Aborted Sudden Cardiac Death: a Clinical Perspective

Postgrad Med J 2001;77:363–370 363

REVIEWS Postgrad Med J: first published as 10.1136/pmj.77.908.363 on 1 June 2001. Downloaded from

Aborted sudden cardiac death: a clinical perspective

P Mazeika

Abstract hypertrophic cardiomyopathy, idiopathic di- Sudden cardiac death in the community lated cardiomyopathy, or arrhythmogenic right remains a major public health problem. ventricular dysplasia, and to around 20% for The purpose of this article is to outline the cardiac arrest survivors in the era before avail- epidemiology, pathophysiology, and im- ability of the implantable cardioverter- mediate treatment of the cardiac arrest defibrillator (ICD).6 victim. The subsequent in-hospital diagnostic evaluation and management will Underlying pathology then be discussed with an emphasis on the Table 1 outlines common and important role of the implantable cardioverter- conditions found in these patients. Major defibrillator. A systematic and evidence predisposing pathological substrates include based approach should help to optimize the presence of a myocardial scar, ventricular patient care. hypertrophy from any cause, the various types (Postgrad Med J 2001;77:363–370) of cardiomyopathy, and a primary electrical abnormality. About 80% of cardiac arrest sur- Keywords: cardiology; implantable cardioverter- vivors have coronary atherosclerosis, 15% have defibrillator; resuscitation; sudden cardiac death non-coronary structural heart disease, and the remaining 5% have no identifiable structural Epidemiology substrate. Sudden cardiac death is defined as unexpected Hypertrophic cardiomyopathy is the com- natural death due to cardiac causes, heralded monest cause of sudden cardiac death in by abrupt loss of consciousness, and occurring athletes aged less than 35 years whereas in within one hour of the onset of acute older age groups coronary artery disease is the 1 symptoms. It is estimated that approximately predominant aetiology. Concussion of the 300 000 cases of sudden cardiac death occur heart from non-penetrating blunt trauma to per year in the United States with about 50 000 the anterior chest (commotio cordis) is a http://pmj.bmj.com/ 2 cases per year in the United Kingdom. recognised cause of sudden death during However, the nature of the condition makes sporting activities and is seen particularly in the estimates of incidence speculative. Around young because of the presence of a more com- 80% of sudden cardiac deaths occur in the pliant chest wall.7 home, 40% are unwitnessed, and bystander Drugs are an important preventable cause of cardiopulmonary resuscitation is initiated in sudden cardiac death. The Cardiac Arrhythmia 3

only 10%–20% of cases. Suppression Trial (CAST) served to highlight on October 1, 2021 by guest. Protected copyright. Because up to 80% of cardiac arrest the dangerous proarrhythmic potential of survivors have coronary artery disease, the epi- antiarrhythmic drugs in patients with underly- 8 University of Chicago demiology of these two conditions run paral- ing structural heart disease. Diuretics have Hospitals, Chicago, lel.4 Some autopsy series have documented sig- been incriminated as a cause of cardiac arrest Illinois, USA niﬁcant coronary atherosclerosis in over 90% in the hypertensive patient.9 This may be of victims.5 This may be because patients with mediated by hypokalaemia or hypomagnesae- Correspondence to: Dr Peter Mazeika, 18 Alma non-coronary pathology are more likely to sur- mia. Road, Sale, Cheshire vive cardiac arrest. In about 5% of victims of sudden death, no M33 4HB, UK The annual risk of sudden cardiac death evidence of structural heart disease can be 3 Submitted 24 August 2000 for the whole population is about 0.1%, rising found. The Unexplained Cardiac Arrest Regis- Accepted 17 October 2000 to an estimated 2%–4% for patients with try of Europe (UCARE) and the Idiopathic

