Drugs 41 (Supp!. 2): 9-15, 1991 0012-6667/91/0200-0009/$03.50/0 © Adis International Limited All rights reserved. DRSUP1965

Can We Predict Sudden Cardiac Death? Thomas M einertz, 1 Thomas H a/mann 1 and Manfred Zehender2 Department of Cardiology, St George Hospital, Hamburg, Federal Republic of Germany 2 Department of Internal Medicine, University of Freiburg, Freiburg, Federal Republic of Germany

Summary

Up to now only 30 to 40% of patients who die suddenly can be identified as likely candidates before the event. Risk factors in these asymptomatic subjects include a familial history of coronary artery disease, high blood cholesterol levels, hypertension, smoking and, more importantly, an abnormal ECG at rest or during exercise. The predictive value of these abnormalities is too low to justify more detailed clinical investigations in most of these asymptomatic subjects. Exceptions might be the group of patients with multiple risk factors and competitive sportsmen. Sudden cardiac death is a well known complication in patients with hypertrophic and dilated cardiomyopathy. Risk factors in hypertrophic cardiomyopathy include a familial history of this disease, syncope and increasing age. Furthermore, in the adult, the presence of nonsustained episodes of ventricular tachycardia during Holter monitoring seems to indicate an increased risk of sudden cardiac death. In idiopathic dilated cardiomyopathy, the presence of frequent episodes of ventricular pairs and/or episodes of ventricular tachycardia during Holter monitoring, together with a reduced left ventricular ejection fraction, characterises the patient at risk of sudden cardiac death. In patients with coronary artery disease, the patient at risk of sudden cardiac death can be identified by investigating the following: coronary anatomy; global and regional left ventricular function; the presence of ischaemia during rest and/or exercise; the presence oflate potentials, by means of the signal-averaged ECG; the presence of spontaneous ventricular arrhythmias (especially sustained and nonsustained ventricular tachycardia); and the results of electrophysiological testing. On the basis of these investigations, 3 subgroups can be distinguished: patients at low risk, medium risk, and high risk of sudden cardiac death.

There is no general agreement on a definition of sudden cardiac death. Simplistic definitions depending on events occurring within 24 hours, 1 hour or minutes of death have been supplemented by definitions that include the clinical presentation and the aetiology of death. Such a definition, related to both the time-course and the clinical setting, was used in the cardiac arrhythmia pilot study (Greene

et al. 1989). From this study it appeared that nearly all cases of sudden cardiac death were arrhythmic in origin, but 25% of those were associated with myocardial ischaemia. Furthermore, it is also clear that ischaemic myocardial dysfunction can occur rapidly and leads to ventricular failure within minutes, followed by secondary ventricular fibrillation or asystole. Therefore, the identification of the

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patient at risk of sudden cardiac death has to be related not only to the potential for electrical instability, but all other factors that might be associated with or promote ventricular fibrillation or asystole.

1. The Asymptomatic Patient At present, only 30 to 40% of patients dying suddenly and unexpectedly can be identified as being at risk before the event. In the remaining patient population, sudden cardiac death is either preceded by only short-lasting clinical symptoms or occurs in a completely asymptomatic individual. It is possible to recognise those asymptomatic patients at increased risk of sudden cardiac death. Risk factors include a familial history of coronary artery disease, high blood cholesterol levels, hypertension, smoking and, more importantly, an abnormal ECG at rest or during exercise. During a 6-year follow-up of 2456 individuals in the Tecumseh Study, 7 patients who died suddenly had normal ECGs, and 38 deaths occurred in those with abnormal ECG findings. The ECG findings associated with a higher incidence of sudden cardiac death included bilateral bundle branch block (EBB), left bundle branch block (LBBB), and signs of previous myocardial infarction. There were 6 cardiac deaths in the group of 124 individuals with signs of left ventricular hypertrophy on ECG (Chiang et al. 1970). In a 4-year follow-up study of 17 705 men, ECG abnormalities associated with an increased risk of sudden cardiac death included intraventricular conduction defects, QRS complex with a Q or QS configuration, abnormal left axis deviation, ST segment depression, and a T-wave abnormality (Pedoe 1978). It is obvious that the ECG abnormalities found in both of the previously mentioned studies suggest an underlying cardiac disease, most probably coronary artery disease with previous myocardial infarction. Fmihermore, left ventricular hypertrophy and interventricular conduction delay seem to be predisposing factors for sudden cardiac death. Although these risk factors can be associated

with sudden cardiac death, the predictive value of these clinical and ECG abnormalities is too low to justify wide use of further clinical investigations in completely asymptomatic patients with one ofthese risk factors. Stress scintigraphy, echocardiography and, when indicated, also coronary angiography can only be recommended in younger asymptomatic patients with multiple risk factors for coronary heart disease and thus for sudden cardiac death. However, there may be another group in whom these investigations are probably justified.

