Running Marathons with Blocked Coronary Arteries and Runners' Risk of Sudden Cardiac Death—Case Report and Review

Introduction Sudden cardiac death (SCD) is described as an event that is nontraumatic, nonviolent, unexpected, and results from sudden cardiac arrest within 6 h of previously witnessed normal health (1). The growth of long-distance running races has been accompanied by studies documenting that prolonged exercise can trigger unheralded ventricular arrhythmias and cardiac arrest in individuals without overt heart disease (2). Running is an excellent means of conditioning the cardiovascular system. The World Health Organization released evidence-based Physical Activity Guidelines, recommending at least 150 min of moderate intensity or 75 min of vigorous-intensity aerobic activity per week, or an equivalent combination of both (3,4). Runners are not immune to organic heart disease. We are presenting a case report of a marathon runner who was asymptomatic with excellent conditioning, had SCD, and was successfully revived. This patient was found to have critical two-vessel asymptomatic coronary artery disease (CAD) until this index event. Case Report A 56-year-old man with no significant medical history was running a half marathon. He had run races in recent months without any symptoms and had improved his timing by extensive training. He had not previously exhibited any unusual symptoms. When he was in the last half mile of the race, he sped up to overtake another athlete. He ran for another 2 min to 3 min, and as he crossed the finish line, he collapsed; however, he does not remember collapsing. There was an emergency medical team on standby who found him in ventricular fibrillation. He was revived with one defibrillation with return of consciousness. He was admitted to a hospital for further care. He was completely asymptomatic when seen by a cardiologist. His initial EKG was normal without any significant ischemic changes. His laboratory work had shown indeterminate troponins. His echocardiogram showed no significant wall motion abnormality or valvular disease. On cardiac catheterization, he was found to have two-vessel obstructive CAD. His right coronary artery (RCA) was 100% occluded for short segment and had collaterals from the left anterior descending artery (LAD). His left circumflex artery (LCX) had 95% stenosis. LAD had nonobstructive CAD. The patient underwent successful angioplasty of his LCX and totally occluded RCA with drug eluting stents. He is consistent with his follow-up and has been running again with similar or lower times (Figs. 1 and 2).Figure 1: Left circumflex coronary artery with 95% stenosis at mid-LCX and post-PCI with stent.Figure 2: RCA 100% occluded chronically and post-PCI with stent with great result.Discussion Vigorous exercise is associated with a transient increase in risk of SCD. Sports, per se, were not a cause of the enhanced mortality, but it can trigger SCD in those athletes who are affected by cardiovascular conditions predisposing to life-threatening ventricular arrhythmias during physical exercise (2,5,6). Most athletes collapse because of hypoperfusion of the brain due to low blood pressure secondary to dehydration and decreased vascular resistance and respond well to hydration and Trendelenburg positioning. Our case was different as the patient had ventricular fibrillation leading to collapse. SCD in athletes occurs most commonly during or shortly after intense training or competition. The most common causes of SCD if below the age of 35 years are hypertrophic cardiomyopathy (36%), followed by coronary artery anomalies (17%), premature CAD, and ion channelopathies (5,7). The majority of athletes who suffer SCD are men (approximately 90%), and a disproportionate number are nonwhite (i.e., 64% [nonwhite] vs 51% [white] of deaths due to cardiovascular disease, P < 0.001) (7). Older studies on the rate of SCD in athletes have produced widely varying estimates ranging from 1:23,000 to 1:300,000, largely because of differing methodology (7). Recent studies with higher methodological quality consistently yielded incidence rates in the range of 1:40,000 to 1:80,000 (8). The incidence of SCD in National Collegiate Athletic Association athletes is significantly higher than frequently cited estimates, with an overall rate of approximately 1:43,000 student-athletes per year (9). The incidence of SCD in older athletes (>35 years) is reportedly more frequent than in younger athletes, with an estimated annual incidence of approximately 1:11,000 to 1:80,000 in men (5,10). The incidence is strikingly lower in women. However, the participation rate for women also is lower, so the absolute incidence may not be significantly different (5,6). The lower incidence of SCD in women could, therefore, be explained by delayed onset of CAD, decreased susceptibility to exercise-provoked plaque disruption, or platelet activation. The predominant pathological finding in older athletes is CAD, accounting for 73% of SCD in joggers and marathon