Is the Older Athlete at Risk for Sudden Cardiac Death?
Editor's Note: Commentary based on Chugh SS, Weiss JB. Sudden cardiac death in the older athlete. J Am Coll Cardiol 2015;65:493-502.
The number of endurance exercise events and the average age of participants have increased over the last few decades.1 The interest in determining the acute risk of sudden cardiac death (SCD) during exercise has also increased. Despite the long-term salutary effects of exercise, vigorous exertion can trigger SCD.2 Nonetheless, SCD during sports activities represent a small fraction of the overall SCD burden. The Oregon Sudden Unexpected Death Study showed that only 5% of all SCD occurred during sports activities.3
In a recently published article in The Journal of the American College of Cardiology, Drs. Chugh and Weiss summarize the current knowledge about SCD in the older athlete.4 The authors defined older athletes as >35 years of age. However, depending on the source, an "older athlete" is variably defined as older than 30, 35, or 40 years of age. This narrative review mentions some of the studies addressing the incidence of SCD in athletes and highlights several recurrent themes, including the low frequency of events, a male predominance, and the large variation in available estimates of SCD. This variance is due to differences in SCD definitions, surveillance methods for case ascertainment, and estimates of the at-risk population. The incidence of SCD in the older athlete population as defined by the authors was not reported. This is not surprising, given the lack of consensus on the definition of "older athletes." It is well known, however, that the vast majority of sports-related deaths occur in individuals older than 35, and that 94% of the sports-related deaths in the Oregon study were in this age group.5
The risk of acute cardiac events is increased during exercise compared to rest, as described in the review. The magnitude of this effect varies from two to 56 times, depending on the study.2,6-9 This risk is particularly higher in individuals with a low level of habitual physical activity6-7 and in those with known disease,10 although the risk can be mitigated by training.6 The authors of the review emphasize that the global mortality benefits derived from regular exercise outweigh the increased risk.4
Chugh and Weiss' manuscript describes the causes of exercise-induced SCD in older athletes. Coronary artery disease (CAD) is the most common cause (80% of the cases), with hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, myocarditis, valvular heart disease, and a small subgroup of unexplained SCD accounting for the rest. Of the cases caused by CAD, two-thirds are due to plaque rupture,11 and the authors appropriately acknowledge the lack of certainty on the precise mechanism of SCD in these individuals. They hypothesize two potential mechanisms: 1) the acute hemodynamic effects of exercise, including increased sympathetic intput on vulnarable coronary plaques and ischemic myocardium; 2) increased arrhythmia from metabolic changes such as hyperkalemia.
The first seems plausible, given the increase in sheer stress and the increased flexing and bending of the coronaries at increased heart rates during exertion. Athletes also appear to have more coronary thrombosis and less atherosclerosis than non-athletes9,11, suggesting that exercise hastens the event. The postmortem studies cited by the authors also suggest that the causes of plaque rupture are different for those events occuring during exertion and those at rest.11 Specifically, events during exertion often have more plaque rupture in the center of the thin fibrous plaque, whereas rupture at rest is often at the shoulder of the plaque (at the junction between the fibrous cap and the arterial wall). The second hypothesis postulated by the authors includes electrolyte dearrangements, which would explain why SCD tends to occurs towards the end of long-distance races. This could be particularly important in people with myocardial fibrosis, which is seen in some athletes, althought its significance is unclear. In fact, both the increased coronary artery calcification and the myocardial fibrosis, cited by the authors as potentially adverse effect of "high level exercise," are controversial and higly debated. Whether these findings lead to clinically meaningful events in older athletes remains to be determined.
There is debate among experts about the best approach to prevent SCD in athletes. The article ends with the authors' clinical approach to risk stratification for SCD in older athletes. They emphasize symptoms, the individual's risk factor profile, and physical exam. However, in high-risk individuals with diabetes, total cholesterol >320, low-density lipoprotein cholesterol >240 mg/dl, a Framingham Risk Score >5%, family history, or a body mass index >28, they recommend an electrocardiogram and a maximal exercise stress test, particularly when there is a large gap between the baseline exercise level and the intended level of activity. Such an approach could detect underlying pathology, but it is unlikely to identify individuals at risk with vulnerable plaques that tend to cause only mild-to-moderate stenosis and are not detected by traditional stress testing or imaging techniques. A graded increase in physical activity at the outset in sport-naïve individuals, as suggested by the authors, makes intuitive sense and probably also helps to decrease injury risk. The proposal of adding low-dose aspirin in middle-aged and older athletes is interesting since some prothrombotic markers are elevated during exertion,12 but it is in contrast to current evidence and clinical trends on its use for primary prevention in the general population.