2. The Athlete and the Competitive Sportsman In a retrospective investigation of 133 recreational and competitive athletes who died suddenly during physical exercise, Siscovick and coworkers (1984) showed that, at a level oflight training, peak exercise was associated with a 56-fold increased risk of sudden cardiac death compared with exercisefree periods. By contrast, at a high training level, the risk of sudden cardiac death under extreme physical stress was elevated only 5-fold (Siscovick et al. 1984). These findings challenge a direct connection between sudden cardiac death and highperformance sports and raise the question of other factors allowing prediction of an increased risk of sudden cardiac death. The incidence of organic changes in athletes who died suddenly under competition conditions is well above 70% in all studies: in the group of athletes < 40 years of age, hypertrophic cardiomyopathy predominated (Maron et al. 1978). In spite of diagnostic problems, this heart disease can be differentiated by echocardiography from physiological, training-induced and, frequently, septal-dominant muscle hypertrophy (Menapace et al. 1982). However, in some endangered athletes who have an unphysiologically strong but symmetrical muscle hypertrophy, a differentiation between training-induced muscle hypertrophy and hypertrophic cardiomyopathy is not possible (Maron et al. 1978). A second group of athletes who died unexpectedlyhad congenital malformations of the heart. Anomalies in the coronary arteries and so-called

Can We Predict Sudden Cardiac Death?

'muscular bridges' are relatively frequent and have increasingly been held responsible for the occurrence of sudden cardiac death. In cases of anomalous origin of the coronary artery from the right sinus Valsalva, the angle of origin at the aortic root increases with increased physical exercise; an origin of the right coronary artery from the left sinus Val salva shifts more sharply to the right during exercise; both mechanisms may result in acute myocardial ischaemia (Maron et al. 1978; discussion). Likewise, so-called 'muscular bridges' may very rarely induce ischaemia during exercise. Interestingly, such bridges are observed in 20% of the general population (Maron et al. 1978; Morales et al. 1980). Acute aortic rupture (e.g. as a consequence of the Marfan syndrome), inflammatory changes or coronary heart disease are much less frequent causes of sudden cardiac death in young athletes. Prodromal symptoms are reported in one-third of the younger athletes before sudden cardiac death (Maron et al. 1978; Opie 1975; Thompson & Stern 1979). In the group of athletes> 40 years of age, the cause of sudden cardiac death is predominantly coronary artery disease. Vuori and coworkers (1978) described 10 cases of sudden cardiac death during sports activities in a long term study involving more than 1 million trained cross-country skiers over 40 years of age. Eight of these individuals had coronary heart disease (Vuori et al. 1978). In another study by the same authors of 68 000 active persons over a 16-year observation period, 339 died during sports activities; 81 % of these had coronary heart disease. A report by Munschek (1977) on autopsy findings in 67 of 124 competitive athletes after sudden cardiac death during athletic activities showed that 59 had coronary heart disease (Munschek 1977). Convincing evidence of coronary artery disease was also found by Opie (1975) in 10 athletes in this age group who died suddenly, and electrical instability caused by coronary artery disease appears to be as important as acute myocardial infarction (Friedman et al. 1972). Therefore, exercise-induced sudden cardiac death in athletes and in active sportsmen is unusual without pre-existing heart disease.

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The cause of sudden cardiac death in those < 40 years of age can be predominantly ascribed to congenital heart disease (such as hypertrophic cardiomyopathy or coronary anomalies). In athletes> 40 years of age, coronary artery disease is the most frequent autopsy finding. Medical examinations (ECG, echocardiogram) might result in a reduction in sudden cardiac death in this population.

