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class="language" data-v-3692cf84><ul class="language-switch" data-v-6b1118dd data-v-3692cf84><li aria-label="English" data-v-6b1118dd><span class="language-option current divider" data-v-6b1118dd>English</span></li><li aria-label="Français" data-v-6b1118dd><span role="button" tabindex="0" href="#" lang="fr" class="language-option" data-v-6b1118dd> Français </span></li></ul></div></div></div></div> <div class="container container__modified" data-v-01274b1d>  <div class="row" data-v-01274b1d><div role="complementary" aria-label="table of content" class="column__left" data-v-01274b1d><div class="col journal-container row" data-v-146270e8 data-v-01274b1d><img src="https://static.cambridge.org/covers/BJW_0_0_0/advances-in-psychiatric-treatment.jpg" alt="" class="journal__image" data-v-146270e8> <a href="/core/journals/advances-in-psychiatric-treatment" class="app-link journal__title app-link__text app-link--underlined" data-v-63dfaf6e data-v-146270e8><span class="text" data-v-63dfaf6e>Advances in Psychiatric Treatment </span> </a> <hr aria-hidden="true" class="separator default" data-v-7036083a data-v-146270e8></div>  <div id="toc" class="table-of-content" data-v-01274b1d><h2>Article contents</h2> <div id="toc-list-wrapper" class="table-of-content__wrapper"><ul id="toc-list" class="list"><li class="list__item"><a href="#sec0" class="list__item__link"><span class="toc-title">Abstract</span></a></li> <li class="list__item"><a href="#footnotes-list" class="list__item__link"><span class="toc-title">Footnotes</span></a></li> <li class="list__item"><a href="#references-list" class="list__item__link"><span class="toc-title">References</span></a></li></ul></div></div></div> <div class="column__main" data-v-01274b1d><div class="row" data-v-01274b1d><div class="column__main__left" data-v-01274b1d><div id="maincontent" class="col" data-v-862424e6 data-v-01274b1d> <hgroup data-v-862424e6><h1 data-v-862424e6>Psychotropic medication and the heart</h1> </hgroup>     <div class="row published-date" data-v-862424e6><p data-v-862424e6> Published online by Cambridge University Press: <strong data-v-862424e6>02 January 2018</strong></p></div>   <div class="contributors-details" data-v-99f6eb26 data-v-862424e6><div class="row contributors" data-v-99f6eb26><div class="col" data-v-99f6eb26><div class="row contributor-type" data-v-792406ce data-v-99f6eb26> <div class="contributor-type__contributor" data-v-792406ce><a href="/core/search?filters%5BauthorTerms%5D=Patrick%20O'Brien&eventCode=SE-AU" class="app-link app-link__text app-link--accent" data-v-63dfaf6e data-v-792406ce><span data-v-63dfaf6e>Patrick O'Brien</span> </a>  <span data-v-792406ce> and</span></div><div class="contributor-type__contributor" data-v-792406ce><a href="/core/search?filters%5BauthorTerms%5D=Femi%20Oyebode&eventCode=SE-AU" class="app-link app-link__text app-link--accent" data-v-63dfaf6e data-v-792406ce><span data-v-63dfaf6e>Femi Oyebode</span> </a>  <span 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target="_blank" href="https://s100.copyright.com/AppDispatchServlet?publisherName=CUP&publication=BJW&title=Psychotropic%20medication%20and%20the%20heart&publicationDate=02%20January%202018&author=Patrick%20O'Brien%2C%20Femi%20Oyebode©right=Copyright%20%C2%A9%20The%20Royal%20College%20of%20Psychiatrists%202003%C2%A0&contentID=10.1192%2Fapt.9.6.414&startPage=414&endPage=423&orderBeanReset=True&volumeNum=9&issueNum=6&oa=" data-test-id="buttonRightLink" class="app-link rights-link d-print-none app-link__text-icon app-link--accent" data-v-63dfaf6e data-v-92ee52a2 data-v-43a4d572><img src="/core/page-component/img/rights-icon.d4a677c.svg" alt="" class="app-icon icon rights" data-v-d2c09870 data-v-63dfaf6e><span class="text" data-v-63dfaf6e>Rights & Permissions </span> <span class="sr-only" data-v-63dfaf6e>[Opens in a new window]</span></a></div> <hr aria-hidden="true" class="separator default" data-v-7036083a></div> <div class="share-modal-overlay" style="display:none;" data-v-43a4d572></div> <div data-spy="scroll" data-target="#toc" class="scrollspy-content" data-v-43a4d572> <div id="sec0" class="col article-abstract sec" data-v-2fa8b348 data-v-43a4d572><div class="abstract-text-container" data-v-2fa8b348><div lang="en"><h2>Abstract</h2>  <div class="abstract-content"><div class="abstract" data-abstract-type="normal"><p>Psychotropic literature in recent years has become very concerned with the cardiac safety of certain psychotropic medication. This paper reviews some of the cardiac factors to be considered in the safer selection of psychotropic drugs for the vulnerable patient in everyday clinical practice.</p></div></div> <hr aria-hidden="true" class="abstract-divider separator default" data-v-7036083a></div></div>   </div>    <dl class="article-details" data-v-6e32a161 data-v-43a4d572><div class="row" data-v-6e32a161><dt class="col-12 col-sm-3 col-md-2_5 title" data-v-6e32a161> Type </dt> <dd class="col content" data-v-6e32a161>Research Article</dd></div> <div class="row" data-v-6e32a161><dt class="col-12 col-sm-3 col-md-2_5 title" data-v-6e32a161> Information </dt> <dd class="col content" data-v-6e32a161><div class="content__journal" data-v-6e32a161><a href="/core/journals/advances-in-psychiatric-treatment" class="app-link app-link__text app-link--underlined" data-v-63dfaf6e data-v-6e32a161><span class="text" data-v-63dfaf6e>Advances in Psychiatric Treatment </span> </a> <span data-v-6e32a161> , <a href="/core/journals/advances-in-psychiatric-treatment/volume/050FE53A6848CED1ABBD99CAC40B95B8" class="app-link app-link__text app-link--underlined" data-v-63dfaf6e data-v-6e32a161><span class="text" data-v-63dfaf6e>Volume 9 </span> </a></span> <span data-v-6e32a161> , <a href="/core/journals/advances-in-psychiatric-treatment/issue/6DCE0C6FE2C8429721BFE511F3462431" class="app-link app-link__text app-link--underlined" data-v-63dfaf6e data-v-6e32a161><span class="text" data-v-63dfaf6e>Issue 6 </span> </a></span> <span data-v-6e32a161>, November 2003</span>  <span data-v-6e32a161>, pp. 414 - 423</span> </div> <div class="doi-data" data-v-6e32a161><div data-v-6e32a161>DOI: <a target="_blank" href="https://doi.org/10.1192/apt.9.6.414" class="app-link app-link__text app-link--accent" data-v-63dfaf6e data-v-6e32a161><span class="text" data-v-63dfaf6e>https://doi.org/10.1192/apt.9.6.414 </span> <span class="sr-only" data-v-63dfaf6e>[Opens in a new window]</span></a></div> </div>  </dd></div>   <div class="row" data-v-6e32a161><dt class="col-12 col-sm-3 col-md-2_5 title" data-v-6e32a161> Copyright </dt> <dd class="col content" data-v-6e32a161><div data-v-6e32a161> Copyright © The Royal College of Psychiatrists 2003 </div></dd></div></dl>  <div id="content-container" class="content-container" data-v-43a4d572><div class="content-box"><div class="article research-article JATS"> <div class="body"> <p class="p"> Several studies have demonstrated higher rates of cardiovascular death among psychiatric patients, particularly those with schizophrenia, compared with the general population (<a class="xref bibr" href="#ref33"><span class="show-for-sr">Reference Waddington, Youssef and Kinsella</span>Waddington <em class="italic">et al</em>, 1998</a>). Cardiac risk factors, including smoking, lack of exercise, obesity, substance-misuse and high autonomic arousal during physical restraint, are overrepresented in psychiatric patients. As psychotropic medication is prescribed for this at-risk population, it becomes necessary to consider its cardiovascular effects. Here we focus on antipsychotics and antidepressants, as the cardiac effects of benzodiazepines and other psychotropics are negligible by comparison.</p> <div class="sec"> <h2 class="A"> Heart rate</h2> <p class="p"> Resting heart rate arising from spontaneous depolarisation of the sinoatrial node is largely determined by vagal parasympathetic tone. Respiratory sinus arrhythmia (heart rate increase) during inspiration and decrease on expiration is a physiological occurrence. It decreases with age, reflects heart rate variability and, like baroreceptor reflex sensitivity, is determined by sympathovagal balance but mainly depends on vagal influences on the sinoatrial node.</p> <p class="p"> Psychotropic drugs possessing antimuscarinic and anticholinergic effects (e.g. all low-potency typical antipsychotics; some atypical antipsychotics, particularly clozapine; most tricyclic antidepressants; non-selective monoamine oxidase inhibitors (MAOIs); and all antiParkinsonian anticholinergics) cause sinus tachycardia which, in otherwise healthy individuals, rarely leads to symptoms and usually remits over time. An exception is clozapine-related myocarditis and cardiomyopathy, presenting with a persisting sinus tachycardia and accompanied by fever, chest pain, palpitations, dyspnoea, ankle oedema or heart failure early on in treatment (<a class="xref bibr" href="#ref17"><span class="show-for-sr">Reference Kilian, Kerr and Lawrence</span>Kilian <em class="italic">et al</em>, 1999</a>) (see below).</p> <p class="p"> In contrast, selective serotonin reuptake inhibitors (SSRIs) produce minor degrees of bradycardia that can usefully reduce cardiac workload and benefit the diseased heart. For example, in one study of elderly patients with depression who also had ischaemic heart disease, fluoxetine 20–60 mg/day induced a 6% asymptomatic decrease in heart rate, whereas nortriptyline, regarded as one of the safer tricyclics in heart disease, increased heart rate by 9%, possibly contributing to more adverse cardiac events (sinus tachycardia, severe angina and ventricular ectopics) (<a class="xref bibr" href="#ref26"><span class="show-for-sr">Reference Roose, Glassman and Attia</span>Roose <em class="italic">et al</em>, 1998<em class="italic">a</em> </a>).</p> <p class="p"> Heart rate variability is reduced in medical, psychiatric and psychological conditions such as myocardial infarction, heart failure, heart transplantation, normal ageing, depression, panic disorder, anger, hostility, stress and diabetic autonomic neuropathy, and by the use of full-dose anticholinergic, anticholinergic antipsychotic, and tricyclic antidepressant therapy (<a class="xref bibr" href="#ref14"><span class="show-for-sr">Reference Gorman and Sloan</span>Gorman & Sloan, 2000</a>). Reduced heart rate variability post-myocardial infarction carries a poor prognosis of increased cardiac mortality and sudden death from unopposed sympathetic arrhythmogenic influences (<a class="xref bibr" href="#ref6"><span class="show-for-sr">Reference Bigger, Breithardt and Camm</span>Bigger <em class="italic">et al</em>, 1996</a>). Anticholinergic medications such as imipramine reduce heart rate variability further by decreasing vagal tone in depression and panic disorder, but the non-anticholinergic paroxetine has the opposite effect.</p> <p class="p"> Clozapine, a powerful anticholinergic, reduces heart rate variability in patients with schizophrenia (<a class="xref bibr" href="#ref1"><span class="show-for-sr">Reference Agelink, Majewski and Wurthmann</span>Agelink <em class="italic">et al</em>, 2001</a>). Normal heart rate variability, however, can be restored by switching from clozapine to olanzapine, possibly reflecting olanzapine's more modest anticholinergic actions. (<a class="xref bibr" href="#ref9"><span class="show-for-sr">Reference Cohen, Loewenthal and Matar</span>Cohen <em class="italic">et al</em>, 2001</a>).</p> <p class="p"> After myocardial infarction, heart rate variability is maximally, but not fully, recovered within 6–12 months. It is not known whether any recovery from psychotropic-induced heart rate variability reduction occurs or whether this carries the same dire cardiac prognosis as for post-myocardial infarction patients (<a class="xref bibr" href="#ref6"><span class="show-for-sr">Reference Bigger, Breithardt and Camm</span>Bigger <em class="italic">et al</em>, 1996</a>).</p> <p class="p"> Strategies for increasing heart rate variability would therefore appear desirable, and these include physical exercise, b-blockade and low-dose anti-cholinergic hyoscine hydrobromide (scopolamine) therapy, which paradoxically increases vagal parasympathetic activity (<a class="xref bibr" href="#ref6"><span class="show-for-sr">Reference Bigger, Breithardt and Camm</span>Bigger <em class="italic">et al</em>, 1996</a>). This paradoxical finding might explain the poorer cardiac outcome in patients with chronic schizophrenia who are not co-treated with anticholinergic medication (<a class="xref bibr" href="#ref33"><span class="show-for-sr">Reference Waddington, Youssef and Kinsella</span>Waddington <em class="italic">et al</em>, 1998</a>).</p> </div> <div class="sec"> <h2 class="A"> Conduction</h2> <p class="p"> Impulses arising in the sinoatrial node spread across the atria to the atrioventricular node, bundle of His, right and left bundle branches and the distal portions of the Purkinje fibres. The PR interval measures the atrioventricular conduction time and the QRS measures conduction from the atrioventricular node through the bundle of His, bundle branches, Purkinje fibres and ventricular myocardium. The QRS is further subdivided into two intervals that can be measured by bundle of His electrocardiography. The first interval (normal range 50–120 ms) reflects the time taken for an impulse to traverse the atrioventricular node, and the second (normal range 35–55 ms) is the time taken to travel the bundle of His, bundle branches and Purkinje fibres (<a class="xref bibr" href="#ref7"><span class="show-for-sr">Reference Burrows, Vohra and Hunt</span>Burrows <em class="italic">et al</em>, 1976</a>).</p> <p class="p"> Tricyclic antidepressants delay cardiac conduction mainly by prolonging the second part of the QRS interval without significantly affecting the first. The effect is dose-dependent, occurring at both therapeutic and toxic doses, particularly with amitriptyline, imipramine and nortriptyline, but not doxepin (<a class="xref bibr" href="#ref7"><span class="show-for-sr">Reference Burrows, Vohra and Hunt</span>Burrows <em class="italic">et al</em>, 1976</a>). It also probably occurs with dothiepin, but to a lesser degree with lofepra-mine; the perceived difference for doxepin, however, may simply reflect lower plasma levels. This effect is unlikely to be of clinical relevance in the otherwise normal heart. However, it might precipitate complete heart block in the presence of pre-existing conduction delay such as bundle branch block or second and higher degrees of heart (atrioventricular) block. In addition, emergent ventricular pacemakers, which would normally produce an idioventricular rhythm, may be suppressed by the antiarrhythmic action of the tricyclics, thus causing ventricular asystole. Tricyclic antidepressants are more likely to produce higher degrees of heart block in patients with pre-existing bundle branch block (QRS >12 ms) rather than first-degree block (PR >200 ms) (<a class="xref bibr" href="#ref25"><span class="show-for-sr">Reference Roose, Glassman and Giardina</span>Roose <em class="italic">et al</em>, 1987</a>) and they should therefore be avoided in all cases of conduction disease beyond first-degree block. None the less, tricyclics are best avoided in patients with any degree of pre-existing conduction delay, because safer alternatives are available with SSRIs.</p> <p class="p"> The cardiotoxicity and mortality from overdose of tricyclic antidepressants is well established. Toxicity arises from sodium (Na<sup class="sup">+</sup>) ion-channel blockade, known as Type 1 antiarrhythmic action. This reduces inward Na<sup class="sup">+</sup> depolarising current at the beginning of the action potential, leading to conduction delay, bradycardia, atrioventricular block, bundle branch block and monomorphic ventricular tachycardia.</p> <p class="p"> Brugada syndrome (<a class="xref boxed-text" href="#B1">Box 1</a>), another cardiac Na<sup class="sup">+</sup> channelopathy, first described in 1992, causes idiopathic ventricular fibrillation in structurally normal hearts and sudden unexpected death in about 30% of untreated cases. It is associated with mutation of the SCN5A gene encoding cardiac Na<sup class="sup">+</sup> channels, causing a reduction of inward Na<sup class="sup">+</sup> depolarising currents. Electrocardiogram (ECG) features characteristically include right bundle branch block and S–T segment elevation in chest leads V1–V3, but normal QT interval (<a class="xref fig" href="#F1">Fig. 1</a>). Overdose of a tricyclic antidepressant may present with these features. Brugada syndrome is a leading cause of death in Thai males, typically during sleep; 40% of those with the syndrome have a family history of sudden death. It has an estimated prevalence in certain populations of up to 3%. </p><section><div class="fig" data-magellan-destination="F1" id="F1"> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig1g.jpeg?pub-status=live" class="aop-lazy-load-image graphic" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig1g.jpeg" data-zoomable="true"></div> <div class="caption"><p class="p"> </p><p class="p"><span class="label">Fig. 1</span> <strong>Brugada syndrome: electrocardiogram demonstrates typical findings of right bundle branch block and elevated S–T segment leads V1–V3. Rhythm: 25 mm/s. (reproduced with permission from <a class="xref bibr" href="#ref2"><span class="show-for-sr">Reference Alings and Wilde</span>Alings & Wild, 1999</a>).</strong> </p> </div></div></section> <p class="p"> </p><div class="boxed-text" data-magellan-destination="B1" id="B1"> <div class="caption"> <p class="p"><span class="label">Box 1</span> <strong>Brugada syndrome</strong> </p> </div> <p class="p"> Cause of ventricular fibrillation and sudden unexpected death</p> <p class="p"> Common in young Thai males</p> <p class="p"> 40% of patients have a family history of sudden death</p> <p class="p"> Structurally normal heart</p> <p class="p"> Characteristic ECG changes of right bundle branch block and S–T segment elevation leads V1–V3</p> <p class="p"> Normal QT interval</p> <p class="p"> Associated with mutation of SCN5A gene, blocking Na<sup class="sup">+</sup> channels</p> <p class="p"> Associated with tricyclic antidepressant/neuroleptic toxicity</p> <p class="p"> May present with sudden death/syncope/seizures</p> </div> <p class="p"> Similar appearances have been reported in overdose with tricyclic antidepressants such as amitriptyline and with antipsychotics, but no case was complicated by ventricular arrhythmia and the characteristic ECG pattern disappeared within days. It appears that Na<sup class="sup">+</sup> channel blockers such as the tricyclics and antipsychotics might provoke Brugada syndrome in otherwise asymptomatic but genetically predisposed individuals.