Table 1 Causes and contributory factors in sudden cardiac death

Condition Examples Coronary atherosclerosis Remote myocardial infarction, acute myocardial infarction, acute myocardial ischaemia, left ventricular aneurysm Cardiomyopathy Hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia, cardiac sarcoid, myocarditis Valvular heart disease Aortic stenosis, prosthetic valve dysfunction Congenital heart disease Eisenmenger’s syndrome, tetralogy of Fallot, transposition of the great arteries, pulmonary vascular obstruction, congenital coronary artery anomaly Electrophysiological abnormality WolV-Parkinson-White syndrome, conduction system disease, congenital long QT syndrome, idiopathic ventricular ﬁbrillation, Brugada syndrome Miscellaneous Coronary artery spasm, Marfan’s syndrome, pulmonary hypertension, drugs (non-cardiac, cardiac, antiarrhythmic, illicit), ruptured sinus of valsalva aneurysm

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Structural or Transient initiating Arrhythmia Fatal arrhythmia Postgrad Med J: first published as 10.1136/pmj.77.908.363 on 1 June 2001. Downloaded from functional substrate event (trigger) mechanisms

Coronary artery disease Myocardial infarction Re-entry Monomorphic ventricular tachycardia Cardiomyopathy Ischaemia/reperfusion Automaticity Polymorphic Valvular heart disease Emotional/physical Triggered activity ventricular tachycardia stress Congenital heart disease Conduction block Ventricular fibrillation Haemodynamic Primary electrical decompensation Cell to cell uncoupling Profound bradycardia abnormality Electrolyte imbalance Asystole Channelopathy Hypoxaemia, acidosis Pulseless electrical activity Neurophysiological interactions

Drugs

Figure 1 Simpliﬁed conceptual framework to aid understanding of the pathophysiology of sudden cardiac death.

Ventricular Fibrillation registry of the United sudden cardiac death in people with estab- States (IVF-US) have recently been established lished coronary atherosclerosis. Rarely, a to gather more information on these cases.10 11 supraventricular arrhythmia can precipitate sudden death.13 Pathophysiology of sudden cardiac death The mechanisms triggering fatal arrhythmias Resuscitation in the community are complex and poorly understood but are The key elements of a community resuscitation likely to vary depending on the underlying programme, represented in the “chain of pathology and probably also between patients survival” motif, are early access, early basic with the same pathology (fig 1). cardiopulmonary resuscitation, early defibrilla- Plaque rupture with superadded thrombus tion, and early advanced cardiac life support in the coronary tree are found at necropsy in (fig 2).14 Victims of cardiac arrest in the many sudden cardiac death victims with community tend to have less comorbidity and coronary atherosclerosis and suggests a role for fewer systemic precipitants than patients who myocardial ischaemia as an initiator of the ter- arrest in hospital.15 minal event. However, only about 20% of car- Bottiger et al reported long term outcome

diac arrest survivors have features of acute after out of hospital cardiac arrest with a physi- http://pmj.bmj.com/ transmural myocardial infarction, although cian staVed emergency response system serving approximately half have evidence of remote an urban/suburban area of 330 000 inhabit- myocardial infarction with a healed scar.12 ants.16 For 338 patients, return of spontaneous Small cardiac enzyme elevations are the rule circulation was seen in 49%, survival to inten- and likely reflect a combination of factors sive care unit admission in 38%, and survival to including non-Q wave myocardial infarction, hospital discharge and one year was achieved in transient circulatory failure, cardiopulmonary 14% and 12% of patients, respectively. Overall, resuscitation, and defibrillation. five lives were saved per 100 000 population on October 1, 2021 by guest. Protected copyright. Clearly, plaque vulnerability, electrical insta- per year. bility, and thrombotic tendency are key patho- physiological issues in the coronary patient. Early in-hospital management Experimental studies in animals with healed As full recovery after cardiac arrest is rarely infarcts have confirmed that superadded is- immediate, restoration of sinus rhythm marks chaemia in this setting is particularly likely to the start and not the end of a resuscitation provoke malignant ventricular arrhythmias. In attempt. Without treatment, irreversible cer- the clinical arena, vigorous unaccustomed ebral dysfunction occurs within about three exercise and profound emotional or psycho- minutes of circulatory arrest. logical stress are well recognised precipitants of Meticulous control of blood gases, pH, and electrolytes in the period immediately after the arrest is necessary. In many cases, this can be achieved only by endotracheal intubation and Early mechanical ventilation of a sedated and Early advanced paralysed patient on the intensive care unit. Early basic Early cardiac The haemodynamics of the period after cardiac access cardiopulmonary defibrillation life arrest are complex and generally require resuscitation support invasive monitoring of arterial, central venous, and pulmonary capillary wedge pressure as well as cardiac output. Myocardial dysfunction with haemodynamic instability is the rule. The Figure 2 The chain of survival. maintenance of an adequate cerebral perfusion