3. Hypertrophic Cardiomyopathy Sudden cardiac death is a well known complication in patients with hypertrophic cardiomyopathy. The overall annual mortality rate in adults is approximately 2.5%, while in children and adolescents it is even higher, at approximately 6% (McKenna et al. 1981a,b). Most of these deaths are sudden and unexpected. In a retrospective analysis, McKenna and coworkers (1981a,b) studied the predictive accuracy of 24 clinical, ECG and haemodynamic variables in 228 children and adults with hypertrophic cardiomyopathy. Discriminant analysis revealed that the combination of young age at diagnosis, syncope and a familial history of hypertrophic cardiomyopathy and sudden cardiac death best predicted sudden death, with a false negative rate of 30%, a false positive rate of 27% and a positive predictive accuracy of 24%. The addition of ECG, haemodynamic and angiographic parameters to the analysis did not significantly improve the predictive accuracy (Newman et al. 1985). Furthermore, echocardiographic parameters such as septal thickness were not useful for predicting sudden cardiac death in this patient population (Maron et al. 1982). The importance of arrhythmias as a determinant of sudden cardiac death in this disease has been repeatedly emphasised. Observations from large cohorts of patients in 2 independent referral centres suggest that adults with episodes of nonsustained ventricular tachycardia during Holter monitoring have an increased annual mortality from sudden cardiac death (Maron et al. 1981; McKenna et al. 1984). According to these studies, nonsustained ventricular tachycardia is a marker of the adult with hypertrophic cardiomyopathy who is at particular

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risk of sudden cardiac death. In children and adolescents, these arrhythmias are rare and other clinical factors (see above) seem to be more predictive. The clinical relevance of the finding that nonsustained ventricular tachycardia observed during 24-hour Holter monitoring identifies adults at risk of sudden cardiac death is still debated. Since more than 50% of the patients with these arrhythmias survive for several years, the positive predictive accuracy of this diagnostic marker is low (22% according to McKenna 1981a,b). Whether programmed electrical stimulation further improves risk stratification in patients with hypertrophic cardiomyopathy has been evaluated in recent years. Electrophysiological studies were performed in high risk patients (previous syncope or cardiac arrest), as well as in asymptomatic patients. Programmed electrical stimulation with up to 2 extrastimuli did not distinguish between patients with cardiac arrest or syncope and asymptomatic patients (Kuck et al. 1987). Other workers have shown that programmed electrical stimulation with up to 2 extrastimuli can initiate sustained ventricular tachycardia (often polymorphic) or ventricular fibrillation in significant numbers of these patients (20 to 40%). The high number of induced arrhythmias can be interpreted as a sign of the electrical vulnerability of the myocardium in this disease. The prognostic importance of these induced arrhythmias remains uncertain and questionable. Only in those patients who have already had an arrhythmic event such as cardiac arrest, ventricular fibrillation, or documented sustained ventricular tachycardia, can the induction of sustained ventricular tachycardia by programmed electrical stimulation be regarded as a meaningful diagnostic marker.

4. Idiopathic Dilated Cardiomyopathy It is now recognised that the incidence of sudden cardiac death is relatively high in patients with idiopathic dilated cardiomyopathy. According to recent reports, about 20 to 40% of all patients with this disease die suddenly and unexpectedly (Dunica & Coumel 1986).

Since most cases of sudden cardiac death are thought to be secondary to an arrhythmia, attention has-recently focused on the detection of ventricular arrhythmias during 24-hour Holter monitoring. Complex and frequent ventricular arrhythmias are exceedingly common in idiopathic dilated cardiomyopathy and short salvos of ventricular tachycardia and episodes of ventricular pairs occur in 25% to 70% of patients with this disease (Dunica & Coumel 1986). The prognostic value of these arrhythmias remains controversial. Several studies support the conclusion that the presence of severe nonsustained ventricular arrhythmias is independently related to overall cardiac mortality. However, it is still debatable whether these arrhythmias can also be regarded as an independent risk marker for sudden cardiac death. We found that patients with reduced left ventricular ejection fractions (below 40%) and a high number of ventricular pairs or episodes of ventricular tachycardia during 24-hour Holter monitoring have a clearly increased risk of sudden cardiac death (Meinertz et al. 1984). Programmed electrical stimulation with up to 2 extrastimuli did not improve the risk stratification in this asymptomatic patient population (Meinertz et al. 1985). Induced polymorphic ventricular tachycardia had no prognostic relevance in this patient population. Sustained monomorphic ventricular tachycardia was induced only in those patients with a history of such an arrhythmia (Das et al. 1986; Poll et al. 1984). Furthermore, we were unable to detect late potentials in a significant number of patients with this disease (Meinertz et al. 1985). Thus, in patients with idiopathic dilated cardiomyopathy and without previous cardiac arrest or syncope, neither programmed electrical stimulation nor conventional signal averaging seem to be of value for risk stratification.