</p> <p class="p"> Type 1 action is also shared with the antiarrhythmic agents encainide, flecainide and moracizine, a phenothiazine analogue. The first placebo-controlled trial of ventricular premature contraction suppression in post-myocardial infarction patients was prematurely stopped because of increased mortality in the encainide and flecainide groups (Cardiac Arrhythmia Suppression Trial II Investigators, 1992). The second trial, run by the same team and reported in the same paper, continued with moracizine <em class="italic">v</em>. placebo alone, but this was also abandoned early because of the significant increase in mortality and cardiac arrest in the moracizine group (3% <em class="italic">v</em>. 0.4%). Consequently, tricyclic antidepressants and other agents possessing type 1 actions should be avoided, where possible, in psychiatric patients with ischaemic heart disease.</p> <p class="p"> The available SSRIs, in contrast, do not tend to prolong cardiac conduction, with the possible exception of minor conduction delays and QTc prolongation (see below) in citalopram overdose. Even with amounts more than 100 times the therapeutic dose of citalopram, however, the effects on cardiac conduction are few and non-cardiogenic seizures, rather than adverse cardiac events, are the more likely (<a class="xref bibr" href="#ref11"><span class="show-for-sr">Reference Glassman</span>Glassman, 1998</a>). In cardiac patients with pre-existing bundle branch block (QRS >120 ms), therapeutic doses of fluoxetine did not prolong conduction (<a class="xref bibr" href="#ref26"><span class="show-for-sr">Reference Roose, Glassman and Attia</span>Roose <em class="italic">et al</em>, 1998<em class="italic">a</em> </a>); neither did paroxetine or sertraline in similar cardiac settings (<a class="xref bibr" href="#ref27"><span class="show-for-sr">Reference Roose, Laghrissi-Thode and Kennedy</span>Roose <em class="italic">et al</em>, 1998<em class="italic">b</em> </a>; <a class="xref bibr" href="#ref13"><span class="show-for-sr">Reference Glassman, O'Connor and Califf</span>Glassman <em class="italic">et al</em>, 2002</a>).</p> <p class="p"> Considering their established benefits on heart rate, heart rate variability, cardiac rhythm and platelet function (see below), SSRIs seem a treatment of choice for cardiac patients with anxious depression.</p> <p class="p"> Although antipsychotic medication shares the type 1 antiarrhythmic actions of the tricyclics, by contrast, there is little published evidence that this is clinically significant in therapeutic doses, although in overdose, thioridazine in particular induces greater conduction delay and QRS widening than other typical antipsychotics. None the less, as for tricyclics, it would seem prudent to exercise caution when using such agents in psychiatric patients with a history of ischaemic heart disease or family history of sudden death, especially in view of their proarrhythmic QT-prolonging effects (see below).</p> </div> <div class="sec"> <h2 class="A"> Rhythm</h2> <p class="p"> Psychotropic impact on cardiac rhythm focuses mainly on the propensity of antipsychotics to affect ventricular repolarisation. Such effects include prolongation of the QT interval (a measure of ventricular repolarisation), a known risk factor for torsade de pointes (‘twisting of the points’), a polymorphic ventricular tachycardia classically associated with long QT interval (<a class="xref fig" href="#F2">Fig. 2</a>). </p><section><div class="fig" data-magellan-destination="F2" id="F2"> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig2g.jpeg?pub-status=live" class="aop-lazy-load-image graphic" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig2g.jpeg" data-zoomable="true"></div> <div class="caption"><p class="p"> </p><p class="p"><span class="label">Fig. 2</span> <strong>A short–long–short sequence of beats followed by an episode of torsade de pointes. The QT interval in the sinus beat immediately preceding the torsade de pointes is 600 ms (reproduced with permission from <a class="xref bibr" href="#ref16"><span class="show-for-sr">Reference Khan</span>Khan, 2002</a>).</strong> </p> </div></div></section> <p class="p"> Repolarisation effects induced by antipsychotics, particularly thioridazine and chlorpromazine, have long been recognised in the form of T-wave changes on the ECG. For example, 58% of patients treated with 100–800 mg thioridazine daily showed some type of T-wave changes (<a class="xref bibr" href="#ref35"><span class="show-for-sr">Reference Wendkos</span>Wendkos, 1967</a>). These have been graded into three categories based on direction, amplitude and T-wave structure: grade 1 (T-wave broadening, blunting without loss of amplitude); grade 2 (loss of amplitude and bifid T-wave); grade 3 (flattened/inverted T-wave). All T-wave changes normalised in the majority of phenothiazine-treated patients after overnight fasting alone, and the remainder reverted to normal after oral potassium administration (<a class="xref fig" href="#F3">Fig. 3</a>). Oral administration of isosorbide dinitrate, potassium or ergot alkaloids also reversed thioridazine-induced T-wave changes, but was unsuccessful in reversing T-wave changes arising from cardiac pathology or quinidine therapy. Hence, it has been suggested that some antipsychotic repolarisation effects may be ‘benign’ (<a class="xref bibr" href="#ref35"><span class="show-for-sr">Reference Wendkos</span>Wendkos, 1967</a>) and that not all are necessarily associated with the more serious cardiac consequences reported in more recent literature (<a class="xref bibr" href="#ref24"><span class="show-for-sr">Reference Reilly, Ayis and Jones</span>Reilly <em class="italic">et al</em>, 2000</a>). The impact of fasting, however, illustrates the effects of diet on ECG changes. </p><section><div class="fig" data-magellan-destination="F3" id="F3"> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig3g.jpeg?pub-status=live" class="aop-lazy-load-image graphic" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig3g.jpeg" data-zoomable="true"></div> <div class="caption"><p class="p"> </p><p class="p"><span class="label">Fig. 3</span> <strong>ECG of a phenothiazine-treated patient: complete normalisation of repolarisation abnormalities by overnight fasting. Left panel: initial non-fasting T-wave changes; right panel: T-wave normalisation after overnight fasting (reproduced with permission from <a class="xref bibr" href="#ref3"><span class="show-for-sr">Reference Alvarez-Mena and Frank</span>Alvarez-Mena & Frank, 1973</a>).</strong> </p> </div></div></section> <p class="p"> The QT-prolonging tendency of antipsychotics, which is shared to a lesser extent by tricyclic antidepressants (<a class="xref bibr" href="#ref24"><span class="show-for-sr">Reference Reilly, Ayis and Jones</span>Reilly <em class="italic">et al</em>, 2000</a>), is based on their capacity to block IKr, the delayed rectifier, the principal repolarising current terminating ventricular action potential in phase 2–3 (<a class="xref fig" href="#F4">Fig. 4</a>). Blockade of IKr (encoded by the HERG gene) may cause sufficient QT prolongation to generate extra potentials, known as early after-depolarisations, and to distort phase 3 of normal repolarisation (<a class="xref" href="#F4">Figs 4</a> & <a class="xref" href="#F5">5</a>). Early after-depolarisations may give rise to ventricular premature beats capable of triggering a run of torsade de pointes, especially if these beats distort the preceding T-wave (R-on-T) or conform to a long–short coupling pattern (<a class="xref fig" href="#F6">Fig. 6</a>). The risk of drug-induced torsade de pointes is increased under certain conditions (<a class="xref boxed-text" href="#B2">Boxes 2</a> & <a class="xref boxed-text" href="#B3">3</a>). </p><section><div class="fig" data-magellan-destination="F4" id="F4"> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig4g.jpeg?pub-status=live" class="aop-lazy-load-image graphic" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig4g.jpeg" data-zoomable="false"></div> <div class="caption"><p class="p"> </p><p class="p"><span class="label">Fig. 4</span> <strong>Schematic representation of the action potential and corresponding ECG phases.</strong> </p> </div></div></section> <section><div class="fig" data-magellan-destination="F5" id="F5"> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig5g.jpeg?pub-status=live" class="aop-lazy-load-image graphic" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig5g.jpeg" data-zoomable="true"></div> <div class="caption"><p class="p"> </p><p class="p"><span class="label">Fig. 5</span> <strong>Schematic representation of IKr block on the QT interval: (a) monophasic action potential (upper trace) and corresponding surface ECG (lower trace) before (B) and after (D) exposure to IKr blocking drug and the effect on the QT interval; (b) prolonged QT interval induces two early after-depolarisations (EADs) in the action potential (arrows), thus giving rise to a run of torsade de pointes on the surface ECG (lower trace). Reproduced with permission from <a class="xref bibr" href="#ref30"><span class="show-for-sr">Reference Tamargo</span>Tamargo (2000)</a>.</strong> </p> </div></div></section> <section><div class="fig" data-magellan-destination="F6" id="F6"> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig6g.jpeg?pub-status=live" class="aop-lazy-load-image graphic" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig6g.jpeg" data-zoomable="true"></div> <div class="caption"><p class="p"> </p><p class="p"><span class="label">Fig. 6</span> <strong>ECG demonstrating long–short coupling sequence. A ventricular premature contraction (B) succeeds a sinus beat (A), leading to a compensatory pause (long cycle ∗); another sinus beat (C), followed by a second ventricular premature contraction (D) (short cycle), triggers a run of torsade de pointes. Reproduced with permission from <a class="xref bibr" href="#ref30"><span class="show-for-sr">Reference Tamargo</span>Tamargo (2000)</a>.</strong> </p> </div></div></section> <p class="p"> </p><div class="boxed-text" data-magellan-destination="B2" id="B2"> <div class="caption"> <p class="p"><span class="label">Box 2</span> <strong>Drugs and conditions associated with acquired long QT syndromes</strong> </p> </div> <p class="p"> Antiarrhythmic drugs</p> <p class="p"> Antipsychotics</p> <p class="p"> Antidepressants</p> <p class="p"> Antihistamines</p> <p class="p"> Antimicrobials</p> <p class="p"> Structural heart disease</p> <p class="p"> Bradycardias</p> <p class="p"> Intracranial lesions</p> <p class="p"> Electrolyte abnormalities</p> <p class="p"> Alcoholism</p> <p class="p"> Anorexia nervosa</p> <p class="p"> Hypothyroidism</p> </div> <p class="p"> </p><div class="boxed-text" data-magellan-destination="B3" id="B3"> <div class="caption"> <p class="p"><span class="label">Box 3</span> <strong>Risk of drug-induced torsade de pointes</strong> </p> </div> <p class="p"> Pre-existing QT prolongation</p> <p class="p"> Pre-existing QT dispersion</p> <p class="p"> Hypokalaemia</p> <p class="p"> Hypomagnesaemia</p> <p class="p"> Severe hypocalcaemia</p> <p class="p"> QT-prolonging co-therapy</p> <p class="p"> Sinus bradycardia <50 bpm</p> <p class="p"> Pre-exisiting polymorphic ventricular premature beats showing R-on-T or long–short cycles</p> </div> <p class="p"> Normal QT values are not universally established because so many variables affect measurement. These include gender (longer in females), time of day (longer in sleep and early morning), diet, heart rate (QTc denotes QT corrected for heart rate using Bazett, Friderica or other regression formulae) and lead selection (longer in leads II, V2 and V3). However, a consensus appears to be emerging of a normal QTc upper limit of 450 ms for males and 470 ms for females, with a ‘red zone’ limit of 500 ms for both genders. <a class="xref bibr" href="#ref5"><span class="show-for-sr">Reference Bednar, Harrigan and Anziano</span>Bednar <em class="italic">et al</em> (2001)</a> warn that intervals in excess of these values should raise concern. In a literature review of 116 torsade de pointes cases associated with non-cardiac treatment, they found that 92% had QTc intervals >500 ms.</p> <p class="p"> In terms of QTc change from baseline on treatment, it has likewise been recommended, notwithstanding a tendency for regression towards the mean, that an increase of 30 ms is a potential cause for concern and that a 60 ms increase is a definite cause for concern (<a class="xref bibr" href="#ref5"><span class="show-for-sr">Reference Bednar, Harrigan and Anziano</span>Bednar <em class="italic">et al</em>, 2001</a>). In addition, a QT dispersion of 40–60 ms is considered acceptable, but it is thought to be pathological when it exceeds 100 ms or is 100% increased from baseline values (the QT dispersion is the difference between the longest and shortest QT on a 12-lead ECG, which is widely although not universally regarded as reflecting repolarisation asynchrony across the entire ventricle and another risk factor for torsade de pointes) (<a class="xref bibr" href="#ref5"><span class="show-for-sr">Reference Bednar, Harrigan and Anziano</span>Bednar <em class="italic">et al</em>, 2001</a>).</p> <p class="p"> Antipsychotics differ in their capacity for QT prolongation. <em class="italic">In vitro</em> studies using HERG-transfected cell lines demonstrate a concentration-dependent effect for IKr blocking (<a class="xref table" href="#T1">Table 1</a>). This is consistent with findings from retrospective systematic clinical studies identifying thioridazine and the tricyclic antidepressants as predictive of QT prolongation (<a class="xref bibr" href="#ref24"><span class="show-for-sr">Reference Reilly, Ayis and Jones</span>Reilly <em class="italic">et al</em>, 2000</a>). </p><div class="table-wrap" data-magellan-destination="T1" id="T1"> <div class="caption"> <p class="p"><span class="label">Table 1</span> <strong>Drug concentrations for blocking HERG tail-currents (IKr) in HERG-transfected cell lines</strong> </p> </div> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tab1.gif?pub-status=live" class="aop-lazy-load-image graphic" width="415" height="159" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tab1.gif" data-zoomable="false"></div> <table class="table no-colsep no-rowsep"> <colgroup class="colgroup"> <col class="col"> <col class="col"> </colgroup> <thead> <tr class="tr rowsep"> <th class="th bottom left" colspan="1" rowspan="1"> <em class="italic">Drug</em> </th> <th class="th bottom left" colspan="1" rowspan="1"> <em class="italic">Potency (in descending order)</em> </th> </tr> </thead> <tbody class="tbody top"> <tr class="tr"> <td class="td bottom left" colspan="1" rowspan="1">Sertindole<sup class="sup">1</sup> </td> <td class="td bottom left" colspan="1" rowspan="1">2.9 nM</td> </tr> <tr class="tr"> <td class="td bottom left" colspan="1" rowspan="1">Haloperidol<sup class="sup">1</sup> </td> <td class="td bottom left" colspan="1" rowspan="1">1.0 μM</td> </tr> <tr class="tr"> <td class="td bottom left" colspan="1" rowspan="1">Thioridazine<sup class="sup">2</sup> </td> <td class="td bottom left" colspan="1" rowspan="1">1.07± 0.06 μM</td> </tr> <tr class="tr"> <td class="td bottom left" colspan="1" rowspan="1">Chlorpromazine<sup class="sup">2</sup> </td> <td class="td bottom left" colspan="1" rowspan="1">1.47±0.03 μM</td> </tr> <tr class="tr"> <td class="td bottom left" colspan="1" rowspan="1">Clozapine<sup class="sup">2</sup> </td> <td class="td bottom left" colspan="1" rowspan="1">2.63±0.12 μM</td> </tr> <tr class="tr rowsep"> <td class="td bottom left" colspan="1" rowspan="1">Amitriptyline<sup class="sup">2</sup> </td> <td class="td bottom left" colspan="1" rowspan="1">10.0±1.1 μM</td> </tr> </tbody> </table> </div> <p class="p"> The prevalence of torsade de pointes in the psychiatric population is unknown, but estimates from antiarrhythmic-induced torsade de pointes in the cardiac population ranges from 3% to 15%. Being associated with entirely non-specific symptoms such as palpitations, dizziness, syncope and seizures, its potential seriousness may be easily misconstrued as primary psychiatric disorder: this can have fatal outcome. Although usually self-limiting, torsade de pointes tends to recur and in 31% of cases progresses to ventricular fibrillation and sudden death.</p> <p class="p"> These QT-prolonging proarrhythmic concerns led to the placing of prescribing restrictions on thioridazine, a voluntary withdrawal of droperidol in the UK by its manufacturer and a complete withdrawal of sertindole from the European market. They have also shifted the cardiac focus onto other increasingly prescribed atypical antipsychotics. For example, after some initial concern the US Food and Drugs Administration requested Study 054 (<a class="xref bibr" href="#ref22">Psychopharmacological Drugs Advisory Committee, 2000</a>) to further clarify the QT-prolonging capacity of ziprasidone and to compare it with olanzapine, risperidone, quetiapine, thioridazine and haloperidol in an open-label randomised 4-week trial involving 183 patients with psychosis. The mean QTc change from baseline was 10 ms greater with ziprasidone than with olanzapine, risperidone and quetiapine, and 10 ms less than with thioridazine; haloperidol demonstrated the least change and all agents showed a dose-dependent effect. Ziprasidone was subsequently licensed for use in the USA, and although a black-box warning was avoided, a bold-type warning of its QT-prolonging capacity was included.</p> <p class="p"> Additional risks factors for QT-prolongation and torsade de pointes in the psychiatric population include deliberate or accidental antipsychotic overdose, effects of concomitant QT-prolonging medication (either indirect such as CYP 450 3A3 and 3A4 inhibitors, fluoxetine, fluvoxamine, grapefruit juice and ketoconazole, or direct such as tricyclic antidepressants, antihistamines and anti-infectives), comorbid substance misuse and, in particular, the effects of high sympathetic arousal during restraint. Such arousal releases large amounts of circulating catecholamines which, in addition to increasing cardiac oxygen consumption, lower serum levels by β-2 adrenergic stimulation of potassium (K<sup class="sup">+</sup>) uptake into skeletal muscle cells. <a class="xref bibr" href="#ref15"><span class="show-for-sr">Reference Hatta, Takahashi and Nakamura</span>Hatta <em class="italic">et al</em> (1999)</a> found a significant negative correlation between serum K<sup class="sup">+</sup> and high <em class="italic">v</em>. low levels of psychotic agitation in acute in-patients (3.59 <em class="italic">v</em>. 