REVIEW TOPIC OF THE WEEK
Sudden Cardiac Death in the Older Athlete
Sumeet S. Chugh, MD,*Joseph B. Weiss, MDyABSTRACT
The overwhelming majority of sports-related sudden deaths occur among those older than 35 years of age. Because increasing numbers of older people are participating in organized endurance and competitive sporting events, the inci-dence of sports-related sudden death in older adults is expected to rise. Older athletes will approach clinical cardiologists for advice regarding theirfitness for participation. It is important to recognize both that strenuous exercise is associated with a transient elevation in risk of sudden cardiac death and that appropriate training substantially reduces this risk. The approach to pre-participation screening for risk of sudden death in the older athlete is a complex issue and at present is largely focused on identifying inducible ischemia due to significant coronary disease. In this brief review, we summarize the current state of knowledge in this area with respect to epidemiology, mechanisms, and approaches to risk stratifi -cation, as viewed from the perspective of the consulting clinical cardiologist. (J Am Coll Cardiol 2015;65:493–502) © 2015 by the American College of Cardiology Foundation.
T
he legend of the first marathon runner,Pheidippides, embodies the popular notion that endurance athletics increase the risk of death. An Athenian messenger approximately 40 years of age, he is fabled to have run from Mara-thon to Athens in 490 B.C., perishing on arrival after proclaiming the Greek victory over the Persians. The beneficial, health-promoting effects of habitual phys-ical and sports activity are undeniable. However, a “sports paradox”exists: some people, most often those not habituated to exercise, experience sports activity–related cardiac arrests, usually associated with underlying heart disease. Middle-aged and older athletes are at significantly higher risk for sudden cardiac death (SCD) compared with younger athletes and are more vulnerable to misconceptions regarding the cardiovascular effects of sports. The burden of SCD during sports needs further evaluation but prob-ably constitutes a small proportion (5% to 6%) of sud-den deaths in the general population(1,2). However, from a societal perspective, sports-related SCD can have a disproportionate impact. People who engage in athletic activity are ostensibly healthier than
most and therefore considered least likely to experi-ence a cardiac arrest. The media attention on sports-related SCD tends to exaggerate the sports paradox and obscure the global health benefits of regular exer-cise. In addition to being cardiologists, both authors of this review are dedicated long-distance runners who seek to put the clinical risks and benefits of aer-obic exercise in scientific balance.
A leisure athlete is“an individual, usually middle-aged or elderly ($35 years), who participates in a variety of informal recreational sports, on either a regular or an inconsistent basis, which do not require systematic training or the pursuit of excellence” (3). For the purpose of this review, the term“older athlete” includes all athletes older than 35 years of age participating in sports at a competitive or masters level or as a leisure activity. Both clinical cardiol-ogists and their patients will benefit from a balanced approach to education, risk stratification, and exer-cise prescription for the middle-aged and older athlete. The goal of this review is to put forth such an approach on the basis of a current and compre-hensive assessment of previously published studies.
From *The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California; and theyDivision of Cardiology, Warren Alpert Medical School of Brown University, Providence, Rhode Island. Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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CURRENT BURDEN AND FUTURE PROJECTIONS
The overwhelming majority of sports-related sudden deaths occur among those 35 years of age or older(4)(Figure 1). Because many such deaths are unwitnessed, the magnitude of the problem is difficult to ascertain. Retro-spective studies of athletes who participate in marathons yield estimates of 0.8 to 2 SCDs per 100,000 marathon runners(4–11). More comprehen-sively, a prospective 5-year study of sports-related SCD in the general population of France reported an annual incidence of 4.6 sports-related SCDs per 1 million residents of France(4). Most of these events occurred in older male athletes, with only 6% (50 of 820) of all cases of sports-related SCDs in young, competitive athletes. When placed in the context of the overall burden of SCD in the general population (600 to 900 per million), sports-related SCDs consti-tute a small subset. Some have reasoned that the absolute burden of sports-related SCD is small and therefore of modest clinical significance. For recrea-tional joggers, however, the annual incidence of SCD is significantly higher: 13 SCDs per 100,000 joggers per year(8).