5. Coronary Artery Disease The mechanism of sudden cardiac death varies markedly in subsets of patients with coronary artery disease. The relative incidence of the various mechanisms during different clinical stages and

Can We Predict Sudden Cardiac Death?

manifestations of coronary artery disease is difficult to ascertain. From a theoretical and practical point of view, 3 major factors are especially relevant for the genesis of sudden cardiac death in this clinical setting: haemodynamic dysfunction, ischaemia and electrical instability. These 3 factors are closely interrelated and are modified by several other factors, such as the influence of the autonomic nervous system, electrolyte imbalance or drug effects. In normal clinical situations, sudden cardiac death is a result of a complex interplay between these factors. However, in a particular patient, only 1 or 2 of these factors may be responsible. For example, in a previously asymptomatic man, a large anterior transmural myocardial infarction may provoke mechanical and electrical cardiac arrest. In another patient with previous myocardial infarction and severely depressed left ventricular function , pulmonary embolism might produce acute right heart failure and third degree atrioventricular block. On the basis of clinical judgments, a distinction between nonarrhythmic and arrhythmic sudden cardiac death could not be made. The risk of sudden cardiac death differs between patient subsets, and stages of coronary artery disease. According to their risk of sudden cardiac death, patients can be subdivided into low risk, medium risk and high risk groups. 5.1 The Low Risk Patient The low risk patient with coronary artery disease has no signs of symptomatic or silent ischaemia during rest or exercise, normal or nearly normal left ventricular function , and a normal ECG. The overall prognosis for these patients is good, and the risk of sudden cardiac death is very low. The presence of simple or complex ventricular arrhythmias during Holter monitoring can not be regarded as an additional risk factor for sudden cardiac death in these patients. Obviously, most patients with coronary artery disease belong to this low risk population. However, since the number of patients in this group is very high, even a slightly increased relative risk for sudden cardiac death will

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result in a significant number of cases in this low risk population. 5.2 The Medium Risk Patient Compared with the low risk coronary artery disease population, patients in the medium risk group have a clearly increased risk of dying suddenly and unexpectedly. Since this is not a homogeneous patient group, the exact estimate of the risk of sudden cardiac death can not be easily given. This patient population consists of at least 3 subgroups with different clinical and pathophysiological characteristics: first, the patients with recent myocardial infarction; second, the patients with unstable angina; and, last, the patients with severely depressed left ventricular function as a consequence of nonrecent myocardial infarction. In the patient with recent myocardial infarction (within the last few months), the prognosis is mainly determined by the degree of left ventricular impairment, the presence of residual ischaemia in the infarcted and noninfarcted areas, and the presence of myocardial electrical instability. The risk stratification of these patients should include the analysis of left ventricular function (treadmill test, radio nuclide angiography during rest and exercise, left ventricular angiography, 2-dimensional echocardiography), stress scintigraphy, coronary angiography, Holter monitoring, ECG monitoring oflate potentials and, in selected patients, programmed electrical stimulation. Although patients with a clearly increased risk of sudden cardiac death can be identified using these diagnostic techniques, the positive predictive value of this diagnostic workup is relatively low. As regards the results of Holter monitoring, risk prediction is limited by the inverse relationship between sensitivity and specificity of the Holter result. For example, the presence of more than 3 premature ventricular contractions per hour during 24-hour Holter monitoring has a high sensitivity but a low specificity for the prediction of sudden cardiac death. By contrast, the presence of frequent premature ventricular contractions (> 30/hour), together with frequent runs of ventricular tachycardia, has a relatively high