3.79 mEq/l), and lower serum K<sup class="sup">+</sup> in more agitated acute in-patients compared with out-patients. Thus, in a control and restraint situation, the QT-prolonging effects of hypokalaemia and intramuscular antipsychotics, together with the potential for hypoxia and myocardial irritability from inadvertent ventilatory embarrassment and greater cardiac strain, may result in the kind of potent proarrhythmic cocktail that prompted the Collge to warn that ‘the risk of sudden cardiotoxic collapse in response to antipsychotic medication given during a period of high physiological arousal should be widely publicised’(<a class="xref bibr" href="#ref28">Royal College of Psychiatrists, 1997</a>).</p> </div> <div class="sec"> <h2 class="A"> Coronary artery disease</h2> <p class="p"> Major and minor depression have an important relationship with coronary artery disease. Many studies have demonstrated a strong association between depression and coronary artery disease: there is increased incidence of the disease in patients with depression who have an otherwise healthy heart, and exacerbation of existing coronary artery disease and cardiac mortality in the 15–20% of post-infarction patients who develop major, and even minor, depression. Even sub-syndromal depressive symptoms therefore increase cardiac risk in coronary artery disease (<a class="xref bibr" href="#ref23"><span class="show-for-sr">Reference Penninx, Beekman and Honig</span>Penninx <em class="italic">et al</em>, 2001</a>). This strong association persists even after controlling for established cardiac risk factors such as smoking and diabetes.</p> <p class="p"> Panic disorder and phobic anxiety states are also associated with increased rates of coronary artery disease and cardiac mortality, possibly mediated by coronary artery spasm and sympathetic-mediated cardiac arrhythmias, but the association is less well studied and documented (<a class="xref bibr" href="#ref19"><span class="show-for-sr">Reference Mansour, Wilkinson and Jennings</span>Mansour <em class="italic">et al</em>, 1998</a>). Serotonin (5-HT) activity represents one possible link between depression, anxiety and coronary artery disease. Activated platelets, apart from platelet factor-4 (PF-4) and b-thromboglobulin (b-TG), release large quantities of serotonin. This has two main effects: first, it causes vasodilation in normal, but vasoconstriction in diseased, coronary vessels; and second, it promotes endothelial vessel dysfunction, with local further platelet activation and endothelial smooth-muscle proliferation, potentially responsible for local atherogenesis.</p> <p class="p"> Levels of PF-4 and b-TG can be assayed, and are higher in patients with coronary artery disease who have depression than in similar patients without depression and in healthy controls (<a class="xref bibr" href="#ref18"><span class="show-for-sr">Reference Laghrissi-Thode, Wagner and Pollock</span>Laghrissi-Thode <em class="italic">et al</em>, 1997</a>).</p> <p class="p"> Because increased platelet activation may thus contribute to atherogenesis, coronary artery disease and sudden death, attempts to reduce platelet activity in 'coronary-prone’ individuals with depression or anxiety may become an important aspect of cardiac risk reduction, especially since aspirin therapy alone does not appear to reduce platelet activity in this population (<a class="xref bibr" href="#ref18"><span class="show-for-sr">Reference Laghrissi-Thode, Wagner and Pollock</span>Laghrissi-Thode <em class="italic">et al</em>, 1997</a>).</p> <p class="p"> Paroxetine appears to be a promising agent in this regard. <a class="xref bibr" href="#ref21"><span class="show-for-sr">Reference Musselman, Marzec and Manatunga</span>Musselman <em class="italic">et al</em> (2000)</a> report a study of 15 patients with depression who showed no evidence of coronary artery disease, although some did have known risk factors for the disease. At the start of the study, all had elevated PF-4 levels. After receiving 20 mg paroxetine daily for 6 weeks, a significant reduction in these levels was observed in both those with and without known risk factors for coronary artery disease. Roose and colleagues found further evidence supporting the use of paroxetine in co-morbid depression or anxiety and coronary artery disease. They compared paroxetine 20–30 mg daily with therapeutic doses of nortriptyline in 81 patients with coronary artery disease and depression. Despite equal antidepressant efficacy after 6 weeks’ treatment, paroxetine had more benefit on cardiac function, including heart rate, heart rate variability, rhythm and adverse cardiac events (<a class="xref bibr" href="#ref27"><span class="show-for-sr">Reference Roose, Laghrissi-Thode and Kennedy</span>Roose <em class="italic">et al</em>, 1998<em class="italic">b</em> </a>).</p> <p class="p"> The best evidence to date for antidepressant intervention in this patient group has come from the Sertraline Antidepressant Heart Attack Randomised Trial (SADHART; <a class="xref bibr" href="#ref13"><span class="show-for-sr">Reference Glassman, O'Connor and Califf</span>Glassman <em class="italic">et al</em>, 2002</a>). A study of 369 patients recently discharged following acute myocardial infarction or unstable angina, who were randomised to sertraline 50–200 mg/day or to placebo, demonstrated treatment safety and efficacy of the antidepressant over placebo.</p> <p class="p"> The safety and benefits of SSRIs, especially paroxetine and fluoxetine, over tricyclic antidepressants on general cardiac function, platelet coagulability and, possibly, atherogenesis appears to recommend their use as psychotropics of first choice in patients with, or at high risk of, coronary artery disease, especially smokers, postmenopausal women and patients with hypertension, diabetes, hyperlipidaemia and/or a strong family history of coronary artery disease.</p> </div> <div class="sec"> <h2 class="A"> Contractility and effects on cardiac muscle</h2> <p class="p"> Radionuclide ventriculography has demonstrated, contrary to original concerns, that psychotropic drugs do not exert a direct negative inotropic effect (<a class="xref bibr" href="#ref26"><span class="show-for-sr">Reference Roose, Glassman and Attia</span>Roose <em class="italic">et al</em>, 1998<em class="italic">a</em> </a>). However, antipsychotics (clozapine in particular) are occasionally associated with an increased risk of myocarditis or cardiomyopathy (<a class="xref bibr" href="#ref17"><span class="show-for-sr">Reference Kilian, Kerr and Lawrence</span>Kilian <em class="italic">et al</em>, 1999</a>). Kilian and colleagues reported 15 cases of myocarditis and 8 of dilated cardiomyopathy at normal daily doses (100–725 mg clozapine) in 8000 Australian patients. All but 3 were male, with a mean age of 36. The myocarditis occurred in the first month of treatment (often from hypersensitive eosinophilic myocarditis), had few specific symptoms and frequently presented with sudden death. Cardiomyopathy developed more slowly, within the first 12 months, usually presented with cough, dyspnoea, palpitations or heart failure, could improve on clozapine discontinuation and appeared to have a better prognosis. These and other reports have led to increased warnings of these cardiac complications in information on prescribing and of the need for early investigation and clozapine cessation in suspect cases.</p> <p class="p"> As eosinophilic myocarditis seems to be the favoured aetiology, blood eosinophilia should be carefully sought. However, a raised plasma level of eosinophil cationic protein, an assayable pro-inflammatory protein released from degranulated eosinophils, seems a preferable marker as it remains elevated even in cases with normal eosinophil counts (<a class="xref bibr" href="#ref4"><span class="show-for-sr">Reference Arima, Kanoh and Kawano</span>Arima <em class="italic">et al</em>, 2002</a>).</p> </div> <div class="sec"> <h2 class="A"> Blood pressure</h2> <p class="p"> Postural (orthostatic) hypotension has many causes but is probably the most common and potentially most troublesome psychotropic side-effect (<a class="xref boxed-text" href="#B4">Box 4</a>). Usually defined as a ≥20 mmHg reduction in systolic blood pressure after 1–3 minutes of standing upright, it may cause symptomatic underperfusion of vital organs, leading to dizziness, blurred vision, fainting, falls, fractures, seizures, strokes and cardiac ischaemia, especially in elderly people. Fainting usually occurs when mean arterial pressure (diastolic plus 1/3 pulse pressure) drops to 70 mmHg or below, corresponding to an upper-arm blood pressure of 90/60 or less.</p> <p class="p"> </p><div class="boxed-text" data-magellan-destination="B4" id="B4"> <div class="caption"> <p class="p"><span class="label">Box 4</span> <strong>Causes of postural hypotension (after <a class="xref bibr" href="#ref10"><span class="show-for-sr">Reference Engstrom and Aminoff</span>Engstrom & Aminoff,1997</a>, with permission)</strong> </p> </div> <p class="p"> <em class="italic">Cardiac pump failure</em> </p> <p class="p"> Myocardial infarction</p> <p class="p"> Myocarditis</p> <p class="p"> Constrictive pericarditis</p> <p class="p"> Aortic stenosis</p> <p class="p"> Tachy- or bradyarrhythmias</p> <p class="p"> <em class="italic">Venous pooling</em> </p> <p class="p"> Alcohol</p> <p class="p"> Postprandial dilatation of splanchnic vessel beds</p> <p class="p"> Vigorous exercise with dilatation of skeletal vessel beds</p> <p class="p"> Hot baths/showers/fever/weather</p> <p class="p"> Prolonged recumbency or standing</p> <p class="p"> <em class="italic">Reduced intravascular volume</em> </p> <p class="p"> Straining-toilet/coughing/lifting</p> <p class="p"> Dehydration/vomiting/diarrhoea</p> <p class="p"> Haemorrhage/burns</p> <p class="p"> Salt-losing nephropathy</p> <p class="p"> Adrenal insufficiency</p> <p class="p"> Diabetes insipidus</p> <p class="p"> <em class="italic">Other causes</em> </p> <p class="p"> Shy–Drager syndrome</p> <p class="p"> Diabetic neuropathy</p> <p class="p"> Alcoholic neuropathy</p> <p class="p"> Porphyria</p> <p class="p"> Anorexia nervosa</p> <p class="p"> Riley–Day syndrome</p> <p class="p"> Chronic fatigue syndrome</p> <p class="p"> <em class="italic">Medications</em> </p> <p class="p"> Antihypertensives</p> <p class="p"> Diuretics/disulfiram</p> <p class="p"> Vasodilators</p> <p class="p"> Alpha- and beta-blockers</p> <p class="p"> Barbiturates/opiates</p> <p class="p"> Neuroleptics/tricyclics/MAOIs</p> </div> <p class="p"> Clinical studies of tricyclic antidepressants focusing mainly on imipramine and nortriptyline found a 20% prevalence of postural hypotension in treated patients. Non-standardised methodology may account for some conflicting findings, but the data suggest, first, a greater tendency to postural hypotension for tertiary tricyclics (e.g. imipramine and amitriptyline) than for secondary (e.g. nor-triptyline); second, that the degree of pretreatment postural blood pressure drop predicts on-treatment symptoms and when this pretreatment orthostatic hypotension was controlled for, removed age by itself as a predictor of postural drop; and third, that (counterintuitively) dose reduction may not relieve symptoms (<a class="xref bibr" href="#ref12"><span class="show-for-sr">Reference Glassman, Bigger and Giardina</span>Glassman <em class="italic">et al</em>, 1979</a>).</p> <p class="p"> There are fewer studies of MAOIs, for which the hypotensive mechanism remains elusive. In patients with depression, phenelzine 60 mg daily induced both a fall in supine systolic blood pressure and a postural drop. In 14% of patients, the latter caused significant symptoms, which reached a maximum after 4 weeks’ treatment. This contrasts with findings for imipramine, where supine blood pressure remained unaffected but the postural effect tended to maximise after 1 week. However, these results might be related to an early rapid dose escalation. Isocarboxazid and tranylcypromine are likewise associated with an 11% and 17% prevalence of symptomatic postural hypotension respectively (<a class="xref bibr" href="#ref34"><span class="show-for-sr">Reference Warrington, Padgham and Lader</span>Warrington <em class="italic">et al</em>, 1989</a>).</p> <p class="p"> Postural hypotension is a well-documented effect of typical antipsychotics, but few systematic studies exist. In a study of 196 chronic in-patients with schizophrenia on stable antipsychotic treatment, symptomatic postural hypotension occurred in 77% within 1 minute, reducing to 17% after 3 minutes, on standing from supine. No other correlation with age, dose or potency of α<sub>1</sub>-adrenergic blocking drug emerged, although thioridazine was associated with greater postural blood pressure drop (<a class="xref bibr" href="#ref29"><span class="show-for-sr">Reference Silver, Kogan and Zlotogorski</span>Silver <em class="italic">et al</em>, 1990</a>).</p> <p class="p"> Atypical antipsychotics pose much less of a problem (with the possible exception of clozapine, where α<sub>1</sub>-adrenergic blockade is generally assumed to be responsible; it tends to occur early in treatment, particularly with rapid dose escalation, but tolerance usually builds up).</p> <p class="p"> Care is needed when co-prescribing psychotropics and antihypertensives. Antipsychotics may, like tricyclics, antagonise centrally acting drugs such as clonidine and methyldopa. These are infrequently used as antihypertensives, but clonidine is popular in psychiatric practice for acute opiate detoxification. However, co-prescribing antipsychotics, especially low-potency typicals such as chlorpro-mazine or the atypicals clozapine or quetiapine, with any of the following may provoke profound postural hypotension: α<sub>1</sub>-adrenergic antagonists (e.g. doxazosin, which is also a treatment for benign prostatic hypertrophy); calcium-channel blockers (e.g. nifedipine); angiotensin-converting enzyme inhibitors (captopril); angiotensin-II receptor antagonists (losartan); or vasodilators (e.g. nitro-prusside). Postural hypotension is also a risk when antipsychotics are taken with β-blockers (probably because of pharmacokinetic interaction) or with diuretics (because of Na<sup class="sup">+</sup> or volume depletion). The same hypotensive effects might be anticipated when tricyclic antidepressants or MAOIs are co-prescribed with peripheral antihypertensive agonists. One possible exception concerns phenelzine, whose hypotensive action was reversed on co-therapy with atenolol (<a class="xref bibr" href="#ref20"><span class="show-for-sr">Reference Merikangas and Merikangas</span>Merikangas & Merikangas, 1995</a>).</p> <p class="p"> Symptomatic postural hypotension is associated with dizziness, blurred vision, syncope, falls and injuries, seizures and myocardial infarction. Effective management should therefore address prevention as well as specific therapy. Patient counselling is the most important aspect of prevention (<a class="xref boxed-text" href="#B5">Box 5</a>). Extra vigilance in older people and patients who are dehydrated or have diabetes or hypertension on treatment is essential.</p> <p class="p"> </p><div class="boxed-text" data-magellan-destination="B5" id="B5"> <div class="caption"> <p class="p"><span class="label">Box 5</span> <strong>Prevention of postural hypotension</strong> </p> </div> <p class="p"> Avoid prolonged standing</p> <p class="p"> Adopt slow, careful posture changes when rising from bed or chair after prolonged rest</p> <p class="p"> Ascend and descend stairs on your bottom</p> <p class="p"> Sit, do not stand, in hot water</p> <p class="p"> Be careful getting out of a hot bath</p> <p class="p"> Be careful in hot environments</p> <p class="p"> Make a tight fist before standing (isometric handgrip exercises have a pressor effect)</p> <p class="p"> Drink cold and caffeinated drinks</p> <p class="p"> Ensure copious fluid intake</p> <p class="p"> Ensure adequate salt intake</p> <p class="p"> Eat frequent but small meals</p> <p class="p"> Avoid alcohol</p> <p class="p"> Avoid vigorous exercise</p> <p class="p"> Wear support stockings</p> <p class="p"> Sleep with the bed head raised by 15–30 cm (a 30° tilt minimises nocturnal diuresis)</p> </div> <p class="p"> In addition to the simple measures shown in <a class="xref boxed-text" href="#B5">Box 5</a>, fludrocortisone therapy might also be necessary. This acts by increasing arteriolar sensitivity to noradrenalin and, in bigger doses, by expanding plasma volume. Doses begin at 50 μg daily, increased by 50 μg increments to a maximum of 300 μg, according to response and level of hypotensive symptoms. The drug can usually be withdrawn after the early weeks of psychotropic treatment, as accomodation to the hypotensive effect usually develops. Fludrocortisone side-effects include fluid overload and heart failure, hypokalaemia and supine hypertension.</p> </div> <div class="sec"> <h2 class="A"> Conclusion</h2> <p class="p"> On the basis of the literature referenced in this paper, it could be argued that all mental health units have ready access to ECG monitoring equipment. Modern machines provide an automated printout that can be of great assistance to the psychiatrist in ECG interpretation, but in cases of doubtful validity, cardiology colleagues are usually most helpful in providing manual interpretation. Clinicians with a particular interest in this field may wish to conduct ECG studies in a greater proportion of their patients or pursue more complex studies involving heart rate variability, which would probably involve collaboration with cardiology services anyway .</p> <p class="p"> Patients already at higher risk of cardiac complications will continue to be closely monitored. The difficulties of widespread monitoring of the psychiatric population, apart from practical considerations, would appear too considerable to justify at present, and cardiologists or other psychiatrists with particular knowledge of the field have not thus far endorsed its introduction.</p> <p class="p"> Monitoring of pulse and blood pressure ought to remain essential components of the psychiatric examination. It could also be argued that psychiatric in-patients perceived to be at greater risk for QTc prolongation might receive more careful monitoring to minimise known risks (especially low serum K<sup class="sup">+</sup> and Mg<sup class="sup">2+</sup>) and have their levels maintained well into the normal range (serum K<sup class="sup">+</sup> > 3.8 mmol/l) by a diet rich in potassium and magnesium or, if necessary, by oral supplementation.</p> <p class="p"> Furthermore, control and restraint procedures for disturbed patients must be careful to avoid any restriction of chest or diaphragmatic ventilation, which might add to any pre-existing cardiac risk. If rapid tranquillisation becomes necessary, and if time and circumstances allow, intramuscular benzo-diazepines (which have negligible cardiotropic effects) could be administered initially, to be followed with an intramuscular antipsychotic given soon after, when the patient has begun to settle.