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Table 2 Selected causes of sudden cardiac death and elements of their diagnostic work-up Postgrad Med J: first published as 10.1136/pmj.77.908.363 on 1 June 2001. Downloaded from

Condition Investigation Coronary artery disease Coronary angiography, stress testing Coronary artery spasm Ergonovine study Myocarditis; sarcoidosis Endomyocardial biopsy Hypertrophic and dilated cardiomyopathy; aortic stenosis Echocardiography Arrhythmogenic right ventricular dysplasia Magnetic resonance imaging, signal averaged electrocardiogram WolV-Parkinson-White syndrome; supraventricular tachycardia Electrophysiological testing Brugada syndrome Pharmacological challenge with a sodium channel blocker Congenital long QT syndrome; hypertrophic cardiomyopathy; Brugada syndrome Family screening, genotyping Illicit drug abuse Blood and urine toxicology screen

pressure, by ensuring an optimal mean arterial Diagnostic evaluation pressure, may be aided by a low to normal car- Survivors of out of hospital cardiac arrest not bon dioxide partial pressure, to minimise associated with acute transmural myocardial cerebral oedema. Close monitoring of haemo- infarction who are neurologically intact require dynamics and urine output can be used to an extensive diagnostic work-up. Two key guide fluid management and circulatory sup- issues are the diagnosis of the underlying sub- port with inotropes, vasodilators and, if neces- strate and the identification of reversible causes sary, the intra-aortic balloon pump. Cardiac of cardiac arrest (table 2). The strong link arrhythmias are extremely common and recur- between coronary artery disease and sudden rent ventricular fibrillation is seen in 10%–20% cardiac death makes coronary angiography, of patients, usually within the first 48 hours of stress testing, and assessment of left ventricular hospitalisation. Persistent ventricular arrhyth- function essential and helps determine the mias may be managed with intravenous need for coronary revascularisation. Left ven- lignocaine (lidocaine) or amiodarone. tricular function is commonly abnormal, often Where arrest complicates acute myocardial severely so, and is the most important determi- 21 infarction, decisions regarding acute percuta- nant of long term outcome in these patients. neous coronary intervention or coronary Among the cardiomyopathies, arrhythmogenic thrombolysis should be made on an individual right ventricular dysplasia is an uncommon but patient basis, carefully weighing the risks versus important cause of malignant ventricular arrhythmias. The diagnostic criteria for this benefits. Restoration of vessel patency at the 22 time of acute infarction may reduce the occur- condition have recently been reported. rence of subsequent ventricular arrhythmias.17 It has been estimated that a precipitant of the These patients should be managed like any arrhythmia can be identified in 25% of cases other acute myocardial infarct. with no obvious trigger in the other 75%. This issue influences the risk of recurrence. Recog- Common respiratory problems in these nised factors include acute myocardial infarc- patients include the adult respiratory distress tion and ischaemia, severe hypokalaemia, syndrome, aspiration, pneumothorax, and rib