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specificity but a low sensitivity for the prediction of sudden cardiac death. In the patient with unstable angina, sudden cardiac death can occur as a result of ventricular fibrillation due to severe ischaemia. Close monitoring of the electrical and haemodynamic situation, and anti-ischaemic therapy may be the best methods for the prevention of sudden cardiac death. Patients with severely depressed left ventricular ejection fraction have an annual mortality rate of 20 to 30%, which is clearly higher than that of patients with a left ventricular ejection fraction above 50% (Moss et al. 1983). In these patients, the degree of left ventricular impairment seems to be by far the most important prognostic factor as regards sudden cardiac death (Ahnve et al. 1986). Patients requiring treatment for congestive heart failure after acute myocardial infarction have a particularly poor prognosis (Dwyer et al. 1986; Packer 1985). Since 30 to 40% of these patients die suddenly, the question arises whether the frequent and complex ventricular arrhythmias found in most of these patients are independent markers of sudden cardiac death. As in the case of patients with idiopathic dilated cardiomyopathy, it is debatable whether these arrhythmias indicate an increased risk of sudden cardiac death or merely reflect the bad overall prognosis. Can we improve risk stratification by looking for abnormalities in the signalaveraged ECG in this group of patients? A number of reports suggest that the absence oflate potentials in this group and in those with recent myocardial infarction indicates a relatively good prognosis. Correspondingly, it has been reported that the presence of late potentials in these patients indicates an increased risk of sudden cardiac death and recurrences of spontaneous ventricular tachycardia. Programmed electrical stimulation has also been repeatedly used in this group of patients. However, at present there is no clinical evidence that routin.e use of this procedure can improve the diagnostic information and help to identify the patients at risk of sudden cardiac death. 5.3 The High Risk Patient The high risk patient with coronary artery disease either has recurrent symptomatic ventricular tachycardia or is a survivor of ventricular fibril-

lation (in the absence of acute myocardial infarction). The annual mortality rate in these patients is 10 to 30%, depending on the severity of the undedying disease, the degree of left ventricular impairment, and the electrophysiological characteristics of the tachycardia. It is generally agreed that this group of patients must be assessed in hospital for coronary status, left ventricular function, residual ischaemia at rest or during exercise, and the presence of an arrhythmogenic substrate.

6. Conclusion Before treating a patient for the prevention of sudden cardiac death, a careful risk stratification is required. For this purpose the following questions have to be answered: 1. What is the underlying cardiac disease and the status of the coronary anatomy? 2. What is the global and regional left ventricular function? 3. Is there any evidence of residual ischaemia during either rest or exercise? 4. Are there markers for an arrhythmogenic substrate and/or a high incidence of complex ventricular arrhythmias (especially frequent episodes of non sustained ventricular tachycardia)? 5. Is there evidence for the presence of late potentials detected by ECG signal-averaging techniques? 6. Is electrophysiological testing required to test for the inducibility of sustained ventricular tachycardia?

References Ahnve S, Gilpin E. Henning H. Curtis G. Collins D, et al. Limitations and advantages of the ejection fraction for defining high risk after acute myocardial infarction. American Journal of Cardioiogy 58: 872-878, 1986 Chiang BN, Perlman LV, Fulton M, Ostrander LD, Epstein FH. Predisposing factors in sudden cardiac death in Tecumseh, Michigan: a prospective study. Circulation 41: 31-37, 1970 Das SK, Morady F, DiCarlo L, Baerman J, Krol R, et al. Prognostic usefulness of programmed ventricular stimulation i'n idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias. American Journal of Cardiology 58: 9981000, 1986 Dunica S, Coumel P. Incidence and mechanisms of sudden death in patients with left ventricular dysfunction. Heart Failure 6: 244-255, 1986 Dwyer EM, Greenberg H, Case RB and the Multicenter Postin-

Can We Predict Sudden Cardiac Death?