</p> <p class="p"> Finally, as there is a possible association with myocarditis and cardiomyopathy, any patients commencing on clozapine could be considered for pre-treatment baseline ECG, chest X-ray, eosinophil counts and eosinophil cationic protein level, repeated as necessary. Subsequent comparison with baseline would help appropriate interpretation of treatment-emergent changes.</p> </div> <div class="sec"> <h2 class="A"> Multiple choice questions</h2> <p class="p"> </p><ol class="list number nomark"> <li class="list-item"> <p class="p"><span class="label">1</span> <strong>Torsade de pointes:</strong> </p> <p class="p"> <ol class="list number nomark"> <li class="list-item"> <p class="p"><span class="label">a</span> is a variety of French perfume</p> </li> <li class="list-item"> <p class="p"><span class="label">b</span> is a polymorphic ventricular tachycardia</p> </li> <li class="list-item"> <p class="p"><span class="label">c</span> is associated with sudden death</p> </li> <li class="list-item"> <p class="p"><span class="label">d</span> is more likely to occur with hypokalaemia</p> </li> <li class="list-item"> <p class="p"><span class="label">e</span> is associated with long–short coupling on the ECG.</p> </li> </ol> </p> </li> <li class="list-item"> <p class="p"><span class="label">2</span> <strong>A prolonged QT interval:</strong> </p> <p class="p"> <ol class="list number nomark"> <li class="list-item"> <p class="p"><span class="label">a</span> is associated with torsade de pointes</p> </li> <li class="list-item"> <p class="p"><span class="label">b</span> may be congenital or acquired</p> </li> <li class="list-item"> <p class="p"><span class="label">c</span> is associated with antipsychotic medication</p> </li> <li class="list-item"> <p class="p"><span class="label">d</span> is more common in women</p> </li> <li class="list-item"> <p class="p"><span class="label">e</span> is associated with HERG/IKR blockade.</p> </li> </ol> </p> </li> <li class="list-item"> <p class="p"><span class="label">3</span> <strong>Myocardial infarction:</strong> </p> <p class="p"> <ol class="list number nomark"> <li class="list-item"> <p class="p"><span class="label">a</span> has a higher incidence in patients with depression who have no cardiac disease</p> </li> <li class="list-item"> <p class="p"><span class="label">b</span> may present with postural hypotension</p> </li> <li class="list-item"> <p class="p"><span class="label">c</span> may be associated with prolonged QT interval</p> </li> <li class="list-item"> <p class="p"><span class="label">d</span> is associated with increased platelet reactivity</p> </li> <li class="list-item"> <p class="p"><span class="label">e</span> is associated with sudden death when complicated by reduced heart rate variability.</p> </li> </ol> </p> </li> <li class="list-item"> <p class="p"><span class="label">4</span> <strong>Tricyclic antidepressants:</strong> </p> <p class="p"> <ol class="list number nomark"> <li class="list-item"> <p class="p"><span class="label">a</span> are type 1 antiarrhythmic agents</p> </li> <li class="list-item"> <p class="p"><span class="label">b</span> block sodium and potassium cardiac channels</p> </li> <li class="list-item"> <p class="p"><span class="label">c</span> are contraindicated in post-myocardial infarction depression</p> </li> <li class="list-item"> <p class="p"><span class="label">d</span> decrease heart rate variability</p> </li> <li class="list-item"> <p class="p"><span class="label">e</span> are a safe treatment for depression in the presence of bundle branch block.</p> </li> </ol> </p> </li> <li class="list-item"> <p class="p"><span class="label">5</span> <strong>Postural hypotension:</strong> </p> <p class="p"> <ol class="list number nomark"> <li class="list-item"> <p class="p"><span class="label">a</span> is a rare complication of psychotropic drug treatment</p> </li> <li class="list-item"> <p class="p"><span class="label">b</span> may be a manifestation of myocarditis</p> </li> <li class="list-item"> <p class="p"><span class="label">c</span> may present with falls, fits or faints</p> </li> <li class="list-item"> <p class="p"><span class="label">d</span> is usually detectable on clinical examination</p> </li> <li class="list-item"> <p class="p"><span class="label">e</span> is more frequent with SSRI than with tricyclic antidepressant therapy.</p> </li> </ol> </p> </li> </ol> </div> <div class="sec"> <h2 class="A"> </h2> <p class="p"> </p><div class="table-wrap" data-magellan-destination="T2" id="T2"> <div class="caption"> <p class="p"> <strong>MCQ answers</strong> </p> </div> <div class="figure-thumb"><img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tabU2.gif?pub-status=live" class="aop-lazy-load-image graphic" width="348" height="126" data-original-image="urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tabU2.gif" data-zoomable="false"></div> <table class="table no-colsep no-rowsep"> <colgroup class="colgroup"> <col class="col"> <col class="col"> <col class="col"> 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colspan="1" rowspan="1">a</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">F</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">a</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">a</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">a</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">a</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">F</td> </tr> <tr class="tr"> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">b</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">b</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">b</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">b</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">b</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> </tr> <tr class="tr"> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">c</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">c</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">c</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">c</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">c</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> </tr> <tr class="tr"> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">d</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">d</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">d</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">d</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">d</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> </tr> <tr class="tr"> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">e</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">e</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">e</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">T</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">e</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">F</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">e</td> <td class="td top no-colsep no-rowsep left" colspan="1" rowspan="1">F</td> </tr> </tbody> </table> </div> </div> </div> <div class="back"> </div> </div></div> <hr aria-hidden="true" class="list-divider separator default" data-v-7036083a> <div id="footnotes-list" class="circle-list"><h2>Footnotes</h2> <div data-type="fulltextNote" id="FN1" class="circle-list__item"> <div class="circle-list__item__indicator"></div> <div class="circle-list__item__grouped"><div class="circle-list__item__grouped__content"> <p class="p"><span class="label">*</span> denotes recommended reading.</p> </div></div></div></div> <hr aria-hidden="true" class="list-divider separator default" data-v-7036083a> <div id="references-list" class="circle-list"><h2>References</h2> <div id="manual_ref-1" aria-flowto="reference-1-content reference-1-button" class="circle-list__item"> <div class="circle-list__item__indicator"></div> <div aria-hidden="true" data-test-hidden="true" class="circle-list__item__number"> </div> <div class="circle-list__item__grouped"><div id="reference-1-content" class="circle-list__item__grouped__content"><span class="name"><span class="surname">Agelink</span>, <span class="given-names">M. 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Rhythm: 25 mm/s. (reproduced with permission from Alings & Wild, 1999).</span></span></span></p></div> </div></div> <hr aria-hidden="true" class="separator dashed" data-v-7036083a data-v-241a4b23></div><div data-v-241a4b23><div class="figures__item" data-v-241a4b23><div class="figures__item__image-box" data-v-241a4b23><button class="figures__ref" data-v-241a4b23> View in content </button> <img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" alt="Figure 1" data-zoomable="true" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig2g.jpeg" data-enlarged-image="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig2g.jpeg" class="graphic" data-v-241a4b23></div> <div data-v-241a4b23><div class="caption" data-v-241a4b23><p data-v-241a4b23><span class="label" data-v-241a4b23>Fig. 2</span> <span data-v-241a4b23><span class="p"><span class="bold">A short–long–short sequence of beats followed by an episode of torsade de pointes. The QT interval in the sinus beat immediately preceding the torsade de pointes is 600 ms (reproduced with permission from Khan, 2002).</span></span></span></p></div> </div></div> <hr aria-hidden="true" class="separator dashed" data-v-7036083a data-v-241a4b23></div><div data-v-241a4b23><div class="figures__item" data-v-241a4b23><div class="figures__item__image-box" data-v-241a4b23><button class="figures__ref" data-v-241a4b23> View in content </button> <img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" alt="Figure 2" data-zoomable="true" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig3g.jpeg" data-enlarged-image="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig3g.jpeg" class="graphic" data-v-241a4b23></div> <div data-v-241a4b23><div class="caption" data-v-241a4b23><p data-v-241a4b23><span class="label" data-v-241a4b23>Fig. 3</span> <span data-v-241a4b23><span class="p"><span class="bold">ECG of a phenothiazine-treated patient: complete normalisation of repolarisation abnormalities by overnight fasting. Left panel: initial non-fasting T-wave changes; right panel: T-wave normalisation after overnight fasting (reproduced with permission from Alvarez-Mena & Frank, 1973).</span></span></span></p></div> </div></div> <hr aria-hidden="true" class="separator dashed" data-v-7036083a data-v-241a4b23></div><div data-v-241a4b23><div class="figures__item" data-v-241a4b23><div class="figures__item__image-box" data-v-241a4b23><button class="figures__ref" data-v-241a4b23> View in content </button> <img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" alt="Figure 3" data-zoomable="true" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig4g.jpeg" data-enlarged-image="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig4g.jpeg" class="graphic" data-v-241a4b23></div> <div data-v-241a4b23><div class="caption" data-v-241a4b23><p data-v-241a4b23><span class="label" data-v-241a4b23>Fig. 4</span> <span data-v-241a4b23><span class="p"><span class="bold">Schematic representation of the action potential and corresponding ECG phases.</span></span></span></p></div> </div></div> <hr aria-hidden="true" class="separator dashed" data-v-7036083a data-v-241a4b23></div><div data-v-241a4b23><div class="figures__item" data-v-241a4b23><div class="figures__item__image-box" data-v-241a4b23><button class="figures__ref" data-v-241a4b23> View in content </button> <img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" alt="Figure 4" data-zoomable="true" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig5g.jpeg" data-enlarged-image="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig5g.jpeg" class="graphic" data-v-241a4b23></div> <div data-v-241a4b23><div class="caption" data-v-241a4b23><p data-v-241a4b23><span class="label" data-v-241a4b23>Fig. 5</span> <span data-v-241a4b23><span class="p"><span class="bold">Schematic representation of IKr block on the QT interval: (a) monophasic action potential (upper trace) and corresponding surface ECG (lower trace) before (B) and after (D) exposure to IKr blocking drug and the effect on the QT interval; (b) prolonged QT interval induces two early after-depolarisations (EADs) in the action potential (arrows), thus giving rise to a run of torsade de pointes on the surface ECG (lower trace). Reproduced with permission from Tamargo (2000).</span></span></span></p></div> </div></div> <hr aria-hidden="true" class="separator dashed" data-v-7036083a data-v-241a4b23></div><div data-v-241a4b23><div class="figures__item" data-v-241a4b23><div class="figures__item__image-box" data-v-241a4b23><button class="figures__ref" data-v-241a4b23> View in content </button> <img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" alt="Figure 5" data-zoomable="true" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig6g.jpeg" data-enlarged-image="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig6g.jpeg" class="graphic" data-v-241a4b23></div> <div data-v-241a4b23><div class="caption" data-v-241a4b23><p data-v-241a4b23><span class="label" data-v-241a4b23>Fig. 6</span> <span data-v-241a4b23><span class="p"><span class="bold">ECG demonstrating long–short coupling sequence. A ventricular premature contraction (B) succeeds a sinus beat (A), leading to a compensatory pause (long cycle ∗); another sinus beat (C), followed by a second ventricular premature contraction (D) (short cycle), triggers a run of torsade de pointes. Reproduced with permission from Tamargo (2000).</span></span></span></p></div> </div></div> <hr aria-hidden="true" class="separator dashed" data-v-7036083a data-v-241a4b23></div><div data-v-241a4b23><div class="figures__item" data-v-241a4b23><div class="figures__item__image-box" data-v-241a4b23><button class="figures__ref" data-v-241a4b23> View in content </button> <img src="data:image/gif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==" alt="Figure 6" data-zoomable="true" data-src="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tab1.gif" data-enlarged-image="https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tab1.gif" class="graphic" data-v-241a4b23></div> <div data-v-241a4b23><div class="caption" data-v-241a4b23><p data-v-241a4b23><span class="label" data-v-241a4b23>Table 1</span> <span data-v-241a4b23><span class="p"><span class="bold">Drug concentrations for blocking HERG tail-currents (IKr) in HERG-transfected cell lines</span></span></span></p></div> </div></div> </div></div>       <div id="comments-tab" class="comments tab-pane" data-v-01f52a0f><a data-comment-type="comment" data-prod-id="57B44305088700ED3221DD5DFB104915" aria-label="Submit a response" class="reply-button comments__response" data-v-01f52a0f> Submit a response </a> <hr aria-hidden="true" class="separator default" data-v-7036083a data-v-01f52a0f> <h2 class="comments__header" data-v-01f52a0f> eLetters </h2> <span data-v-01f52a0f>No eLetters have been published for this article.</span></div>  <div id="metrics-tab" publication-date="02 January 2018" class="metrics tab-pane" data-v-c41a0c86><div class="app-loader" data-v-c41a0c86></div></div></div></div> </div> <div role="complementary" aria-label="related contents" class="column__main__right" data-v-01274b1d><div class="access-block row access-status" 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Oyebode",searchUrl:"\u002Fcore\u002Fsearch?filters%5BauthorTerms%5D=Femi%20Oyebode&eventCode=SE-AU",orcidUrl:e}]},translators:{contributors:[],label:"Translated by"}},collections:[],publishedDate:"02 January 2018",keywords:[],openPracticeBadges:[],doi:{url:"https:\u002F\u002Fdoi.org\u002F10.1192\u002Fapt.9.6.414",value:"10.1192\u002Fapt.9.6.414"},copyright:{statement:["Copyright © The Royal College of Psychiatrists 2003 "],holder:[E],year:[2003]},creativeCommons:e,acceptedManuscript:b,type:"research-article",pageRange:{range:"414 - 423",firstPage:"414",lastPage:"423"},typeDescription:"Research Article",commentsCount:F,topicsAndSubtopics:e},journal:{id:G,title:o,titleSlug:H,mnemonic:"BJW",titleHistory:[{productId:G,title:o},{productId:I,title:w}],isFirstView:b,journalSlug:H,isCompanion:b,parentCompanionJournalName:o,associatedParentCollection:e,paymentInfo:{prices:{"£":{price:26,sku:p,skuNew:l,currency:"£"},"€":{price:31,sku:p,skuNew:l,currency:"€"},US$:{price:36,sku:p,skuNew:l,currency:"US$"},AU$:{price:51,sku:p,skuNew:l,currency:"AU$"}}},url:J,firstViewUrl:"\u002Fcore\u002Fjournals\u002Fadvances-in-psychiatric-treatment\u002Ffirstview",coverUrl:"https:\u002F\u002Fstatic.cambridge.org\u002Fcovers\u002FBJW_0_0_0\u002Fadvances-in-psychiatric-treatment.jpg",submitMaterialsUrl:"\u002Fcore\u002Fjournals\u002Fadvances-in-psychiatric-treatment\u002Finformation\u002Fauthor-instructions\u002Fsubmitting-your-materials",hasHistory:c,latestTitle:w,latestId:I,hasPastTitle:c,issue:{id:"6DCE0C6FE2C8429721BFE511F3462431",number:"6",title:"Issue 6",publishedDate:"November 2003",printPublishTimestamp:1067644800000,url:K},volume:{id:"050FE53A6848CED1ABBD99CAC40B95B8",number:"9",title:"Volume 9",publishedDate:"March 2003",printPublishTimestamp:1046476800000,url:"\u002Fcore\u002Fjournals\u002Fadvances-in-psychiatric-treatment\u002Fvolume\u002F050FE53A6848CED1ABBD99CAC40B95B8"}},abstract:{textAbstracts:[{title:"Abstract",content:"\u003Cdiv class=\"abstract\" data-abstract-type=\"normal\"\u003E\u003Cp\u003EPsychotropic literature in recent years has become very concerned with the cardiac safety of certain psychotropic medication. This paper reviews some of the cardiac factors to be considered in the safer selection of psychotropic drugs for the vulnerable patient in everyday clinical practice.\u003C\u002Fp\u003E\u003C\u002Fdiv\u003E",lang:L}]},content:{html:"\u003Cdiv class=\"article research-article JATS\"\u003E\n \n \u003Cdiv class=\"body\"\u003E\n \u003Cp class=\"p\"\u003E Several studies have demonstrated higher rates of cardiovascular death among psychiatric patients, particularly those with schizophrenia, compared with the general population (\u003Ca class=\"xref bibr\" href=\"#ref33\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Waddington, Youssef and Kinsella\u003C\u002Fspan\u003EWaddington \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003C\u002Fa\u003E). Cardiac risk factors, including smoking, lack of exercise, obesity, substance-misuse and high autonomic arousal during physical restraint, are overrepresented in psychiatric patients. As psychotropic medication is prescribed for this at-risk population, it becomes necessary to consider its cardiovascular effects. Here we focus on antipsychotics and antidepressants, as the cardiac effects of benzodiazepines and other psychotropics are negligible by comparison.