supraventricular tachycardia, and drug proar- http://pmj.bmj.com/ fractures. Some degree of aspiration is prob- rhythmia. ably an inevitable consequence of cardiopul- Acute Q wave myocardial infarction is seen monary resuscitation. Gastric decompression in about 20% of patients who have coronary with a nasogastric tube and prophylactic atherosclerosis as the underlying pathology. antibiotics should be considered. Seizures sec- Moderate cardiac enzyme elevations compat- ondary to anoxic encephalopathy occur fre- ible with periarrest non-Q wave myocardial quently and may require anticonvulsants. infarction are very common but may also be Residual permanent cognitive impairment is due to transient circulatory arrest, cardiopul- on October 1, 2021 by guest. Protected copyright. seen in a significant minority of cardiac arrest monary resuscitation, and defibrillation. As it is survivors. As in all critically ill patients, the risk generally not possible to make the distinction of stress ulceration should be countered with with certainty, these findings do not preclude appropriate medications such as ranitidine or recommendation of an ICD. sucralfate. Acute myocardial ischaemia can precipitate Unfortunately, many patients who are ini- ventricular fibrillation. These patients give a tially resuscitated die within 72 hours from history of angina before collapse and usually persistent cerebral or myocardial dysfunction have angiographic evidence of severe coronary after arrest. However, in the period immedi- artery disease with physiological data confirm- ately after resuscitation it is not possible to reli- ing reversible ischaemia. The diagnosis is more ably predict long term outcome and therefore secure if there is no wall motion abnormality all patients should be managed aggressively. In and left ventricular function is normal. patients who are unconscious when admitted Severe hypokalaemia (potassium <2.5 to hospital, the prognosis becomes more unfa- mmol/l), often related to diuretic use, can trig- vourable the longer coma persists. In one study, ger a fatal ventricular arrhythmia. However, in 25% of patients who regained consciousness the period after resuscitation, hypokalaemia did so by the time of admission, 71% by day 1, may be due to the eVects of catecholamine 86% by day 2, and 92% by day 3.18 The usual release and therefore can be a consequence practice is to provide full support in the inten- rather than a cause of the cardiac arrest. sive care unit for at least 72 hours. A persistent Ventricular arrhythmias secondary to various vegetative state may develop in a small minor- medications, antiarrhythmic agents, and illicit ity of survivors.19 20 drugs such as cocaine are an important

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27 Aetiology Reversible Mixed Non-reversible patients after recent myocardial infarction. Where ACE inhibitors are not tolerated or Postgrad Med J: first published as 10.1136/pmj.77.908.363 on 1 June 2001. Downloaded from Treatment Correct reversible Correct reversible ICD contraindicated, alternatives include nitrates factors factors + ICD plus hydralazine and treatment with a specific angiotensin II receptor blocker such as losartan.28 The Randomized Aldactone Evaluation Study (RALES) found that spironolactone, an CAD Myocardial ischaemia Myocardial ischaemia No myocardial ischaemia aldosterone receptor blocker, substantially re- No previous MI Previous MI Previous MI duces the risk of both morbidity and death among patients with severe heart failure.29 Normal LV function Impaired LV function Impaired LV function Spironolactone 25–50 mg per day or placebo Treatment Coronary Coronary ICD was added to conventional treatment with an revascularisation revascularisation + ICD ACE inhibitor, loop diuretic and digoxin, and Figure 3 Management of the cardiac arrest survivor (CAD, coronary artery disease; after a mean follow up of 24 months, total ICD, implantable cardioverter-defibrillator; LV,left ventricular; MI, myocardial infarction). mortality was reduced from 46% in the placebo group to 35% in the spironolactone group preventable cause of cardiac arrest. Class Ia (p<0.001). Sudden death was also reduced and class III agents as well as many non-cardiac (p=0.02) and the authors speculated that these medications, such as antihistamines, antide- beneficial eVects might arise by the avoidance pressants, and major tranquillisers can prolong of potassium loss or the prevention of myocar- the QT interval and cause torsade de pointes dial fibrosis. tachycardia by generating early afterdepolarisa- The value of â-blockade in patients after tions. myocardial infarction is well established.30 More recently, treatment with â-blockers in General aspects of management patients with chronic stable heart failure has As approximately 80% of cardiac arrest survi- been shown to reduce all-cause mortality and vors have coronary atherosclerosis, it is impera- prevent sudden death in three prospective ran- tive that all coronary risk factors such as hyper- domised trials. These were the US Carvedilol tension, hypercholesterolaemia, cigarette Heart Failure Study,31 the Metoprolol CR/XL smoking, diabetes, and obesity are managed Randomized Intervention Trial in Congestive aggressively. Regular exercise on a cardiac Heart Failure (MERIT-HF),32 and the Cardiac rehabilitation programme may, by increasing InsuYciency Bisoprolol Study II (CIBIS II).33 vagal tone, be protective. Anxiety and depres- The addition of carvedilol (3.125–50 mg twice sion are not uncommon and require early rec- a day), controlled release metoprolol (12.5– ognition, counselling, and psychological sup- 200 mg once a day), or bisoprolol (1.25–10 mg 23 port. once a day) to conventional treatment was For patients with coronary atherosclerosis, eVective and well tolerated. These studies aspirin 75–325 mg/day should be prescribed included patients with both ischaemic and