farction Research Group: association between transient pulmonary congestion during acute myocardial infarction and high incidence of death in six months. American Journal of Cardiology 58: 900-905, 1986 Friedman M, Manwaring JH, Roseman RH. Instantaneous exercise and sudden death. Journal of the American Medical Association 225: 1319-1323, 1972 Greene HL, Richardson OW, Barker AH, Roden OM, Capone RJ, et al. and the CAPS investigators. Classification of death after myocardial infarction as arrhythmic or nonarrhythmic (The Cardiac Arrhythmia Pilot Study). American Journal of Cardiology 63: 1-6, 1989 Kuck KH , Kunze KP, Geiger M, Costard A, Schluter M. Programmed electrical stimulation in patients with hypertrophic cardiomyopathy: results in patients with and without cardiac arrest or snycope. Cardiac Arrhythmias 22: 367-376, 1987 Maron BJ, Roberts WC, Edwards JE, McAllister HA, Epstein SE. Sudden death in patients with hypertrophic cardiomyopathy: characterization of 26 patients without functional limitations. American Journal of Cardiology 41: 803, 1978 Maron BJ, Roberts We, Epstein SE. Sudden death in hypertrophic cardiomyopathy: a profile of 78 patients. Circulation 65: 1388-1394, 1982 Maron BJ, Savage DO, Wolfson JK, Epstein SE. Prognostic significance in 24 hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: a prospective study. American Journal of Cardiology 48: 252-257, 1981 McKenna WJ, Deanfield J, Faruqui A, England 0, Oakley CM, et al. Prognosis in hypertrophic cardiomyopathy. American Journal of Cardiology 47: 532-538, 1981a McKenna WJ, England 0, Doi YL, Deanfield JE, Oakley CM, et al. Arrhythmia in hypertrophic cardiomyopathy. I. Influence on prognosis. British Heart Journal 46: 168-172, 1981b McKenna WJ. Harris L, Rowland E, Kleinebenne A, Krikler OM, et al. Amiodarone for long term management of patients with hypertrophic cardiomyopathy. American Journal of Cardiology 54: 802-810, 1984 Meinertz T, Hofmann T, Kasper W, Treese N, Bechtold H, et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. American Journal of Cardiology 53: 902-907, 1984 Meinertz T, Treese N, Kasper W, Geibel A, Hofmann T, et al.

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Determinants of prognosis in idiopathic dilated cardiomyopathy as determined by programmed electrical stimulation. American Journal of Cardiology 56: 337-341, 1985 Menapace FJ, Hammer WJ, Rityer TF. Left ventricular size in competitive weight lifters: an echocardiographic study. Medicine and Science in Sports and Exercise 3: 141-144, 1982 Morales AR, Romanelli R, Boucek RJ. The neural LAD coronary artery, strenuous exercise and sudden death. Circulation 62: 230, 1980 Moss AJ, Bigger TJ, Case RB, Gillespie JA, Goldstein RE, et al. The multicenter postinfarction research group: risk stratification and survival after myocardial infarction. New England Journal of Medicine 390: 331 .. 336, 1983 Munschek H. Ursachen des akuten TQdes beim Sport in der Bundesrepublik. Sportarzt und Sportmedizin 5: 133, 1977 Newman H, Sugrue DO, Oakley CM, Goodwin JF, McKenna WJ. Relation ofleft ventricular function and prognosis in hypertrophic cardiomyopathy: an angiographic study. Journal of the American College of Cardiology 5: 1064-1074, 1985 Opie LH. Sudden death and sports. Lancet 3: 263-267, 1975 Packer M. Sudden unexpected death in patients with congestive heart failure: a second frontier. Circulation 72: 681-685, 1985 Pedoe HOT. Predictability of sudden death from resting electrocardiogram: effect of previous manifestations of coronary heart disease. British Heart Journal 4040: 630-635, 1978 Poll OS, Marchlinski FE, Buxton AE, Doherty JU, Waxman HL, et al. Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy. Circulation 70: 451-456, 1984 Siscovick 0, Weiss N, Fletcher R, Lasky T. The incidence of primary cardiac arrest during vigorous exercise. New England Journal of Medicine 311: 874-876, 1984 Thompson PO, Stern MP. Death during jogging or running. Journal of the American Medical Association 242: 1265-1270, 1979 V uori I, Makarainen M, Lasselainen A. Sudden death and physical activity. Cardiology 63: 287-295, 1978

Correspondence and reprints: Prof. Dr T. Meinertz, II. Med. Klinik, AK SI Georg, Lohrntihlenstrasse 5, 2000 Hamburg I, Federal Republic of Germany.

Can we predict sudden cardiac death?

Up to now only 30 to 40% of patients who die suddenly can be identified as likely candidates before the event. Risk factors in these asymptomatic subj...
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