Mss20666 886..897

Habitual physical activity reduces coronary heart disease events, but vigorous activity can also acutely and transiently increase the risk of sudden cardiac death and acute myocardial infarction in susceptible persons. This scientific statement discusses the potential cardiovascular complications of exercise, their pathological substrate, and their incidence and suggests strategies to reduce these complications. Exercise-associated acute cardiac events generally occur in individuals with structural cardiac disease. Hereditary or congenital cardiovascular abnormalities are predominantly responsible for cardiac events among young individuals, whereas atherosclerotic disease is primarily responsible for these events in adults. The absolute rate of exercise-related sudden cardiac death varies with the prevalence of disease in the study population. The incidence of both acute myocardial infarction and sudden death is greatest in the habitually least physically active individuals. No strategies have been adequately studied to evaluate their ability to reduce exercise-related acute cardiovascular events. Maintaining physical fitness through regular physical activity may help to reduce events because a disproportionate number of events occur in least physically active subjects performing unaccustomed physical activity. Other strategies, such as screening patients before participation in exercise, excluding high-risk patients from certain activities, promptly evaluating possible prodromal symptoms, training fitness personnel for emergencies, and encouraging patients to avoid high-risk activities, appear prudent but have not been systematically evaluated. R egular physical activity is widely advocated by the medical community in part because substantial epidemiological, clinical, and basic science evidence suggests that physical activity and exercise training delay the development of atherosclerosis and reduce the incidence of coronary heart disease (CHD) events (1–4). Nevertheless, vigorous physical activity can also acutely and transiently increase the risk of acute myocardial infarction (AMI) and sudden cardiac death (SCD) in susceptible individuals (5–7). This scientific statement presents the cardiovascular complications of vigorous exercise, their pathophysiological substrate, and their incidence in specific patient groups and evaluates strategies directed at reducing these complications. The goal is to provide healthcare professionals with the information they need to advise patients more accurately about the benefits and risks of physical activity. Most studies of exercise-related cardiovascular events have examined events associated with sports participation in young subjects and with vigorous exercise in adults. Vigorous exercise is usually defined as an absolute exercise work rate of at least 6 metabolic equivalents (METs), which is historically assumed to equal an oxygen uptake (V̇O2) of 21 mLIkg Imin. Six METs approximates the energy requirements of activities such as jogging. Six METs is an arbitrary threshold and does not account for the fact that the myocardial oxygen demands of any physical activity are more closely related to the V̇O2 requirements relative to maximal exercise capacity than to the absolute work rate per se. Consequently, exercise work rates G 6 METs may still place considerable stress on the cardiovascular systems of unfit and older individuals. PATHOPHYSIOLOGICAL BASIS FOR EXERTION-RELATED CARDIOVASCULAR EVENTS Exercise-associated acute cardiac events generally occur in individuals with structural cardiac disease. 0195-9131/07/3905-0886/0 MEDICINE & SCIENCE IN SPORTS & EXERCISE Copyright 2007 by the American Heart Association and the American College of Sports Medicine DOI: 10.1249/mss.0b013e3180574e0e This joint position paper was authored by the American College of Sports Medicine and the American Heart Association. The content appears in AHA style. This paper is being published concurrently in Medicine & Science in Sports & Exercise and in Circulation. SPECIAL COMMUNICATIONS 886 SP EC IA L C O M M U N IC AT IO N S Pathological Findings in Young Individuals Among young individuals, variously defined as G 30 or G 40 years of age, the most frequent pathological findings are hereditary or congenital cardiovascular abnormalities (8–10), including hypertrophic cardiomyopathy; coronary artery anomalies (eg, anomalous coronary artery origin, acute angle takeoff and ostial ridges, or intramyocardial course) (11,12); aortic stenosis; aortic dissection and rupture probably associated with connective tissue defects such as Marfan syndrome; mitral valve prolapse; arrhythmogenic right ventricular cardiomyopathy; and arrhythmias, including those resulting from accessory atrioventricular pathways and channelopathies such as the long-QT syndrome. Myocarditis also is associated with exercise-related deaths in young individuals. Ventricular arrhythmias are the immediate cause of death in these conditions, except for Marfan syndrome, in which aortic rupture is often the proximate cause (Table 1). Pathological Findings in Adults In contrast to young subjects, coronary artery disease (CAD) is the most frequent pathological finding among older individuals who die during exertion (13,14). Among previously asymptomatic adults, evidence of acute coronary artery plaque disruption, including plaque rupture or erosion, with acute thrombotic occlusion is common (14). The mechanism by which vigorous exercise provokes such events is not defined, but suggested triggering mechanisms (15,16) include increased wall stress from increases in heart rate and blood pressure, exercise-induced coronary artery spasm in diseased artery segments (17), and increased flexing of atherosclerotic epicardial coronary arteries (15), leading to plaque disruption and thrombotic occlusion. Vigorous exercise also could provoke acute coronary thrombosis by deepening