Several additional factors contribute to the clinical and public health importance of SCD in the older
athlete. The number of older Americans is steadily increasing and is expected to double by 2035, reach-ing 70 million. By 2040, 21% of the U.S. population will be older than 65 years of age (currently 13.7%) (12). As the population ages, a burgeoning subgroup of older athletes is participating in leisure and orga-nized sports. The popularity of endurance sports, especially running, is significantly on the rise in the United States. For example, there are approximately 20,000,000 participants in foot races in the United States annually. Of these, 54% are older than 35 years of age and 57% are male. The number of participants has been growing steadily for the past 15 years(13) (Figure 2). These trends are driven by the growing awareness of the health benefits of exercise activity but are matched by increasing levels of cardiovascu-lar risk among aspiring older athletes. According to recently published studies, the overwhelming ma-jority of sports-related SCDs have occurred in men, with a 9:1 ratio of men to women experiencing SCD during sports (11). Potential explanations include lower participation rates for women in marathons or similar events. Because women tend to develop atherosclerosis about 10 years later than men, the participation rate of women at risk may be even lower. As the demographics of endurance athletics change along with the population, we anticipate that increasing numbers of older women will pursue endurance athletics. However, women clearly enjoy the advantage of a lower likelihood of overall SCD, and the possibility remains that they have a special advantage during physical activity.
EVIDENCE FOR TRANSIENT ELEVATION IN RISK WITH EXERCISE, COUNTERED BY A PROTECTIVE EFFECT OF REGULAR EXERCISE Several now-classic studies showed an increased risk of SCD and myocardial infarction (MI) during strenuous exercise. Siscovick et al. (7) interviewed the spouses of 133 men with SCD without known prior heart disease and reported a significant in-crease in relative risk with exercise, but this effect strongly depended on the habitual exercise level. Among sedentary people, the relative risk of SCD during exercise was increased 56-fold compared with other times. This contrasted strikingly with the lower relative risk during exercise of 5 for men with the highest level of habitual activity. Despite the residual 5-fold increased risk of SCD during vigorous activity, men with the highest habitual level of physical activity had a substantially lower relative risk (0.4) of global SCD compared with sedentary controls.
FIGURE 1 Relationship Between Age and Sports-Related Sudden Deaths
120 100 80 60 40 20 0 15 20 25 30 35 40 45 50 55 60 65 70 75 Age, Years Number of Spor ts -R elated SD s
Distribution by age of sports-related sudden deaths (SDs) in the overall population(blue) and among young competitive athletes(red)in a nationwide, 5-year study in France, showing that the vast majority occurred in those 35 years of age and older. Reprinted with permission from Marijon et al.(4).
A B B R E V I A T I O N S A N D A C R O N Y M S CAC= coronary artery calcium CAD= coronary artery disease MET= metabolic equivalent MI= myocardial infarction RV= right ventricular SCD= sudden cardiac death
This “paradox of exercise” was confirmed by 2 other important epidemiological studies: one study of exercise-related MI, the most common substrate for SCD, and a second study of exercise-related SCD. Mittleman et al. (14) reported an overall increased relative risk of MI during exercise of 5.9. They also found an extraordinary 50-fold difference between sedentary patients (relative risk of MI associated with exertion of 107) and active patients (relative risk: 2.4). They showed a clear dose-response effect, and the greater the frequency of weekly exertion, the greater the reduction in relative risk of MI (Figure 3). Although SCD was not evaluated, the congruence of their findings with those of Siscovick et al. (7) for SCD is striking. A third prospective analysis, conducted by Albert et al. (10) from the Physicians Health Study, showed very similar findings. The overall relative risk of SCD within 30 min of vigorous exercise was 16.9. For those who exercised less than once per week, the relative risk was 74.1; for those who exercised $5 times per week, the relative risk was 10.9. These 3 seminal studies confirm both the increased risk of MI and SCD associated with exercise and the beneficial effect of regular exercise to reduce this risk.
The magnitudes of the risk reduction attributed to frequent exercise are impressive, in the range of 7- to 10-fold lowered risk for exercise-associated SCD and 50-fold reduction for exercise-associated MI. The global mortality benefits of exercise, we reiterate, far outweigh the increased risk (Table 1). Multiple studies confirm a dose-related beneficial impact of regular exercise on global cardiovascular risk, which is inde-pendent of sex, ethnicity, and probably of age. The magnitude of the risk reduction is comparable to or exceeds that of statin therapy and extends beyond cardiovascular risk to cancer. Moderate exercise (30 min of moderate activity 5 times per week) re-duces cardiovascular risk by 20%, and high levels of exercise (30 min of vigorous activity 5 times per week) reduce cardiovascular risk by 30% to 40%(15). These benefits are enhanced by the observed addi-tional impact of regular exercise on the risk of cancer. Over an 8-year period, regular high levels of exercise in healthy people were associated with a 70% reduc-tion in age-adjusted all-cause mortality in men and an 80% reduction in women(16).