indefinitely, unless contraindicated. A recent non-ischaemic heart failure in functional class http://pmj.bmj.com/ overview of 145 randomised trials of prolonged 2–4 and raise the possibility that â-blockade antiplatelet treatment versus control in about may prevent sudden death by an antifibrillatory 70 000 patients concluded that in a wide range eVect. of patients at high risk of occlusive vascular Although there is no direct evidence that any disease aspirin oVers worthwhile protection of the drugs outlined above are of value in the against myocardial infarction, stroke, and cardiac arrest survivor, their benefits are likely death.24 to extend to most of these patients. Lipid lowering treatment with a hydroxy- on October 1, 2021 by guest. Protected copyright. methyglutaryl coenzyme A reductase inhibitor Coronary revascularisation has been shown to reduce total mortality in Cardiac arrest in patients with coronary patients with coronary artery disease in several atherosclerosis occurs in three overlapping set- clinical trials. For example, the Scandinavian tings: acute myocardial infarction; transient Simvastatin Survival Study (4S) showed that myocardial ischaemia without infarction; and simvastatin significantly improved survival and ventricular arrhythmias arising from a previ- reduced the occurrence of major coronary ous, healed, myocardial infarct (fig 3). events and need for myocardial revascularisa- A small group of patients have myocardial tion in patients with angina pectoris or ischaemia as the primary cause of cardiac previous myocardial infarction with a raised arrest. Collapse typically occurs in relation to serum cholesterol despite dietary measures.25 exercise, there is an antecedent history of chest Cardiac arrest survivors with congestive pain but no evidence of acute infarction and heart failure should be treated with an subsequent stress testing reveals severe ischae- angiotensin converting enzyme (ACE) inhibi- mia with a large amount of jeopardised tor as there is overwhelming evidence that they myocardium. Cardiac catheterisation shows confer prognostic benefit.26 Clinical trials in severe proximal multivessel disease and normal patients after infarct have also shown that these global left ventricular systolic function with no drugs reduce mortality. A recent meta-analysis evidence of a regional wall motion abnormality. of 15 clinical trials involving over 15 000 Most experts agree that these patients can be patients found that ACE inhibitor treatment managed with coronary revascularisation alone significantly reduced total mortality, cardiovas- without cardioverter-defibrillator implanta- cular death, and sudden cardiac death in tion, with decisions between coronary artery

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Table 3 Implantable cardioverter deﬁbrillator (ICD) secondary prevention trials Postgrad Med J: first published as 10.1136/pmj.77.908.363 on 1 June 2001. Downloaded from

AVID CIDS CASH No of patients 1016 659 349 No of patients with ventricular ﬁbrillation (%) 455 (45) 314 (48) ? Mean patient age (years) 65 63 ∼57 Per cent with CAD 81 82 ∼80 Mean left ventricular ejection fraction (%) 32 34 ∼40 Antiarrhythmic drug group treatment Amiodarone, sotalol Amiodarone Amiodarone, metoprolol Mean follow up (months) 18.2 35.4 24 Primary endpoint Total mortality Total mortality Total mortality Two year total mortality in ICD group (%) 18 15 12 Two year total mortality in AAD group (%) 25 21 20 p Value <0.02 0.142 0.047