existing coronary fissures, augmenting catecholamine-induced platelet aggregation, or both. Spontaneous coronary plaque fissures are common and have been reported in 9% of subjects dying in motor vehicle accidents or by suicide and in 17% of people dying of noncoronary atherosclerosis (18). This observation suggests that mildly fissured coronary plaques require some exacerbating event such as vigorous physical activity to induce coronary thrombosis. An increase in thrombogenicity also could contribute to coronary thrombosis after plaque rupture or erosion. Increased platelet activation has been reported in sedentary individuals who engage in unaccustomed high-intensity exercise but not in physically conditioned individuals (19,20). Because circulating catecholamine levels are related more closely to the relative intensity of exercise for the individual than to the absolute exercise intensity, it is likely that platelet activation also is related to the relative intensity of the exercise session (21). Among individuals with symptomatic CHD, pathophysiological processes may include plaque disruption as above or ischemia-induced ventricular fibrillation from peri-infarction, ischemic tissue, or scar (22). Vigorous physical exertion, which increases myocardial oxygen demand and simultaneously shortens diastole and coronary perfusion time, may induce myocardial ischemia and malignant cardiac arrhythmias. Reduced coronary perfusion can be exacerbated by a decrease in venous return secondary to abrupt cessation of activity, which possibly explains the clinical observation that collapse not infrequently occurs immediately after exercise. Ischemia can alter depolarization, repolarization, and conduction velocity and thereby trigger threatening ventricular arrhythmias (Fig. 1). In addition, myocardial ischemia (23), sodium-potassium shifts with exercise, increased catecholamine levels, and TABLE 1. Cardiovascular causes of exercise-related SCD in young athletes.* Van Camp et al. (8) (n = 100),† % Maron et al. (9) (n = 134), % Corrado et al. (25) (n = 55),‡ % Hypertrophic cardiomyopathy 51 36 1 Probable hypertrophic cardiomyopathy 5 10 Coronary anomalies§ 18 23 9 Valvular and subvalvular aortic stenosis 8 4 Possible myocarditis 7 3 5 Dilated and nonspecific cardiomyopathy 7 3 1 Atherosclerotic CAD 3 2 10 Aortic dissection/rupture 2 5 1 Arrhythmogenic right ventricular cardiomyopathy 1 3 11 Myocardial scarring 3 Mitral valve prolapse 1 2 6 Other congenital abnormalities 1.5 Long-QT syndrome 0.5 1 Wolff-Parkinson-White syndrome 1 1 Cardiac conduction disease 3 Cardiac sarcoidosis 0.5 Coronary artery aneurysm 1 Normal heart at necropsy 7 2 1 Pulmonary thromboembolism 1 * Ages ranged from 13 to 24 (8), 12 to 40 (9), and 12 to 35 years (25) for the 3 studies, respectively. Van Kamp et al. (8) and Maron et al. (9) used the same database and include many of the same athletes. All (8), 90% (9), and 89% (25) had symptom onset during or within 1 hour of training or competition. † Total exceeds 100% because several athletes had multiple abnormalities. ‡ Includes some athletes whose deaths were not associated with recent exertion. § Includes aberrant artery origin and course, tunneled arteries, and other abnormalities. Exercise and Acute CV Events Medicine & Science in Sports & Exercised 887 SPEC IA L C O M M U N IC ATIO N S circulating free fatty acids may all increase the risks of ventricular arrhythmias (24). THE IMPORTANCE OF AGE AND PATHOLOGICAL SUBSTRATE The present scientific statement addresses the risks of exercise in both young and adult individuals, but it is critically important to recognize that these age groups have markedly different causes of exercise-related deaths and therefore markedly different risk-to-benefit ratios for vigorous exercise. The causes of exercise-related events are not strictly separated by age, given that, for example, some young individuals with genetic defects in the lowdensity lipoprotein receptor may develop premature CAD, whereas some older individuals may present with structural congenital cardiac abnormalities. Nevertheless, the predominant pathological cause of exercise-related events in adults is occult CAD. Habitual vigorous physical activity appears to reduce the incidence of CHD events, and cardiac rehabilitation appears to reduce the risk of CHD death in patients with diagnosed disease, although neither conclusion has been proved by a randomized, controlled clinical trial. Thus, the benefits of physical activity in those with or at risk for CHD appear to outweigh the risks. This situation is markedly different in young individuals with diagnosed or occult heart disease. Such subjects rarely die of CHD during exercise, and the clinical course of the responsible conditions such as hypertrophic cardiomyopathy and anomalous coronary arteries is not improved by vigorous exercise. Consequently, in populations with these diagnosed or occult cardiac diseases, the health risks of vigorous physical activity almost certainly exceed the benefits. Moderate physical activity may be justified in such patients on the basis of social and selfimage considerations, as well as the benefits of physical activity in preventing obesity, obesity-related health problems, and atherosclerosis, all of which would further exacerbate the individual’s cardiac risk. INCIDENCE OF EXERCISE-RELATED ACUTE CARDIOVASCULAR EVENTS The absolute risk of an exercise-related cardiovascular event varies with the prevalence of diagnosed or occult cardiac disease in the study population but appears to be extremely low in ostensibly healthy subjects. Because of the rarity of exercise-related cardiovascular events, studies examining its incidence are limited by small sample sizes and large confidence intervals. In addition, small changes in the number of events can produce large changes in the calculated incidence. Given these caveats, estimates are available for various patient groups.