runners (11). This is consistent with observations that vigorous exercise can trigger acute myocardial infarction, with annual incidence rates at about 1:600 to 1:4,000 of apparently healthy individuals (5,7,11). Large prospective epidemiologic studies consistently document reduced rates of CAD with regular exercise. Physical inactivity is a strong predictor of mortality, with lower risk being directly proportional to exercise capacity (5,6). Regular exercise also substantially decreases the overall risk of SCD in both men and women (10). For example, in a case series of 133 men with primary cardiac arrest, the relative risk of SCD during vigorous exercise versus rest was 56-fold for those with low levels of habitual exercise, compared with a relative risk of five-fold for those at the highest level of regular exercise (5). Regular exercise also lowers the probability of an exertion-triggered myocardial infarction, with a relative risk of 1.3 versus 6.9 for men who exercised four or more times per week versus less than four times per week, respectively (5,6). Running, even 5 to 10 min·d−1 at slow speeds <6 miles·h−1, is associated with markedly reduced risk of death from all causes and cardiovascular diseases. These studies motivate healthy, but sedentary individuals, to begin and continue running for substantial and attainable mortality benefits (3,6). With these significant data in mind and given the low overall incidence of exercise-induced SCD, the benefits of routine vigorous exercise outweigh the small risk of SCD, particularly in older individuals. A reduced long-term disability and marked survival advantage of older runners compared with a control group in a large study (12) with a 21-year follow-up period argued strongly that long-term benefits of vigorous exercise far outweigh any real or theoretical risks of SCD. Screening Before Participation The screening of runners before participating in a marathon or of the general public before starting vigorous exercise has been controversial. Because the main cause of death among older marathon runners is CAD, the screening tool of choice is resting ECG and the exercise stress test. No randomized controlled trials have addressed the utility of exercise testing in asymptomatic individuals, even those pursuing a vigorous exercise program or competition. As such, published guidelines are based on expert consensus and thus differ among writing groups (6). The American College of Cardiology and the American Heart Association Task Force considered exercise testing a class II indication for asymptomatic persons with diabetes mellitus who are planning to start vigorous exercise. The American College of Sports Medicine provided similar recommendations, whereas the U.S. Preventive Services Task Force found insufficient evidence for routine stress testing and resting ECG before exercise training and did not endorse it. A significant shortcoming of exercise testing is insensitivity for predicting acute coronary events, most of which result from plaque rupture of non–flow-limiting epicardial coronary lesions. There also are more practical issues of cost-effectiveness of performing exercise tests on many participants, as well as unnecessary secondary and often invasive testing that would be needed to discriminate true- from false-positive stress test results in a low-risk population. Overall, a more careful strategy seems to be one of prevention and attention to symptoms for obstructive CAD, which both the patient and the physician tend to ignore when they occur in highly fit individuals (5,6). It is a known fact that survival from SCD is highly dependent on the time interval from the onset of arrest to first defibrillation. Rapid defibrillation is easier to guarantee for sporting events held in an enclosed space but much more difficult to achieve for a marathon race. Because cardiac arrests occur most commonly in the latter stages of the race, a good approach is to increase the density of automatic external defibrillators and medical response teams in the last 4 to 6 miles of the marathon. Conclusions As with other forms of vigorous exercise, marathon running is associated with a transient increase in, but exceedingly low risk of SCD. Although coronary events are the primary cause, widespread screening of runners with stress testing is not useful or cost-effective. Deployment of rapid medical response teams and automatic defibrillators has been shown to have a significant impact on survival after cardiac arrest during a marathon. Screening programs with a history and physical examination are recommended for high school and collegiate sports participants. For older individuals who are likely to have undetected CAD and are exercising for physical fitness, caution regarding the level of activity and type of symptoms that are frequently associated with CAD may help prevent SCD. A robust association of long-distance running with improved quality of life and longevity is certainly encouraging news for the running community.