AAD, antiarrhythmic drug; AVID, Antiarrhythmics Versus Implantable Defibrillators Study; CAD, coronary artery disease; CASH, Cardiac Arrest Study Hamburg; CIDS, Canadian Implantable Defibrillator Study. bypass grafting and percutaneous coronary The implantable intervention being made on an individual case cardioverter-defibrillator basis. Implantation of a cardioverter-defibrillator is At the other end of the clinical spectrum are the most important element of treatment for patients with previous myocardial infarction the cardiac arrest survivor and has been shown who collapse while resting and give no history to improve survival in several clinical trials of preceding chest pain or limiting angina. (table 3). The Antiarrhythmics Versus Im- Stress testing typically reveals minimal or no plantable Defibrillator (AVID) study observed reversible ischaemia. Cardiac catheterisation clinical benefit from ICD therapy only in shows non-critical coronary artery disease and patients with a left ventricular ejection fraction depressed global left ventricular function with <35%.36 Furthermore, the average unadjusted a fixed wall motion abnormality. Implantation length of additional life associated with ICD of a cardioverter-defibrillator without con- therapy in AVID was only 2.7 months after comitant coronary revascularisation is appro- three years of follow up raising the issue of priate. Many patients fall between these competing causes of death and what pro- extremes and require both coronary revascularisation and an ICD. As the procedural risk of portion of total mortality is device preventable cardioverter-defibrillator implantation is in these patients (fig 4). The Cardiac Arrest higher in patients with untreated myocardial Study Hamburg (CASH) trial also had a ischaemia, coronary revascularisation should propafenone group which was discontinued be undertaken first. early after a significant excess mortality was 437 Observational data from the Coronary Ar- observed. It is possible that the smaller ICD tery Surgery Study (CASS) registry supports benefit found in the Canadian Implantable this approach.34 A comparison of medical with Defibrillator Study (CIDS) was due to its surgical treatment in 13 476 patients using longer duration of follow up compared with multivariate techniques found that coronary AVID as the two studies were of similar statis- http://pmj.bmj.com/ artery bypass grafting significantly reduced the tical power.38 One would expect deaths that incidence of sudden cardiac death and total were not device preventable to become more mortality over five years of follow up. The relief prominent with longer follow up. of myocardial ischaemia may have reduced or Based on the above studies the American eliminated the events triggering malignant College of Cardiology/American Heart Associ- ventricular arrhythmias in these patients. Simi- ation guidelines list cardiac arrest due to lar positive findings were reported from Seattle

ventricular tachycardia or ventricular fibrilla- on October 1, 2021 by guest. Protected copyright. by Every et al in 265 survivors of out of hospi- tion without a transient or reversible cause as a tal cardiac arrest resuscitated between 1970 class I indication for ICD therapy.39 Outcome and 1988.35 data from the AVID registry which includes trial eligible randomised, eligible non- randomised, and ineligible patients has recently been reported.40 A surprise finding was Non- Not Non- Non- that cardiac arrest survivors with or without an sudden device cardiac arrhythmic identifiable transient or correctable cause for death preventable the arrhythmia had a similarly poor prognosis: mortality was 18% compared with 17% during a mean follow up of 17 months. Clinical judg- Total ment regarding the presence of a reversible mortality factor may be inaccurate raising the possibility that ICD therapy may be beneficial for a broader range of patients than previously thought, especially if the left ventricular Sudden Cardiac Arrhythmic Device ejection fraction is <35%. death preventable Technological advances have greatly reduced the size of cardioverter-defibrillators such that transvenous prepectoral implantation under conscious sedation is now routine and has a Figure 4 What proportion of total mortality is device preventable? mortality risk of less than 1%. Current devices