\u003C\u002Fp\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Heart rate\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E Resting heart rate arising from spontaneous depolarisation of the sinoatrial node is largely determined by vagal parasympathetic tone. Respiratory sinus arrhythmia (heart rate increase) during inspiration and decrease on expiration is a physiological occurrence. It decreases with age, reflects heart rate variability and, like baroreceptor reflex sensitivity, is determined by sympathovagal balance but mainly depends on vagal influences on the sinoatrial node.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Psychotropic drugs possessing antimuscarinic and anticholinergic effects (e.g. all low-potency typical antipsychotics; some atypical antipsychotics, particularly clozapine; most tricyclic antidepressants; non-selective monoamine oxidase inhibitors (MAOIs); and all antiParkinsonian anticholinergics) cause sinus tachycardia which, in otherwise healthy individuals, rarely leads to symptoms and usually remits over time. An exception is clozapine-related myocarditis and cardiomyopathy, presenting with a persisting sinus tachycardia and accompanied by fever, chest pain, palpitations, dyspnoea, ankle oedema or heart failure early on in treatment (\u003Ca class=\"xref bibr\" href=\"#ref17\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Kilian, Kerr and Lawrence\u003C\u002Fspan\u003EKilian \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1999\u003C\u002Fa\u003E) (see below).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E In contrast, selective serotonin reuptake inhibitors (SSRIs) produce minor degrees of bradycardia that can usefully reduce cardiac workload and benefit the diseased heart. For example, in one study of elderly patients with depression who also had ischaemic heart disease, fluoxetine 20–60 mg\u002Fday induced a 6% asymptomatic decrease in heart rate, whereas nortriptyline, regarded as one of the safer tricyclics in heart disease, increased heart rate by 9%, possibly contributing to more adverse cardiac events (sinus tachycardia, severe angina and ventricular ectopics) (\u003Ca class=\"xref bibr\" href=\"#ref26\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Roose, Glassman and Attia\u003C\u002Fspan\u003ERoose \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003Cem class=\"italic\"\u003Ea\u003C\u002Fem\u003E\n \u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Heart rate variability is reduced in medical, psychiatric and psychological conditions such as myocardial infarction, heart failure, heart transplantation, normal ageing, depression, panic disorder, anger, hostility, stress and diabetic autonomic neuropathy, and by the use of full-dose anticholinergic, anticholinergic antipsychotic, and tricyclic antidepressant therapy (\u003Ca class=\"xref bibr\" href=\"#ref14\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Gorman and Sloan\u003C\u002Fspan\u003EGorman & Sloan, 2000\u003C\u002Fa\u003E). Reduced heart rate variability post-myocardial infarction carries a poor prognosis of increased cardiac mortality and sudden death from unopposed sympathetic arrhythmogenic influences (\u003Ca class=\"xref bibr\" href=\"#ref6\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Bigger, Breithardt and Camm\u003C\u002Fspan\u003EBigger \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1996\u003C\u002Fa\u003E). Anticholinergic medications such as imipramine reduce heart rate variability further by decreasing vagal tone in depression and panic disorder, but the non-anticholinergic paroxetine has the opposite effect.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Clozapine, a powerful anticholinergic, reduces heart rate variability in patients with schizophrenia (\u003Ca class=\"xref bibr\" href=\"#ref1\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Agelink, Majewski and Wurthmann\u003C\u002Fspan\u003EAgelink \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2001\u003C\u002Fa\u003E). Normal heart rate variability, however, can be restored by switching from clozapine to olanzapine, possibly reflecting olanzapine's more modest anticholinergic actions. (\u003Ca class=\"xref bibr\" href=\"#ref9\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Cohen, Loewenthal and Matar\u003C\u002Fspan\u003ECohen \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2001\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E After myocardial infarction, heart rate variability is maximally, but not fully, recovered within 6–12 months. It is not known whether any recovery from psychotropic-induced heart rate variability reduction occurs or whether this carries the same dire cardiac prognosis as for post-myocardial infarction patients (\u003Ca class=\"xref bibr\" href=\"#ref6\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Bigger, Breithardt and Camm\u003C\u002Fspan\u003EBigger \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1996\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Strategies for increasing heart rate variability would therefore appear desirable, and these include physical exercise, b-blockade and low-dose anti-cholinergic hyoscine hydrobromide (scopolamine) therapy, which paradoxically increases vagal parasympathetic activity (\u003Ca class=\"xref bibr\" href=\"#ref6\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Bigger, Breithardt and Camm\u003C\u002Fspan\u003EBigger \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1996\u003C\u002Fa\u003E). This paradoxical finding might explain the poorer cardiac outcome in patients with chronic schizophrenia who are not co-treated with anticholinergic medication (\u003Ca class=\"xref bibr\" href=\"#ref33\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Waddington, Youssef and Kinsella\u003C\u002Fspan\u003EWaddington \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Conduction\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E Impulses arising in the sinoatrial node spread across the atria to the atrioventricular node, bundle of His, right and left bundle branches and the distal portions of the Purkinje fibres. The PR interval measures the atrioventricular conduction time and the QRS measures conduction from the atrioventricular node through the bundle of His, bundle branches, Purkinje fibres and ventricular myocardium. The QRS is further subdivided into two intervals that can be measured by bundle of His electrocardiography. The first interval (normal range 50–120 ms) reflects the time taken for an impulse to traverse the atrioventricular node, and the second (normal range 35–55 ms) is the time taken to travel the bundle of His, bundle branches and Purkinje fibres (\u003Ca class=\"xref bibr\" href=\"#ref7\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Burrows, Vohra and Hunt\u003C\u002Fspan\u003EBurrows \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1976\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Tricyclic antidepressants delay cardiac conduction mainly by prolonging the second part of the QRS interval without significantly affecting the first. The effect is dose-dependent, occurring at both therapeutic and toxic doses, particularly with amitriptyline, imipramine and nortriptyline, but not doxepin (\u003Ca class=\"xref bibr\" href=\"#ref7\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Burrows, Vohra and Hunt\u003C\u002Fspan\u003EBurrows \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1976\u003C\u002Fa\u003E). It also probably occurs with dothiepin, but to a lesser degree with lofepra-mine; the perceived difference for doxepin, however, may simply reflect lower plasma levels. This effect is unlikely to be of clinical relevance in the otherwise normal heart. However, it might precipitate complete heart block in the presence of pre-existing conduction delay such as bundle branch block or second and higher degrees of heart (atrioventricular) block. In addition, emergent ventricular pacemakers, which would normally produce an idioventricular rhythm, may be suppressed by the antiarrhythmic action of the tricyclics, thus causing ventricular asystole. Tricyclic antidepressants are more likely to produce higher degrees of heart block in patients with pre-existing bundle branch block (QRS >12 ms) rather than first-degree block (PR >200 ms) (\u003Ca class=\"xref bibr\" href=\"#ref25\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Roose, Glassman and Giardina\u003C\u002Fspan\u003ERoose \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1987\u003C\u002Fa\u003E) and they should therefore be avoided in all cases of conduction disease beyond first-degree block. None the less, tricyclics are best avoided in patients with any degree of pre-existing conduction delay, because safer alternatives are available with SSRIs.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E The cardiotoxicity and mortality from overdose of tricyclic antidepressants is well established. Toxicity arises from sodium (Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E) ion-channel blockade, known as Type 1 antiarrhythmic action. This reduces inward Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E depolarising current at the beginning of the action potential, leading to conduction delay, bradycardia, atrioventricular block, bundle branch block and monomorphic ventricular tachycardia.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Brugada syndrome (\u003Ca class=\"xref boxed-text\" href=\"#B1\"\u003EBox 1\u003C\u002Fa\u003E), another cardiac Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E channelopathy, first described in 1992, causes idiopathic ventricular fibrillation in structurally normal hearts and sudden unexpected death in about 30% of untreated cases. It is associated with mutation of the SCN5A gene encoding cardiac Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E channels, causing a reduction of inward Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E depolarising currents. Electrocardiogram (ECG) features characteristically include right bundle branch block and S–T segment elevation in chest leads V1–V3, but normal QT interval (\u003Ca class=\"xref fig\" href=\"#F1\"\u003EFig. 1\u003C\u002Fa\u003E). Overdose of a tricyclic antidepressant may present with these features. Brugada syndrome is a leading cause of death in Thai males, typically during sleep; 40% of those with the syndrome have a family history of sudden death. It has an estimated prevalence in certain populations of up to 3%.\n\u003C\u002Fp\u003E\u003Csection\u003E\u003Cdiv class=\"fig\" data-magellan-destination=\"F1\" id=\"F1\"\u003E\n \n \n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig1g.jpeg?pub-status=live\" class=\"aop-lazy-load-image graphic\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig1g.jpeg\" data-zoomable=\"true\"\u003E\u003C\u002Fdiv\u003E\n \u003Cdiv class=\"caption\"\u003E\u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EFig. 1\u003C\u002Fspan\u003E \n \u003Cstrong\u003EBrugada syndrome: electrocardiogram demonstrates typical findings of right bundle branch block and elevated S–T segment leads V1–V3. Rhythm: 25 mm\u002Fs. (reproduced with permission from \u003Ca class=\"xref bibr\" href=\"#ref2\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Alings and Wilde\u003C\u002Fspan\u003EAlings & Wild, 1999\u003C\u002Fa\u003E).\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\u003C\u002Fdiv\u003E\u003C\u002Fsection\u003E\n \n \u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cdiv class=\"boxed-text\" data-magellan-destination=\"B1\" id=\"B1\"\u003E\n \n \u003Cdiv class=\"caption\"\u003E\n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EBox 1\u003C\u002Fspan\u003E \n \u003Cstrong\u003EBrugada syndrome\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cp class=\"p\"\u003E Cause of ventricular fibrillation and sudden unexpected death\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Common in young Thai males\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E 40% of patients have a family history of sudden death\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Structurally normal heart\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Characteristic ECG changes of right bundle branch block and S–T segment elevation leads V1–V3\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Normal QT interval\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Associated with mutation of SCN5A gene, blocking Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E channels\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Associated with tricyclic antidepressant\u002Fneuroleptic toxicity\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E May present with sudden death\u002Fsyncope\u002Fseizures\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \n \u003Cp class=\"p\"\u003E Similar appearances have been reported in overdose with tricyclic antidepressants such as amitriptyline and with antipsychotics, but no case was complicated by ventricular arrhythmia and the characteristic ECG pattern disappeared within days. It appears that Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E channel blockers such as the tricyclics and antipsychotics might provoke Brugada syndrome in otherwise asymptomatic but genetically predisposed individuals.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Type 1 action is also shared with the antiarrhythmic agents encainide, flecainide and moracizine, a phenothiazine analogue. The first placebo-controlled trial of ventricular premature contraction suppression in post-myocardial infarction patients was prematurely stopped because of increased mortality in the encainide and flecainide groups (Cardiac Arrhythmia Suppression Trial II Investigators, 1992). The second trial, run by the same team and reported in the same paper, continued with moracizine \u003Cem class=\"italic\"\u003Ev\u003C\u002Fem\u003E. placebo alone, but this was also abandoned early because of the significant increase in mortality and cardiac arrest in the moracizine group (3% \u003Cem class=\"italic\"\u003Ev\u003C\u002Fem\u003E. 0.4%). Consequently, tricyclic antidepressants and other agents possessing type 1 actions should be avoided, where possible, in psychiatric patients with ischaemic heart disease.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E The available SSRIs, in contrast, do not tend to prolong cardiac conduction, with the possible exception of minor conduction delays and QTc prolongation (see below) in citalopram overdose. Even with amounts more than 100 times the therapeutic dose of citalopram, however, the effects on cardiac conduction are few and non-cardiogenic seizures, rather than adverse cardiac events, are the more likely (\u003Ca class=\"xref bibr\" href=\"#ref11\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Glassman\u003C\u002Fspan\u003EGlassman, 1998\u003C\u002Fa\u003E). In cardiac patients with pre-existing bundle branch block (QRS >120 ms), therapeutic doses of fluoxetine did not prolong conduction (\u003Ca class=\"xref bibr\" href=\"#ref26\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Roose, Glassman and Attia\u003C\u002Fspan\u003ERoose \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003Cem class=\"italic\"\u003Ea\u003C\u002Fem\u003E\n \u003C\u002Fa\u003E); neither did paroxetine or sertraline in similar cardiac settings (\u003Ca class=\"xref bibr\" href=\"#ref27\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Roose, Laghrissi-Thode and Kennedy\u003C\u002Fspan\u003ERoose \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003Cem class=\"italic\"\u003Eb\u003C\u002Fem\u003E\n \u003C\u002Fa\u003E; \u003Ca class=\"xref bibr\" href=\"#ref13\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Glassman, O'Connor and Califf\u003C\u002Fspan\u003EGlassman \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2002\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Considering their established benefits on heart rate, heart rate variability, cardiac rhythm and platelet function (see below), SSRIs seem a treatment of choice for cardiac patients with anxious depression.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Although antipsychotic medication shares the type 1 antiarrhythmic actions of the tricyclics, by contrast, there is little published evidence that this is clinically significant in therapeutic doses, although in overdose, thioridazine in particular induces greater conduction delay and QRS widening than other typical antipsychotics. None the less, as for tricyclics, it would seem prudent to exercise caution when using such agents in psychiatric patients with a history of ischaemic heart disease or family history of sudden death, especially in view of their proarrhythmic QT-prolonging effects (see below).\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Rhythm\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E Psychotropic impact on cardiac rhythm focuses mainly on the propensity of antipsychotics to affect ventricular repolarisation. Such effects include prolongation of the QT interval (a measure of ventricular repolarisation), a known risk factor for torsade de pointes (‘twisting of the points’), a polymorphic ventricular tachycardia classically associated with long QT interval (\u003Ca class=\"xref fig\" href=\"#F2\"\u003EFig. 2\u003C\u002Fa\u003E).\n\u003C\u002Fp\u003E\u003Csection\u003E\u003Cdiv class=\"fig\" data-magellan-destination=\"F2\" id=\"F2\"\u003E\n \n \n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig2g.jpeg?pub-status=live\" class=\"aop-lazy-load-image graphic\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig2g.jpeg\" data-zoomable=\"true\"\u003E\u003C\u002Fdiv\u003E\n \u003Cdiv class=\"caption\"\u003E\u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EFig. 2\u003C\u002Fspan\u003E \n \u003Cstrong\u003EA short–long–short sequence of beats followed by an episode of torsade de pointes. The QT interval in the sinus beat immediately preceding the torsade de pointes is 600 ms (reproduced with permission from \u003Ca class=\"xref bibr\" href=\"#ref16\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Khan\u003C\u002Fspan\u003EKhan, 2002\u003C\u002Fa\u003E).