Sports-associated SCD in older adults represents a small proportion of the overall SCD burden. We should strive to maximize both safety and promotion of sports activity in the older athlete given the overall benefits of exercise on cardiovascular mortality, even at low doses. Implementing physical exercise programs with a gradual increase in physical activity could be a safe and inexpensive intervention to mitigate the risk of sports-related SCD. Also, since 36% of sports-related SCD victims in the Oregon project had classical prodromal symptoms, it is important that active adults know these symptoms and receive prompt medical attention.
- Running USA. Statistics. 2015 (Running USA website). Available at: http://www.runningusa.org/statistics. Accessed 7/5/2015.
- Albert CM, Mittleman MA, Chae CU, Lee IM, Hennekens CH, Manson JE. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med 2000;343:1355-61.
- Marijion E, Uy-Evanado A, Reinier K, et al. Sudden cardiac arrest during sports activity in middle age. Circulation 2015;131:1384-91.
- Chugh SS, Weiss JB. Sudden cardiac death in the older athlete. J Am Coll Cardiol 2015;65:493-502.
- Marijon E, Tafflet M, Celermajer DS, et al. Sports-related sudden death in the general population. Circulation 2011;124:672-81.
- Mittleman MA, Maclure M, Tofler GH, Sherwood JB, Goldberg RJ, Muller JE. Triggering of acute myocardial infarction by heavy physical exertion. N Engl J Med 1993;329:1677-83.
- Siscovick DS, Weiss NS, Fletcher RH, Lasky T. The incidence of primary cardiac arrest during vigorous exercise. N Engl J Med 1984;311:874-7
- Hallqvist J, Moller J, Ahlbom A, Diderichsen F, Reuterwall C, de Faire U. Does heavy physical exertion trigger myocardial infarction? A case-crossover analysis nested in a population-based case-referent study. Am J Epidemiol 2000;151:459-67.
- Giri S, Thompson PD, Kiernan FJ, et al. Clinical and angiographic characteristics of exertion-related acute myocardial infarction. JAMA 1999;282:1731-6.
- Thompson PD, Franklin BA, Balady GJ, et al. Exercise and acute cardiovascular events placing the risks into perspective: A scientific statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism and the Council on Clinical Cardiology. Circulation 2007;115:2358-68.
- Burke AP, Farb A, Malcolm GT, Liang Y, Smialek JE, Virmani R. Plaque rupture and sudden death related to exertion in men without coronary artery disease. JAMA 1999;281:921-6.
- Siegel AJ, Stec JJ, Lipinska I, et al. Effect of marathon running on inflammatory and hemostatic markers. Am J Cardiol 2001;88:918-20.
Clinical Topics: Arrhythmias and Clinical EP, Diabetes and Cardiometabolic Disease, Dyslipidemia, Heart Failure and Cardiomyopathies, Prevention, Sports and Exercise Cardiology, Stable Ischemic Heart Disease, Atherosclerotic Disease (CAD/PAD), Implantable Devices, Genetic Arrhythmic Conditions, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Lipid Metabolism, Nonstatins, Exercise, Sports and Exercise and ECG and Stress Testing
Keywords: Arrhythmias, Cardiac, Arrhythmogenic Right Ventricular Dysplasia, Aspirin, Atherosclerosis, Athletes, Body Mass Index, Cardiomyopathy, Hypertrophic, Cholesterol, Cholesterol, LDL, Consensus, Constriction, Pathologic, Coronary Artery Disease, Coronary Thrombosis, Cost of Illness, Death, Sudden, Cardiac, Diabetes Mellitus, Electrocardiography, Electrolytes, Exercise, Exercise Test, Heart Rate, Hyperkalemia, Lipoproteins, LDL, Middle Aged, Motor Activity, Myocarditis, Myocardium, Physical Exertion, Primary Prevention, Prodromal Symptoms, Risk Factors, Sports
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