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are multiprogrammable with extensive diag- cardiac transplantation. This drug has a nostic features including event counters, epi- complex pharmacological profile, multiple Postgrad Med J: first published as 10.1136/pmj.77.908.363 on 1 June 2001. Downloaded from sode logs, and stored electrograms, which are mechanisms of action, and the potential for very helpful for troubleshooting. serious side eVects with long term treatment Biphasic shocks result in a substantially including pulmonary fibrosis, hepatic toxicity, lower defibrillation threshold and have there- and thyroid dysfunction. Close monitoring is fore replaced the monophasic waveform. Bidi- therefore essential. Amiodarone has a half life rectional shock vectors involving two lead coils of 30–100 days and therefore peak eVect and the ICD casing oVer advantages over con- occurs only after several weeks of treatment ventional bipolar or single coil unipolar con- with an oral loading dose. figurations and are in common use. Defibrilla- The Cardiac Arrest in Seattle: Conventional tion thresholds around 10 J are usual and tend versus Amiodarone Drug Evaluation (CAS- to be lower with device implantation on the left CADE) study compared empiric amiodarone side. It may be appropriate to abbreviate to a Holter or electrophysiological study defibrillation threshold testing in some patients guided alternative antiarrhythmic agent (most with poor cardiac function to minimise proce- commonly quinidine or procainamide) in 228 dural risk. Current systems use integrated survivors of out of hospital ventricular fibrilla- bipolar sensing between the lead tip electrode tion.43 Survival free of cardiac death, resusci- and the large distal coil which theoretically tated ventricular fibrillation, or a syncopal defi- makes oversensing more likely. Leads with true brillator shock at two years was 82% for dedicated bipolar sensing may be superior but amiodarone compared with 69% for conven- are diYcult to manufacture and not yet gener- tional treatment (p=0.007). A recent meta- ally available. Device testing at implant is done analysis of 15 randomised trials of amiodarone at the least sensitive setting. If sensing of for the prevention of sudden cardiac death ventricular fibrillation is adequate the device is found that amiodarone significantly reduced generally programmed to a more sensitive level total mortality by 10% (placebo controlled trial which provides a fourfold safety margin, only) to 19% (all trials).44 Mortality reductions making oversensing more likely in the long were similar in trials enrolling patients after term. Similarly, when programming shock myocardial infarction (21%), with left ven- therapy in the ventricular fibrillation zone, the tricular dysfunction (22%), and after cardiac first shock administered should have a 10 J arrest (25%). safety margin over the defibrillation threshold Approximately one third of cardioverter- as this threshold rises by about5Jinaround defibrillator recipients also receive antiarrhyth- 50% of patients over the ensuing months. mic medication, most commonly for the For most cardiac arrest survivors a single control of coexisting supraventricular arrhyth- chamber ICD suYces. Detection enhance- mias such as atrial fibrillation. Another impor- ments such as stability algorithms, onset crite- tant indication is frequent device discharges, ria, and arrhythmia duration have also helped which, if unchecked, can substantially reduce to reduce the frequency of shocks triggered by the ICD’s usual five year longevity. Patient’s

sinus tachycardia, atrial fibrillation, or non- presenting with multiple appropriate shocks http://pmj.bmj.com/ sustained ventricular tachycardia. are generally admitted to hospital and stabi- Devices can be configured to provide diVer- lised with intravenous lignocaine or procaina- ent therapies in diVerent tachycardia cycle mide. If recurrent ventricular tachycardia length zones. For rapid ventricular tachycardia persists, intravenous or oral amiodarone com- or ventricular fibrillation, a high energy shock is bined with a â-blocker is usually eVective.45 appropriate first line treatment. Cardiac arrest Sotalol (160–320 mg per day) has been shown survivors often experience sustained mono- to significantly reduce the probability of an morphic ventricular tachycardia of intermedi- appropriate first shock and also to prevent the on October 1, 2021 by guest. Protected copyright. ate cycle length which is pace terminable and occurrence of shocks for supraventricular therefore it is well worth adding a antitachycar- arrhythmias in a double blind placebo control- dia pacing zone.41 led clinical trial.46 Defibrillator follow up is scheduled for every The possibility of an adverse drug-device three months as a minimum and patients interaction should always be borne in mind. should be encouraged to carry personal identi- Many drugs, including amiodarone and cal- fication and information about their device cium channel blockers, especially verapamil, with them at all times. Patients should not drive may increase the defibrillation threshold, for six months after implantation and for six sometimes dramatically. Antiarrhythmic drugs months after each subsequent shock. Commer- can also slow the ventricular tachycardia cycle cial driving should be prohibited indefinitely.42 length below the detection rate or increase shock frequency through proarrhythmic ef- Other aspects of arrhythmia fects. management Some patients continue to experience fre- Amiodarone is a potential alternative treatment quent device discharges or have sustained ven- if cardioverter-defibrillator implantation is tricular tachycardia below the ICD rate cut oV contraindicated or refused. Contraindications despite optimal antiarrhythmic drug treatment. include major cerebral dysfunction after arrest, Strickberger et al prospectively evaluated the significant psychiatric morbidity, terminal ill- utility of adjunctive radiofrequency catheter ness with life expectancy less than six months, ablation of ventricular tachycardia in this situ- and functional class 4 drug refractory heart ation.47 Ablation of the clinical arrhythmia was failure in patients who are not candidates for successful in 76% of 21 consecutive patients