POTENTIAL MECHANISMS OF EXERCISE-INDUCED SCD
In older athletes, coronary artery disease (CAD) is the most common cause of sports-related SCD, iden-tified in more than 80% of cases. The remaining
sports-related cases of SCD are attributable to a number of other problems, such as hypertrophic car-diomyopathy, arrhythmogenic right ventricular (RV) dysplasia, myocarditis, valvular heart disease, and a small but distinct subgroup of unexplained SCD (11,17–19). For the cases with significant associated
FIGURE 2 Increasing Numbers of U.S. Athletes Complete Running Races
57% 43% 44% 56% 45% 55% 53% 47% 2000 58% 42% 1995 32% 68% 20,000,000 10,000,000 0 1990 2005 2010 2011 2012 2013 1990 Female Male 1995 2000 2005 2010 2011 2012 2013 1,199,200 2,215,500 3,619,600 4,494,400 6,929,000 7,685,700 8,699,000 10,844,200 6,835,000 8,180,800 6,288,300 6,071,000 4,947,600 4,998,400 4,708,000 3,597,800 Male Female 75% 25% 52% 48%
Between 1990 and 2013, the number of participating athletes who completed running races in the United States increased significantly tow20 million per year; 54% were older than 65 years of age, and 57% were male. Reprinted with permission from State of the Sport(13).
FIGURE 3 The Greater the Frequency of Weekly Exertion,
the Greater the Reduction in Relative Risk of MI
107 19.4 8.6 2.4 180 160 140 120 100 R elativ e Risk of Onset of MI
Frequency of Physical Exertion per Week 80 60 40 20 0 0 1-2 3-4 ≥5
A clear dose-response effect of exertion on the relative risk of MI was demonstrated. Modified with permission from Mittleman et al.(14). MI¼myocardial infarction.
CAD, the mechanism of sudden death is incompletely understood. Although ischemic ventricular arrhythmia is thefinal common pathway, the triggers have yet to be established. Hypothetical mechanisms include sym-pathetic activation, electrolyte and metabolic factors, activation of the hemostatic system, and hemody-namic effects on vulnerable coronary plaque. Exercise-related sympathetic activity may sensitize vulnerable myocardium to ischemia and arrhythmia. Prolonged exercise produces electrolyte abnormalities that may also contribute. It is striking that the overwhelming majority of sudden deaths occu in thefinal quartile of marathons and that marathons are associated with greater risk than half-marathons (9,11). Both findings support an electrolyte/metabolic contribution to risk of SCD. One recent retrospective study also raised the question of whether heat stroke is an underdiagnosed cause of death in long-distance races(20).
Postmortem studies strongly support roles for plaque rupture, hemostasis, and thrombosis. In a comparative pathological study of plaque mor-phology in men whose death was temporally linked to physical or emotional stress versus men who died at rest(21), acute plaque rupture was evident at au-topsy in 68% of the stress-related deaths compared with 23% of the deaths at rest (p<0.001). Similarly, hemorrhage into the plaque was found in 71% of stress-related SCDs compared with 41% of SCDs at rest (p¼0.007). Stress-related plaque rupture occurred in the central, thin-capped plaque, while plaque rupture that occurred at rest was found in the shoulders of plaque (Figure 4). Increased subjacent vasa vasorum was identified as a likely source of underlying hem-orrhage in stress-related plaque rupture, whereas plaque rupture at rest was remote from the vasa vasorum. On this basis, the authors suggest that he-modynamic factors contribute to stress-related pla-que rupture as the substrate for sports-related SCD. How habitual exercise confers protection against plaque rupture is not known, but both hemodynamic and tissue effects are potential contributors. POTENTIAL HAZARDS AT THE HIGH END OF THE EXERCISE SPECTRUM
Although high levels of habitual exercise clearly reduce all-cause mortality, the benefits at the highest levels of exercise may come at a price. Emerging
TABLE 1 A Long-Term Protective Effect of
Regular Exercise Counters the Transient Risk of Exercise In sedentary people, the relative risk of sudden death during exercise
increases by 56-fold
For those habituated to regular exercise, this risk increases by only 5-fold
Regular exercise of mild to moderate intensity provides a 7-fold to 10-fold risk reduction for sudden cardiac death and a 50-fold risk reduction for myocardial infarction
Leisure running, even 5 to 10 min per day at slow speeds (<6 miles/h), is associated with substantial mortality benefits
FIGURE 4 Comparison of Plaque Rupture With Exertion and at Rest
Plaque Rupture With Exertion Plaque Rupture at Rest
Vasa Vasorum Necrotic Core L HP Th Fibrous Cap HP Th L
Plaque rupture with exertion(left)is characterized by a relatively thinfibrous cap, relatively numerous vasa vasorum, and rupture in the midcap. In contrast, plaque rupture at rest(right)is depicted at the junction of thefibrous cap and the arterial wall. Reprinted with permission from Burke et al.(21). HP¼hemorrhage into plaque; L¼lumen; Th¼thrombus.
evidence proposes 2 adverse cardiovascular conse-quences of exercise at the high end: 1) accumulation of coronary artery calcium (CAC) with myocardial fibrosis; and 2) RV fibrosis secondary to episodic
volume/pressure overload. Mohlenkamp et al.