\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\u003C\u002Fdiv\u003E\u003C\u002Fsection\u003E\n \n \u003Cp class=\"p\"\u003E Repolarisation effects induced by antipsychotics, particularly thioridazine and chlorpromazine, have long been recognised in the form of T-wave changes on the ECG. For example, 58% of patients treated with 100–800 mg thioridazine daily showed some type of T-wave changes (\u003Ca class=\"xref bibr\" href=\"#ref35\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Wendkos\u003C\u002Fspan\u003EWendkos, 1967\u003C\u002Fa\u003E). These have been graded into three categories based on direction, amplitude and T-wave structure: grade 1 (T-wave broadening, blunting without loss of amplitude); grade 2 (loss of amplitude and bifid T-wave); grade 3 (flattened\u002Finverted T-wave). All T-wave changes normalised in the majority of phenothiazine-treated patients after overnight fasting alone, and the remainder reverted to normal after oral potassium administration (\u003Ca class=\"xref fig\" href=\"#F3\"\u003EFig. 3\u003C\u002Fa\u003E). Oral administration of isosorbide dinitrate, potassium or ergot alkaloids also reversed thioridazine-induced T-wave changes, but was unsuccessful in reversing T-wave changes arising from cardiac pathology or quinidine therapy. Hence, it has been suggested that some antipsychotic repolarisation effects may be ‘benign’ (\u003Ca class=\"xref bibr\" href=\"#ref35\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Wendkos\u003C\u002Fspan\u003EWendkos, 1967\u003C\u002Fa\u003E) and that not all are necessarily associated with the more serious cardiac consequences reported in more recent literature (\u003Ca class=\"xref bibr\" href=\"#ref24\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Reilly, Ayis and Jones\u003C\u002Fspan\u003EReilly \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2000\u003C\u002Fa\u003E). The impact of fasting, however, illustrates the effects of diet on ECG changes.\n\u003C\u002Fp\u003E\u003Csection\u003E\u003Cdiv class=\"fig\" data-magellan-destination=\"F3\" id=\"F3\"\u003E\n \n \n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig3g.jpeg?pub-status=live\" class=\"aop-lazy-load-image graphic\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig3g.jpeg\" data-zoomable=\"true\"\u003E\u003C\u002Fdiv\u003E\n \u003Cdiv class=\"caption\"\u003E\u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EFig. 3\u003C\u002Fspan\u003E \n \u003Cstrong\u003EECG of a phenothiazine-treated patient: complete normalisation of repolarisation abnormalities by overnight fasting. Left panel: initial non-fasting T-wave changes; right panel: T-wave normalisation after overnight fasting (reproduced with permission from \u003Ca class=\"xref bibr\" href=\"#ref3\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Alvarez-Mena and Frank\u003C\u002Fspan\u003EAlvarez-Mena & Frank, 1973\u003C\u002Fa\u003E).\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\u003C\u002Fdiv\u003E\u003C\u002Fsection\u003E\n \n \u003Cp class=\"p\"\u003E The QT-prolonging tendency of antipsychotics, which is shared to a lesser extent by tricyclic antidepressants (\u003Ca class=\"xref bibr\" href=\"#ref24\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Reilly, Ayis and Jones\u003C\u002Fspan\u003EReilly \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2000\u003C\u002Fa\u003E), is based on their capacity to block IKr, the delayed rectifier, the principal repolarising current terminating ventricular action potential in phase 2–3 (\u003Ca class=\"xref fig\" href=\"#F4\"\u003EFig. 4\u003C\u002Fa\u003E). Blockade of IKr (encoded by the HERG gene) may cause sufficient QT prolongation to generate extra potentials, known as early after-depolarisations, and to distort phase 3 of normal repolarisation (\u003Ca class=\"xref\" href=\"#F4\"\u003EFigs 4\u003C\u002Fa\u003E & \u003Ca class=\"xref\" href=\"#F5\"\u003E5\u003C\u002Fa\u003E). Early after-depolarisations may give rise to ventricular premature beats capable of triggering a run of torsade de pointes, especially if these beats distort the preceding T-wave (R-on-T) or conform to a long–short coupling pattern (\u003Ca class=\"xref fig\" href=\"#F6\"\u003EFig. 6\u003C\u002Fa\u003E). The risk of drug-induced torsade de pointes is increased under certain conditions (\u003Ca class=\"xref boxed-text\" href=\"#B2\"\u003EBoxes 2\u003C\u002Fa\u003E & \u003Ca class=\"xref boxed-text\" href=\"#B3\"\u003E3\u003C\u002Fa\u003E).\n\u003C\u002Fp\u003E\u003Csection\u003E\u003Cdiv class=\"fig\" data-magellan-destination=\"F4\" id=\"F4\"\u003E\n \n \n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig4g.jpeg?pub-status=live\" class=\"aop-lazy-load-image graphic\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig4g.jpeg\" data-zoomable=\"false\"\u003E\u003C\u002Fdiv\u003E\n \u003Cdiv class=\"caption\"\u003E\u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EFig. 4\u003C\u002Fspan\u003E \n \u003Cstrong\u003ESchematic representation of the action potential and corresponding ECG phases.\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\u003C\u002Fdiv\u003E\u003C\u002Fsection\u003E\n \u003Csection\u003E\u003Cdiv class=\"fig\" data-magellan-destination=\"F5\" id=\"F5\"\u003E\n \n \n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig5g.jpeg?pub-status=live\" class=\"aop-lazy-load-image graphic\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig5g.jpeg\" data-zoomable=\"true\"\u003E\u003C\u002Fdiv\u003E\n \u003Cdiv class=\"caption\"\u003E\u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EFig. 5\u003C\u002Fspan\u003E \n \u003Cstrong\u003ESchematic representation of IKr block on the QT interval: (a) monophasic action potential (upper trace) and corresponding surface ECG (lower trace) before (B) and after (D) exposure to IKr blocking drug and the effect on the QT interval; (b) prolonged QT interval induces two early after-depolarisations (EADs) in the action potential (arrows), thus giving rise to a run of torsade de pointes on the surface ECG (lower trace). Reproduced with permission from \u003Ca class=\"xref bibr\" href=\"#ref30\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Tamargo\u003C\u002Fspan\u003ETamargo (2000)\u003C\u002Fa\u003E.\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\u003C\u002Fdiv\u003E\u003C\u002Fsection\u003E\n \u003Csection\u003E\u003Cdiv class=\"fig\" data-magellan-destination=\"F6\" id=\"F6\"\u003E\n \n \n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig6g.jpeg?pub-status=live\" class=\"aop-lazy-load-image graphic\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_fig6g.jpeg\" data-zoomable=\"true\"\u003E\u003C\u002Fdiv\u003E\n \u003Cdiv class=\"caption\"\u003E\u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EFig. 6\u003C\u002Fspan\u003E \n \u003Cstrong\u003EECG demonstrating long–short coupling sequence. A ventricular premature contraction (B) succeeds a sinus beat (A), leading to a compensatory pause (long cycle ∗); another sinus beat (C), followed by a second ventricular premature contraction (D) (short cycle), triggers a run of torsade de pointes. Reproduced with permission from \u003Ca class=\"xref bibr\" href=\"#ref30\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Tamargo\u003C\u002Fspan\u003ETamargo (2000)\u003C\u002Fa\u003E.\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\u003C\u002Fdiv\u003E\u003C\u002Fsection\u003E\n \n \u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cdiv class=\"boxed-text\" data-magellan-destination=\"B2\" id=\"B2\"\u003E\n \n \u003Cdiv class=\"caption\"\u003E\n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EBox 2\u003C\u002Fspan\u003E \n \u003Cstrong\u003EDrugs and conditions associated with acquired long QT syndromes\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cp class=\"p\"\u003E Antiarrhythmic drugs\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Antipsychotics\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Antidepressants\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Antihistamines\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Antimicrobials\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Structural heart disease\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Bradycardias\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Intracranial lesions\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Electrolyte abnormalities\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Alcoholism\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Anorexia nervosa\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Hypothyroidism\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \n \u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cdiv class=\"boxed-text\" data-magellan-destination=\"B3\" id=\"B3\"\u003E\n \n \u003Cdiv class=\"caption\"\u003E\n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EBox 3\u003C\u002Fspan\u003E \n \u003Cstrong\u003ERisk of drug-induced torsade de pointes\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cp class=\"p\"\u003E Pre-existing QT prolongation\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Pre-existing QT dispersion\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Hypokalaemia\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Hypomagnesaemia\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Severe hypocalcaemia\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E QT-prolonging co-therapy\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Sinus bradycardia <50 bpm\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Pre-exisiting polymorphic ventricular premature beats showing R-on-T or long–short cycles\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \n \u003Cp class=\"p\"\u003E Normal QT values are not universally established because so many variables affect measurement. These include gender (longer in females), time of day (longer in sleep and early morning), diet, heart rate (QTc denotes QT corrected for heart rate using Bazett, Friderica or other regression formulae) and lead selection (longer in leads II, V2 and V3). However, a consensus appears to be emerging of a normal QTc upper limit of 450 ms for males and 470 ms for females, with a ‘red zone’ limit of 500 ms for both genders. \u003Ca class=\"xref bibr\" href=\"#ref5\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Bednar, Harrigan and Anziano\u003C\u002Fspan\u003EBednar \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E (2001)\u003C\u002Fa\u003E warn that intervals in excess of these values should raise concern. In a literature review of 116 torsade de pointes cases associated with non-cardiac treatment, they found that 92% had QTc intervals >500 ms.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E In terms of QTc change from baseline on treatment, it has likewise been recommended, notwithstanding a tendency for regression towards the mean, that an increase of 30 ms is a potential cause for concern and that a 60 ms increase is a definite cause for concern (\u003Ca class=\"xref bibr\" href=\"#ref5\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Bednar, Harrigan and Anziano\u003C\u002Fspan\u003EBednar \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2001\u003C\u002Fa\u003E). In addition, a QT dispersion of 40–60 ms is considered acceptable, but it is thought to be pathological when it exceeds 100 ms or is 100% increased from baseline values (the QT dispersion is the difference between the longest and shortest QT on a 12-lead ECG, which is widely although not universally regarded as reflecting repolarisation asynchrony across the entire ventricle and another risk factor for torsade de pointes) (\u003Ca class=\"xref bibr\" href=\"#ref5\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Bednar, Harrigan and Anziano\u003C\u002Fspan\u003EBednar \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2001\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Antipsychotics differ in their capacity for QT prolongation. \u003Cem class=\"italic\"\u003EIn vitro\u003C\u002Fem\u003E studies using HERG-transfected cell lines demonstrate a concentration-dependent effect for IKr blocking (\u003Ca class=\"xref table\" href=\"#T1\"\u003ETable 1\u003C\u002Fa\u003E). This is consistent with findings from retrospective systematic clinical studies identifying thioridazine and the tricyclic antidepressants as predictive of QT prolongation (\u003Ca class=\"xref bibr\" href=\"#ref24\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Reilly, Ayis and Jones\u003C\u002Fspan\u003EReilly \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2000\u003C\u002Fa\u003E).\n\u003C\u002Fp\u003E\u003Cdiv class=\"table-wrap\" data-magellan-destination=\"T1\" id=\"T1\"\u003E\n \n \u003Cdiv class=\"caption\"\u003E\n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003ETable 1\u003C\u002Fspan\u003E \n \u003Cstrong\u003EDrug concentrations for blocking HERG tail-currents (IKr) in HERG-transfected cell lines\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tab1.gif?pub-status=live\" class=\"aop-lazy-load-image graphic\" width=\"415\" height=\"159\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tab1.gif\" data-zoomable=\"false\"\u003E\u003C\u002Fdiv\u003E\n \u003Ctable class=\"table no-colsep no-rowsep\"\u003E\n \u003Ccolgroup class=\"colgroup\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003C\u002Fcolgroup\u003E\n \u003Cthead\u003E\n \u003Ctr class=\"tr rowsep\"\u003E\n \u003Cth class=\"th bottom left\" colspan=\"1\" rowspan=\"1\"\u003E\n \u003Cem class=\"italic\"\u003EDrug\u003C\u002Fem\u003E\n \u003C\u002Fth\u003E\n \u003Cth class=\"th bottom left\" colspan=\"1\" rowspan=\"1\"\u003E\n \u003Cem class=\"italic\"\u003EPotency (in descending order)\u003C\u002Fem\u003E\n \u003C\u002Fth\u003E\n \u003C\u002Ftr\u003E\n \u003C\u002Fthead\u003E\n \n \u003Ctbody class=\"tbody top\"\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003ESertindole\u003Csup class=\"sup\"\u003E1\u003C\u002Fsup\u003E\n \u003C\u002Ftd\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003E2.9 nM\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003EHaloperidol\u003Csup class=\"sup\"\u003E1\u003C\u002Fsup\u003E\n \u003C\u002Ftd\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003E1.0 μM\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003EThioridazine\u003Csup class=\"sup\"\u003E2\u003C\u002Fsup\u003E\n \u003C\u002Ftd\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003E1.07± 0.06 μM\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003EChlorpromazine\u003Csup class=\"sup\"\u003E2\u003C\u002Fsup\u003E\n \u003C\u002Ftd\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003E1.47±0.03 μM\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003EClozapine\u003Csup class=\"sup\"\u003E2\u003C\u002Fsup\u003E\n \u003C\u002Ftd\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003E2.63±0.12 μM\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr rowsep\"\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003EAmitriptyline\u003Csup class=\"sup\"\u003E2\u003C\u002Fsup\u003E\n \u003C\u002Ftd\u003E\n \u003Ctd class=\"td bottom left\" colspan=\"1\" rowspan=\"1\"\u003E10.0±1.1 μM\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003C\u002Ftbody\u003E\n \u003C\u002Ftable\u003E\n \u003C\u002Fdiv\u003E\n \n \u003Cp class=\"p\"\u003E The prevalence of torsade de pointes in the psychiatric population is unknown, but estimates from antiarrhythmic-induced torsade de pointes in the cardiac population ranges from 3% to 15%. Being associated with entirely non-specific symptoms such as palpitations, dizziness, syncope and seizures, its potential seriousness may be easily misconstrued as primary psychiatric disorder: this can have fatal outcome. Although usually self-limiting, torsade de pointes tends to recur and in 31% of cases progresses to ventricular fibrillation and sudden death.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E These QT-prolonging proarrhythmic concerns led to the placing of prescribing restrictions on thioridazine, a voluntary withdrawal of droperidol in the UK by its manufacturer and a complete withdrawal of sertindole from the European market. They have also shifted the cardiac focus onto other increasingly prescribed atypical antipsychotics. For example, after some initial concern the US Food and Drugs Administration requested Study 054 (\u003Ca class=\"xref bibr\" href=\"#ref22\"\u003EPsychopharmacological Drugs Advisory Committee, 2000\u003C\u002Fa\u003E) to further clarify the QT-prolonging capacity of ziprasidone and to compare it with olanzapine, risperidone, quetiapine, thioridazine and haloperidol in an open-label randomised 4-week trial involving 183 patients with psychosis. The mean QTc change from baseline was 10 ms greater with ziprasidone than with olanzapine, risperidone and quetiapine, and 10 ms less than with thioridazine; haloperidol demonstrated the least change and all agents showed a dose-dependent effect. Ziprasidone was subsequently licensed for use in the USA, and although a black-box warning was avoided, a bold-type warning of its QT-prolonging capacity was included.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Additional risks factors for QT-prolongation and torsade de pointes in the psychiatric population include deliberate or accidental antipsychotic overdose, effects of concomitant QT-prolonging medication (either indirect such as CYP 450 3A3 and 3A4 inhibitors, fluoxetine, fluvoxamine, grapefruit juice and ketoconazole, or direct such as tricyclic antidepressants, antihistamines and anti-infectives), comorbid substance misuse and, in particular, the effects of high sympathetic arousal during restraint. Such arousal releases large amounts of circulating catecholamines which, in addition to increasing cardiac oxygen consumption, lower serum levels by β-2 adrenergic stimulation of potassium (K\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E) uptake into skeletal muscle cells. \u003Ca class=\"xref bibr\" href=\"#ref15\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Hatta, Takahashi and Nakamura\u003C\u002Fspan\u003EHatta \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E (1999)\u003C\u002Fa\u003E found a significant negative correlation between serum K\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E and high \u003Cem class=\"italic\"\u003Ev\u003C\u002Fem\u003E. low levels of psychotic agitation in acute in-patients (3.59 \u003Cem class=\"italic\"\u003Ev\u003C\u002Fem\u003E. 3.79 mEq\u002Fl), and lower serum K\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E in more agitated acute in-patients compared with out-patients. Thus, in a control and restraint situation, the QT-prolonging effects of hypokalaemia and intramuscular antipsychotics, together with the potential for hypoxia and myocardial irritability from inadvertent ventilatory embarrassment and greater cardiac strain, may result in the kind of potent proarrhythmic cocktail that prompted the Collge to warn that ‘the risk of sudden cardiotoxic collapse in response to antipsychotic medication given during a period of high physiological arousal should be widely publicised’(\u003Ca class=\"xref bibr\" href=\"#ref28\"\u003ERoyal College of Psychiatrists, 1997\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Coronary artery disease\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E Major and minor depression have an important relationship with coronary artery disease. Many studies have demonstrated a strong association between depression and coronary artery disease: there is increased incidence of the disease in patients with depression who have an otherwise healthy heart, and exacerbation of existing coronary artery disease and cardiac mortality in the 15–20% of post-infarction patients who develop major, and even minor, depression. Even sub-syndromal depressive symptoms therefore increase cardiac risk in coronary artery disease (\u003Ca class=\"xref bibr\" href=\"#ref23\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Penninx, Beekman and Honig\u003C\u002Fspan\u003EPenninx \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2001\u003C\u002Fa\u003E). This strong association persists even after controlling for established cardiac risk factors such as smoking and diabetes.