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with coronary artery disease and signiﬁcantly 16 Bottiger BW, Grabner C, Bauer H, et al. Long term outcome

after out-of-hospital cardiac arrest with physician staVed Postgrad Med J: first published as 10.1136/pmj.77.908.363 on 1 June 2001. Downloaded from improved quality of life in these cases. Bundle emergency medical services: the Utstein style applied to a branch re-entrant ventricular tachycardia is midsized urban/suburban area. Heart 1999;82:674–9. 17 Vatterott PJ, Hammill SC, Bailey KR, et al. Late potentials uncommon but uniquely amenable to catheter on signal-averaged electrocardiograms and patency of the ablation and therefore should always be sought infarct-related artery in survivors of acute myocardial at electrophysiological testing in such patients. infarction. J Am Coll Cardiol 1991;17:330–7. 18 Longstreth WT, Inui TS, Cobb LA, et al. Neurological As previously mentioned, Wang et al found that recovery after out-of-hospital cardiac arrest. Ann Intern Med supraventricular tachycardia was the cause of 1983;98:588–92. 19 Multi-Society Task Force on PVS. Medical aspects of the aborted sudden cardiac death in 13 (4.5%) of persistent vegetative state (first of two parts). N Engl J Med 290 consecutive patients referred for electro- 1994;330:1499–508. 13 20 Multi-Society Task Force on PVS. Medical aspects of the physiological evaluation. This uncommon persistent vegetative state (second of two parts). N Engl J clinical scenario is important to recognise as Med 1994;330:1572–9. 21 Ritchie JL, Hallstrom AP, Troubaugh GB, et al. Out-of- many of these patients can be cured by catheter hospital sudden coronary death: rest and exercise radionu- ablation and cardioverter-defibrillator implan- clide left ventricular function in survivors. Am J Cardiol tation is unnecessary. 1985;55:645–51. 22 McKenna WJ, Thiene G, Nava A, et al. Diagnosis of Rarely, infranodal conduction system disease arrhythmogenic right ventricular dysplasia/cardiomyopathy. presents as a bradyarrhythmic cardiac arrest Br Heart J 1994;71:215–18. 23 Arteaga WJ, Windle JR. The quality of life of patients with and permanent pacing, rather than defibrillator life-threatening arrhythmias. Arch Intern Med 1995;155: implantation, is indicated.48 Recent evidence 2086–91. 24 Antiplatelet Trialists’ Collaboration. Collaborative overview suggests that isolated congenital complete of randomized trials of antiplatelet therapy-I: prevention of heart block may not be as benign a condition as death, myocardial infarction, and stroke by prolonged 49 antiplatelet therapy in various categories of patients. BMJ previously thought. In a large follow up study, 1994;308:81–106. there was a high incidence of Stokes-Adams 25 Scandinavian Simvastatin Survival Study Group. Rand- omized trial of cholesterol lowering in 4444 patients with attacks with considerable mortality from the coronary heart disease: the Scandinavian Simvastatin 49 first episode. Prophylactic permanent pace- Survival Study (4S). 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Medical Anniversary

Sir George Pickering, 26 June 1904 George Pickering (1904–80) was born in Whalton, Northumberland, son of a schoolteacher with strong farming traditions. He was educated at Dulwich, Pembroke College, Cambridge, and St Thomas’ where he qualiﬁed in 1928. He became professor of medicine at St Mary’s in 1939 and Oxford in 1956. His research provided the basis of the epidemiology of blood pressure in populations, and he brought numeracy into clinical thinking. He was a devoted historian of medicine and helped to found the Osler Club of London (1928). He died on 3 September 1980.—D G James http://pmj.bmj.com/ on October 1, 2021 by guest. Protected copyright.