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Panic disorder and phobic anxiety states are also associated with increased rates of coronary artery disease and cardiac mortality, possibly mediated by coronary artery spasm and sympathetic-mediated cardiac arrhythmias, but the association is less well studied and documented (\u003Ca class=\"xref bibr\" href=\"#ref19\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Mansour, Wilkinson and Jennings\u003C\u002Fspan\u003EMansour \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003C\u002Fa\u003E). Serotonin (5-HT) activity represents one possible link between depression, anxiety and coronary artery disease. Activated platelets, apart from platelet factor-4 (PF-4) and b-thromboglobulin (b-TG), release large quantities of serotonin. This has two main effects: first, it causes vasodilation in normal, but vasoconstriction in diseased, coronary vessels; and second, it promotes endothelial vessel dysfunction, with local further platelet activation and endothelial smooth-muscle proliferation, potentially responsible for local atherogenesis.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Levels of PF-4 and b-TG can be assayed, and are higher in patients with coronary artery disease who have depression than in similar patients without depression and in healthy controls (\u003Ca class=\"xref bibr\" href=\"#ref18\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Laghrissi-Thode, Wagner and Pollock\u003C\u002Fspan\u003ELaghrissi-Thode \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1997\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Because increased platelet activation may thus contribute to atherogenesis, coronary artery disease and sudden death, attempts to reduce platelet activity in 'coronary-prone’ individuals with depression or anxiety may become an important aspect of cardiac risk reduction, especially since aspirin therapy alone does not appear to reduce platelet activity in this population (\u003Ca class=\"xref bibr\" href=\"#ref18\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Laghrissi-Thode, Wagner and Pollock\u003C\u002Fspan\u003ELaghrissi-Thode \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1997\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Paroxetine appears to be a promising agent in this regard. \u003Ca class=\"xref bibr\" href=\"#ref21\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Musselman, Marzec and Manatunga\u003C\u002Fspan\u003EMusselman \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E (2000)\u003C\u002Fa\u003E report a study of 15 patients with depression who showed no evidence of coronary artery disease, although some did have known risk factors for the disease. At the start of the study, all had elevated PF-4 levels. After receiving 20 mg paroxetine daily for 6 weeks, a significant reduction in these levels was observed in both those with and without known risk factors for coronary artery disease. Roose and colleagues found further evidence supporting the use of paroxetine in co-morbid depression or anxiety and coronary artery disease. They compared paroxetine 20–30 mg daily with therapeutic doses of nortriptyline in 81 patients with coronary artery disease and depression. Despite equal antidepressant efficacy after 6 weeks’ treatment, paroxetine had more benefit on cardiac function, including heart rate, heart rate variability, rhythm and adverse cardiac events (\u003Ca class=\"xref bibr\" href=\"#ref27\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Roose, Laghrissi-Thode and Kennedy\u003C\u002Fspan\u003ERoose \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003Cem class=\"italic\"\u003Eb\u003C\u002Fem\u003E\n \u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E The best evidence to date for antidepressant intervention in this patient group has come from the Sertraline Antidepressant Heart Attack Randomised Trial (SADHART; \u003Ca class=\"xref bibr\" href=\"#ref13\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Glassman, O'Connor and Califf\u003C\u002Fspan\u003EGlassman \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2002\u003C\u002Fa\u003E). A study of 369 patients recently discharged following acute myocardial infarction or unstable angina, who were randomised to sertraline 50–200 mg\u002Fday or to placebo, demonstrated treatment safety and efficacy of the antidepressant over placebo.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E The safety and benefits of SSRIs, especially paroxetine and fluoxetine, over tricyclic antidepressants on general cardiac function, platelet coagulability and, possibly, atherogenesis appears to recommend their use as psychotropics of first choice in patients with, or at high risk of, coronary artery disease, especially smokers, postmenopausal women and patients with hypertension, diabetes, hyperlipidaemia and\u002For a strong family history of coronary artery disease.\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Contractility and effects on cardiac muscle\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E Radionuclide ventriculography has demonstrated, contrary to original concerns, that psychotropic drugs do not exert a direct negative inotropic effect (\u003Ca class=\"xref bibr\" href=\"#ref26\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Roose, Glassman and Attia\u003C\u002Fspan\u003ERoose \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1998\u003Cem class=\"italic\"\u003Ea\u003C\u002Fem\u003E\n \u003C\u002Fa\u003E). However, antipsychotics (clozapine in particular) are occasionally associated with an increased risk of myocarditis or cardiomyopathy (\u003Ca class=\"xref bibr\" href=\"#ref17\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Kilian, Kerr and Lawrence\u003C\u002Fspan\u003EKilian \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1999\u003C\u002Fa\u003E). Kilian and colleagues reported 15 cases of myocarditis and 8 of dilated cardiomyopathy at normal daily doses (100–725 mg clozapine) in 8000 Australian patients. All but 3 were male, with a mean age of 36. The myocarditis occurred in the first month of treatment (often from hypersensitive eosinophilic myocarditis), had few specific symptoms and frequently presented with sudden death. Cardiomyopathy developed more slowly, within the first 12 months, usually presented with cough, dyspnoea, palpitations or heart failure, could improve on clozapine discontinuation and appeared to have a better prognosis. These and other reports have led to increased warnings of these cardiac complications in information on prescribing and of the need for early investigation and clozapine cessation in suspect cases.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E As eosinophilic myocarditis seems to be the favoured aetiology, blood eosinophilia should be carefully sought. However, a raised plasma level of eosinophil cationic protein, an assayable pro-inflammatory protein released from degranulated eosinophils, seems a preferable marker as it remains elevated even in cases with normal eosinophil counts (\u003Ca class=\"xref bibr\" href=\"#ref4\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Arima, Kanoh and Kawano\u003C\u002Fspan\u003EArima \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 2002\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Blood pressure\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E Postural (orthostatic) hypotension has many causes but is probably the most common and potentially most troublesome psychotropic side-effect (\u003Ca class=\"xref boxed-text\" href=\"#B4\"\u003EBox 4\u003C\u002Fa\u003E). Usually defined as a ≥20 mmHg reduction in systolic blood pressure after 1–3 minutes of standing upright, it may cause symptomatic underperfusion of vital organs, leading to dizziness, blurred vision, fainting, falls, fractures, seizures, strokes and cardiac ischaemia, especially in elderly people. Fainting usually occurs when mean arterial pressure (diastolic plus 1\u002F3 pulse pressure) drops to 70 mmHg or below, corresponding to an upper-arm blood pressure of 90\u002F60 or less.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cdiv class=\"boxed-text\" data-magellan-destination=\"B4\" id=\"B4\"\u003E\n \n \u003Cdiv class=\"caption\"\u003E\n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EBox 4\u003C\u002Fspan\u003E \n \u003Cstrong\u003ECauses of postural hypotension (after \u003Ca class=\"xref bibr\" href=\"#ref10\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Engstrom and Aminoff\u003C\u002Fspan\u003EEngstrom & Aminoff,1997\u003C\u002Fa\u003E, with permission)\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cp class=\"p\"\u003E \n \u003Cem class=\"italic\"\u003ECardiac pump failure\u003C\u002Fem\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Myocardial infarction\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Myocarditis\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Constrictive pericarditis\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Aortic stenosis\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Tachy- or bradyarrhythmias\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Cem class=\"italic\"\u003EVenous pooling\u003C\u002Fem\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Alcohol\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Postprandial dilatation of splanchnic vessel beds\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Vigorous exercise with dilatation of skeletal vessel beds\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Hot baths\u002Fshowers\u002Ffever\u002Fweather\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Prolonged recumbency or standing\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Cem class=\"italic\"\u003EReduced intravascular volume\u003C\u002Fem\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Straining-toilet\u002Fcoughing\u002Flifting\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Dehydration\u002Fvomiting\u002Fdiarrhoea\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Haemorrhage\u002Fburns\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Salt-losing nephropathy\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Adrenal insufficiency\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Diabetes insipidus\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Cem class=\"italic\"\u003EOther causes\u003C\u002Fem\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Shy–Drager syndrome\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Diabetic neuropathy\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Alcoholic neuropathy\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Porphyria\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Anorexia nervosa\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Riley–Day syndrome\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Chronic fatigue syndrome\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Cem class=\"italic\"\u003EMedications\u003C\u002Fem\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Antihypertensives\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Diuretics\u002Fdisulfiram\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Vasodilators\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Alpha- and beta-blockers\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Barbiturates\u002Fopiates\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Neuroleptics\u002Ftricyclics\u002FMAOIs\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \n \u003Cp class=\"p\"\u003E Clinical studies of tricyclic antidepressants focusing mainly on imipramine and nortriptyline found a 20% prevalence of postural hypotension in treated patients. Non-standardised methodology may account for some conflicting findings, but the data suggest, first, a greater tendency to postural hypotension for tertiary tricyclics (e.g. imipramine and amitriptyline) than for secondary (e.g. nor-triptyline); second, that the degree of pretreatment postural blood pressure drop predicts on-treatment symptoms and when this pretreatment orthostatic hypotension was controlled for, removed age by itself as a predictor of postural drop; and third, that (counterintuitively) dose reduction may not relieve symptoms (\u003Ca class=\"xref bibr\" href=\"#ref12\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Glassman, Bigger and Giardina\u003C\u002Fspan\u003EGlassman \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1979\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E There are fewer studies of MAOIs, for which the hypotensive mechanism remains elusive. In patients with depression, phenelzine 60 mg daily induced both a fall in supine systolic blood pressure and a postural drop. In 14% of patients, the latter caused significant symptoms, which reached a maximum after 4 weeks’ treatment. This contrasts with findings for imipramine, where supine blood pressure remained unaffected but the postural effect tended to maximise after 1 week. However, these results might be related to an early rapid dose escalation. Isocarboxazid and tranylcypromine are likewise associated with an 11% and 17% prevalence of symptomatic postural hypotension respectively (\u003Ca class=\"xref bibr\" href=\"#ref34\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Warrington, Padgham and Lader\u003C\u002Fspan\u003EWarrington \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1989\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Postural hypotension is a well-documented effect of typical antipsychotics, but few systematic studies exist. In a study of 196 chronic in-patients with schizophrenia on stable antipsychotic treatment, symptomatic postural hypotension occurred in 77% within 1 minute, reducing to 17% after 3 minutes, on standing from supine. No other correlation with age, dose or potency of α\u003Csub\u003E1\u003C\u002Fsub\u003E-adrenergic blocking drug emerged, although thioridazine was associated with greater postural blood pressure drop (\u003Ca class=\"xref bibr\" href=\"#ref29\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Silver, Kogan and Zlotogorski\u003C\u002Fspan\u003ESilver \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E, 1990\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Atypical antipsychotics pose much less of a problem (with the possible exception of clozapine, where α\u003Csub\u003E1\u003C\u002Fsub\u003E-adrenergic blockade is generally assumed to be responsible; it tends to occur early in treatment, particularly with rapid dose escalation, but tolerance usually builds up).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Care is needed when co-prescribing psychotropics and antihypertensives. Antipsychotics may, like tricyclics, antagonise centrally acting drugs such as clonidine and methyldopa. These are infrequently used as antihypertensives, but clonidine is popular in psychiatric practice for acute opiate detoxification. However, co-prescribing antipsychotics, especially low-potency typicals such as chlorpro-mazine or the atypicals clozapine or quetiapine, with any of the following may provoke profound postural hypotension: α\u003Csub\u003E1\u003C\u002Fsub\u003E-adrenergic antagonists (e.g. doxazosin, which is also a treatment for benign prostatic hypertrophy); calcium-channel blockers (e.g. nifedipine); angiotensin-converting enzyme inhibitors (captopril); angiotensin-II receptor antagonists (losartan); or vasodilators (e.g. nitro-prusside). Postural hypotension is also a risk when antipsychotics are taken with β-blockers (probably because of pharmacokinetic interaction) or with diuretics (because of Na\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E or volume depletion). The same hypotensive effects might be anticipated when tricyclic antidepressants or MAOIs are co-prescribed with peripheral antihypertensive agonists. One possible exception concerns phenelzine, whose hypotensive action was reversed on co-therapy with atenolol (\u003Ca class=\"xref bibr\" href=\"#ref20\"\u003E\u003Cspan class=\"show-for-sr\"\u003EReference Merikangas and Merikangas\u003C\u002Fspan\u003EMerikangas & Merikangas, 1995\u003C\u002Fa\u003E).\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Symptomatic postural hypotension is associated with dizziness, blurred vision, syncope, falls and injuries, seizures and myocardial infarction. Effective management should therefore address prevention as well as specific therapy. Patient counselling is the most important aspect of prevention (\u003Ca class=\"xref boxed-text\" href=\"#B5\"\u003EBox 5\u003C\u002Fa\u003E). Extra vigilance in older people and patients who are dehydrated or have diabetes or hypertension on treatment is essential.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cdiv class=\"boxed-text\" data-magellan-destination=\"B5\" id=\"B5\"\u003E\n \n \u003Cdiv class=\"caption\"\u003E\n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003EBox 5\u003C\u002Fspan\u003E \n \u003Cstrong\u003EPrevention of postural hypotension\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cp class=\"p\"\u003E Avoid prolonged standing\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Adopt slow, careful posture changes when rising from bed or chair after prolonged rest\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Ascend and descend stairs on your bottom\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Sit, do not stand, in hot water\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Be careful getting out of a hot bath\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Be careful in hot environments\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Make a tight fist before standing (isometric handgrip exercises have a pressor effect)\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Drink cold and caffeinated drinks\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Ensure copious fluid intake\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Ensure adequate salt intake\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Eat frequent but small meals\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Avoid alcohol\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Avoid vigorous exercise\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Wear support stockings\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Sleep with the bed head raised by 15–30 cm (a 30° tilt minimises nocturnal diuresis)\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \n \u003Cp class=\"p\"\u003E In addition to the simple measures shown in \u003Ca class=\"xref boxed-text\" href=\"#B5\"\u003EBox 5\u003C\u002Fa\u003E, fludrocortisone therapy might also be necessary. This acts by increasing arteriolar sensitivity to noradrenalin and, in bigger doses, by expanding plasma volume. Doses begin at 50 μg daily, increased by 50 μg increments to a maximum of 300 μg, according to response and level of hypotensive symptoms. The drug can usually be withdrawn after the early weeks of psychotropic treatment, as accomodation to the hypotensive effect usually develops. Fludrocortisone side-effects include fluid overload and heart failure, hypokalaemia and supine hypertension.\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Conclusion\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E On the basis of the literature referenced in this paper, it could be argued that all mental health units have ready access to ECG monitoring equipment. Modern machines provide an automated printout that can be of great assistance to the psychiatrist in ECG interpretation, but in cases of doubtful validity, cardiology colleagues are usually most helpful in providing manual interpretation. Clinicians with a particular interest in this field may wish to conduct ECG studies in a greater proportion of their patients or pursue more complex studies involving heart rate variability, which would probably involve collaboration with cardiology services anyway .\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Patients already at higher risk of cardiac complications will continue to be closely monitored. The difficulties of widespread monitoring of the psychiatric population, apart from practical considerations, would appear too considerable to justify at present, and cardiologists or other psychiatrists with particular knowledge of the field have not thus far endorsed its introduction.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Monitoring of pulse and blood pressure ought to remain essential components of the psychiatric examination. It could also be argued that psychiatric in-patients perceived to be at greater risk for QTc prolongation might receive more careful monitoring to minimise known risks (especially low serum K\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E and Mg\u003Csup class=\"sup\"\u003E2+\u003C\u002Fsup\u003E) and have their levels maintained well into the normal range (serum K\u003Csup class=\"sup\"\u003E+\u003C\u002Fsup\u003E > 3.8 mmol\u002Fl) by a diet rich in potassium and magnesium or, if necessary, by oral supplementation.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Furthermore, control and restraint procedures for disturbed patients must be careful to avoid any restriction of chest or diaphragmatic ventilation, which might add to any pre-existing cardiac risk. If rapid tranquillisation becomes necessary, and if time and circumstances allow, intramuscular benzo-diazepines (which have negligible cardiotropic effects) could be administered initially, to be followed with an intramuscular antipsychotic given soon after, when the patient has begun to settle.\u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E Finally, as there is a possible association with myocarditis and cardiomyopathy, any patients commencing on clozapine could be considered for pre-treatment baseline ECG, chest X-ray, eosinophil counts and eosinophil cationic protein level, repeated as necessary. Subsequent comparison with baseline would help appropriate interpretation of treatment-emergent changes.\u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E Multiple choice questions\u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Col class=\"list number nomark\"\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003E1\u003C\u002Fspan\u003E \n \u003Cstrong\u003ETorsade de pointes:\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Col class=\"list number nomark\"\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ea\u003C\u002Fspan\u003E is a variety of French perfume\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Eb\u003C\u002Fspan\u003E is a polymorphic ventricular tachycardia\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ec\u003C\u002Fspan\u003E is associated with sudden death\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ed\u003C\u002Fspan\u003E is more likely to occur with hypokalaemia\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ee\u003C\u002Fspan\u003E is associated with long–short coupling on the ECG.\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003C\u002Fol\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003E2\u003C\u002Fspan\u003E \n \u003Cstrong\u003EA prolonged QT interval:\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Col class=\"list number nomark\"\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ea\u003C\u002Fspan\u003E is associated with torsade de pointes\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Eb\u003C\u002Fspan\u003E may be congenital or acquired\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ec\u003C\u002Fspan\u003E is associated with antipsychotic medication\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ed\u003C\u002Fspan\u003E is more common in women\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ee\u003C\u002Fspan\u003E is associated with HERG\u002FIKR blockade.\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003C\u002Fol\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003E3\u003C\u002Fspan\u003E \n \u003Cstrong\u003EMyocardial infarction:\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Col class=\"list number nomark\"\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ea\u003C\u002Fspan\u003E has a higher incidence in patients with depression who have no cardiac disease\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Eb\u003C\u002Fspan\u003E may present with postural hypotension\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ec\u003C\u002Fspan\u003E may be associated with prolonged QT interval\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ed\u003C\u002Fspan\u003E is associated with increased platelet reactivity\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ee\u003C\u002Fspan\u003E is associated with sudden death when complicated by reduced heart rate variability.\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003C\u002Fol\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003E4\u003C\u002Fspan\u003E \n \u003Cstrong\u003ETricyclic antidepressants:\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Col class=\"list number nomark\"\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ea\u003C\u002Fspan\u003E are type 1 antiarrhythmic agents\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Eb\u003C\u002Fspan\u003E block sodium and potassium cardiac channels\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ec\u003C\u002Fspan\u003E are contraindicated in post-myocardial infarction depression\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ed\u003C\u002Fspan\u003E decrease heart rate variability\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ee\u003C\u002Fspan\u003E are a safe treatment for depression in the presence of bundle branch block.\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003C\u002Fol\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003E5\u003C\u002Fspan\u003E \n \u003Cstrong\u003EPostural hypotension:\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003Cp class=\"p\"\u003E \n \u003Col class=\"list number nomark\"\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ea\u003C\u002Fspan\u003E is a rare complication of psychotropic drug treatment\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Eb\u003C\u002Fspan\u003E may be a manifestation of myocarditis\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ec\u003C\u002Fspan\u003E may present with falls, fits or faints\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ed\u003C\u002Fspan\u003E is usually detectable on clinical examination\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003Cli class=\"list-item\"\u003E\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003Ee\u003C\u002Fspan\u003E is more frequent with SSRI than with tricyclic antidepressant therapy.\u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003C\u002Fol\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fli\u003E\n \u003C\u002Fol\u003E\n \n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"sec\"\u003E\n \u003Ch2 class=\"A\"\u003E \u003C\u002Fh2\u003E\n \u003Cp class=\"p\"\u003E \n \u003C\u002Fp\u003E\u003Cdiv class=\"table-wrap\" data-magellan-destination=\"T2\" id=\"T2\"\u003E\n \u003Cdiv class=\"caption\"\u003E\n \u003Cp class=\"p\"\u003E \n \u003Cstrong\u003EMCQ answers\u003C\u002Fstrong\u003E\n \u003C\u002Fp\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"figure-thumb\"\u003E\u003Cimg src=\"data:image\u002Fgif;base64,R0lGODlhAQABAIAAAMLCwgAAACH5BAAAAAAALAAAAAABAAEAAAICRAEAOw==\" data-src=\"https:\u002F\u002Fstatic.cambridge.org\u002Fbinary\u002Fversion\u002Fid\u002Furn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tabU2.gif?pub-status=live\" class=\"aop-lazy-load-image graphic\" width=\"348\" height=\"126\" data-original-image=\"urn:cambridge.org:id:binary:20180620095945424-0499:S1355514600000821:S1355514600000821_tabU2.gif\" data-zoomable=\"false\"\u003E\u003C\u002Fdiv\u003E\n \u003Ctable class=\"table no-colsep no-rowsep\"\u003E\n \u003Ccolgroup class=\"colgroup\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003Ccol class=\"col\"\u003E\n \u003C\u002Fcolgroup\u003E\n \u003Ctbody class=\"tbody top\"\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E1\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E2\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E3\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E4\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E5\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003E\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ea\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003EF\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ea\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ea\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ea\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ea\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003EF\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Eb\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Eb\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Eb\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Eb\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Eb\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ec\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ec\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ec\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ec\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ec\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ed\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ed\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ed\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ed\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ed\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003Ctr class=\"tr\"\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ee\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ee\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ee\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003ET\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ee\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003EF\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003Ee\u003C\u002Ftd\u003E\n \u003Ctd class=\"td top no-colsep no-rowsep left\" colspan=\"1\" rowspan=\"1\"\u003EF\u003C\u002Ftd\u003E\n \u003C\u002Ftr\u003E\n \u003C\u002Ftbody\u003E\n \u003C\u002Ftable\u003E\n \u003C\u002Fdiv\u003E\n \n \u003C\u002Fdiv\u003E\n \u003C\u002Fdiv\u003E\n \u003Cdiv class=\"back\"\u003E\n \n \n \u003C\u002Fdiv\u003E\n\u003C\u002Fdiv\u003E",tableOfContent:[],footnotes:[],fulltextNotes:[{content:"\n \n \u003Cp class=\"p\"\u003E\u003Cspan class=\"label\"\u003E*\u003C\u002Fspan\u003E denotes recommended reading.\u003C\u002Fp\u003E\n ",targetId:"FN1",displayNumber:q}],references:[{id:"manual_ref-1",displayNumber:a,existInContent:b,content:"\u003Cspan class=\"name\"\u003E\u003Cspan class=\"surname\"\u003EAgelink\u003C\u002Fspan\u003E, \u003Cspan class=\"given-names\"\u003EM. W.\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E, \u003Cspan class=\"name\"\u003E\u003Cspan class=\"surname\"\u003EMajewski\u003C\u002Fspan\u003E, \u003Cspan class=\"given-names\"\u003ET.\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E, \u003Cspan class=\"name\"\u003E\u003Cspan class=\"surname\"\u003EWurthmann\u003C\u002Fspan\u003E, \u003Cspan class=\"given-names\"\u003EC.\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E \n \u003Cem class=\"italic\"\u003Eet al\u003C\u002Fem\u003E (\u003Cspan class=\"year\"\u003E2001\u003C\u002Fspan\u003E) \u003Cspan class=\"article-title\"\u003EEffects of newer atypical antipsychotics on autonomic neurocardiac function: a comparison between amisulpride, olanzapine, sertindole, and clozapine\u003C\u002Fspan\u003E. \u003Cspan class=\"source\"\u003EJournal of Clinical Psychopharmacology\u003C\u002Fspan\u003E, \u003Cspan class=\"volume\"\u003E21\u003C\u002Fspan\u003E, \u003Cspan class=\"fpage\"\u003E8\u003C\u002Fspan\u003E–\u003Cspan class=\"lpage\"\u003E13\u003C\u002Fspan\u003E.\u003Ca class='ref-link' target='_blank' aria-label='CrossRef link for Effects of newer atypical antipsychotics on autonomic neurocardiac function: a comparison between amisulpride, olanzapine, sertindole, and clozapine' href=https:\u002F\u002Fdx.doi.org\u002F10.1097\u002F00004714-200102000-00003\u003ECrossRef\u003C\u002Fa\u003E\u003Ca class='ref-link' target='_blank' aria-label='Google Scholar link for Effects of newer atypical antipsychotics on autonomic neurocardiac function: a comparison between amisulpride, olanzapine, sertindole, and clozapine' 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H.\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E (\u003Cspan class=\"year\"\u003E1967\u003C\u002Fspan\u003E) \u003Cspan class=\"article-title\"\u003ECardiac changes related to phenothiazine, with special reference to thioridazine\u003C\u002Fspan\u003E. \u003Cspan class=\"source\"\u003EJournal of the American Geriatrics Society\u003C\u002Fspan\u003E, \u003Cspan class=\"volume\"\u003E15\u003C\u002Fspan\u003E, \u003Cspan class=\"fpage\"\u003E20\u003C\u002Fspan\u003E–\u003Cspan class=\"lpage\"\u003E28\u003C\u002Fspan\u003E.\u003Ca class='ref-link' target='_blank' aria-label='Google Scholar link for Cardiac changes related to phenothiazine, with special reference to thioridazine' href=https:\u002F\u002Fscholar.google.com\u002Fscholar_lookup?title=Cardiac+changes+related+to+phenothiazine%2C+with+special+reference+to+thioridazine&author=Wendkos+M.+H.&publication+year=1967&journal=Journal+of+the+American+Geriatrics+Society&volume=15&pages=20-28\u003EGoogle Scholar\u003C\u002Fa\u003E",item:[{googleScholarLink:"https:\u002F\u002Fscholar.google.com\u002Fscholar_lookup?title=Cardiac+changes+related+to+phenothiazine%2C+with+special+reference+to+thioridazine&author=Wendkos+M.+H.&publication+year=1967&journal=Journal+of+the+American+Geriatrics+Society&volume=15&pages=20-28",openUrlParams:{genre:g,atitle:aX,jtitle:aY,title:aY,volume:"15",artnum:"65b2ba27495e210001ee22fa",spage:"20",epage:"28",date:"1967",sid:f,aulast:a,aufirst:a,doi:e,au:a},innerRefId:"ref35",title:aX,doi:e,crossRefLink:a,pubMedLink:a}]}],figures:[{contentId:"F1",label:"Fig. 1",description:"\u003Cspan class=\"p\"\u003E\u003Cspan class=\"bold\"\u003EBrugada syndrome: electrocardiogram demonstrates typical findings of right bundle branch block and elevated S–T segment leads V1–V3. Rhythm: 25 mm\u002Fs. (reproduced with permission from Alings & Wild, 1999).\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E",thumbnailSrc:aZ,enlargedSrc:aZ,attrib:[]},{contentId:"F2",label:"Fig. 2",description:"\u003Cspan class=\"p\"\u003E\u003Cspan class=\"bold\"\u003EA short–long–short sequence of beats followed by an episode of torsade de pointes. The QT interval in the sinus beat immediately preceding the torsade de pointes is 600 ms (reproduced with permission from Khan, 2002).\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E",thumbnailSrc:a_,enlargedSrc:a_,attrib:[]},{contentId:"F3",label:"Fig. 3",description:"\u003Cspan class=\"p\"\u003E\u003Cspan class=\"bold\"\u003EECG of a phenothiazine-treated patient: complete normalisation of repolarisation abnormalities by overnight fasting. Left panel: initial non-fasting T-wave changes; right panel: T-wave normalisation after overnight fasting (reproduced with permission from Alvarez-Mena & Frank, 1973).\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E",thumbnailSrc:a$,enlargedSrc:a$,attrib:[]},{contentId:"F4",label:"Fig. 4",description:"\u003Cspan class=\"p\"\u003E\u003Cspan class=\"bold\"\u003ESchematic representation of the action potential and corresponding ECG phases.\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E",thumbnailSrc:ba,enlargedSrc:ba,attrib:[]},{contentId:"F5",label:"Fig. 5",description:"\u003Cspan class=\"p\"\u003E\u003Cspan class=\"bold\"\u003ESchematic representation of IKr block on the QT interval: (a) monophasic action potential (upper trace) and corresponding surface ECG (lower trace) before (B) and after (D) exposure to IKr blocking drug and the effect on the QT interval; (b) prolonged QT interval induces two early after-depolarisations (EADs) in the action potential (arrows), thus giving rise to a run of torsade de pointes on the surface ECG (lower trace). Reproduced with permission from Tamargo (2000).\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E",thumbnailSrc:bb,enlargedSrc:bb,attrib:[]},{contentId:"F6",label:"Fig. 6",description:"\u003Cspan class=\"p\"\u003E\u003Cspan class=\"bold\"\u003EECG demonstrating long–short coupling sequence. A ventricular premature contraction (B) succeeds a sinus beat (A), leading to a compensatory pause (long cycle ∗); another sinus beat (C), followed by a second ventricular premature contraction (D) (short cycle), triggers a run of torsade de pointes. Reproduced with permission from Tamargo (2000).\u003C\u002Fspan\u003E\u003C\u002Fspan\u003E",thumbnailSrc:bc,enlargedSrc:bc,attrib:[]},{contentId:"T1",label:"Table 1",description:"\u003Cspan class=\"p\"\u003E\u003Cspan class=\"bold\"\u003EDrug concentrations for blocking HERG tail-currents (IKr) in HERG-transfected cell 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