(22)quantified CAC, as measured by computed to-mography, and late gadolinium enhancement, as
measured by magnetic resonance imaging, for
myocardialfibrosis in 108 apparently healthy, expe-rienced male marathon runners older than 50 years of age(22). Higher levels of accumulation of CAC were found in runners matched to controls on the basis of the Framingham risk score. However, accumulation of CAC was not significantly different from that of age-matched controls. Therefore, marathon runners had lower Framingham risk profiles, without lower CAC scores. Among 102 marathon runners, 12% had
detectable late gadolinium enhancement in patterns consistent both with CAD scar and in a diffuse, patchy fashion; Breuckmann et al. (23) reported a similar prevalence. They also identified a statistically
signi-ficant association between late gadolinium
en-hancement and CAC. The implications of these results are that endurance athletes may not be protected from accumulation of coronary calcium. It is important to recognize that this study did not support an adverse impact of endurance athletics on either CAC or car-diovascular events.
The acute effects of marathon running on RV size and function have also been evaluated. RV pressures and dimensions were consistently elevated at the conclusion of marathons compared with pre-race measurements. RV function also suffers transiently. In a study of 60 nonelite participants in the Boston
FIGURE 5 Leisure-Time Running Reduces All-Cause and Cardiovascular Mortality Risk
0.2 0.4 0.6 0.8 1.0 0.2 0.4 0.6 0.8 1.0 X X X X X X X X X X X X
*
*
*
*
*
*
Quintiles of Running Characteristics Hazard Ratios of Cardiov
a
scular Mor
tality
Hazard Ratios of All
-Cause Mor tality
X
*
Time (min/wk) Distance (miles/wk) Frequency (times/wk) Total amount (MET-min/wk) Speed (mph) 0 <51 51-80 81-119 120-175≥
176 0 <6 6-8 9-12 13-19≥
20 0 1-2 3 4 5≥
6 0 <506 506-812 813-1199 1200-1839≥
1840 0 <6.0 6.0-6.6 6.7-7.0 7.1-7.5≥
7.6*
*
*
*
*
*
Non-RunnersRunning 1 to 3 times per week appears to provide the same level of risk reduction as higher frequency or intensity of running. In this study, participants were classified into 6 groups: nonrunners (reference group) and 5 quintiles of each running characteristic. Hazard ratios of all-cause and cardiovascular mortality by running characteristics (weekly running time, distance, frequency, total amount, and speed) are shown. All HRs were adjusted for baseline age (years), sex, examination year, smoking status (never, former, or current), alcohol consumption (heavy drinker or not), other physical activities except running (0, 1 to 499, or$500 MET-minutes/week), and parental history of cardiovascular disease (yes or no). All p values for HRs across running characteristics were<0.05 for all-cause and cardio-vascular mortality except for running frequency of$6 times/week (p¼0.11) and speed of<6.0 miles/h (p¼0.10) for cardiovascular mortality. Reproduced with permission from Lee et al.(26).
Marathon (mean age of 41 years), Neilan et al.
(24) found approximately 2-fold elevations of
N-terminal pro–B-type natriuretic peptide and in-creased cardiac troponin T levels in 60%, with 40% exceeding the threshold usually used to diagnose MI. The increased levels of biomarkers correlated with impaired left ventricular diastolic function, increased pulmonary artery pressures, and RV
dys-function. One of the more remarkable findings
in this study pertains to the role of training in rela-tion to these markers of myocardial injury and dysfunction. Virtually all indexes of RV function and the pulmonary artery pressures were more severely affected in the least well-trained athletes
compared with the best. La Gerche et al. (25)
comparing marathon runners with ultraendurance athletes, confirmed the findings of transient RV dysfunction. They observed elevations of cardiac troponin T, B-type natriuretic peptide, and RV vol-umes with declines in RV function immediately after these endurance events. They also found that release of cardiac troponin T strongly correlated with a decline in RV ejection fraction, particularly in ultra-triathletes (r¼0.746; p¼0.003). Although the
acute effects all reversed in the days after the events, they found late gadolinium enhancement in 12.8% of the athletes, which correlated with a modest reduc-tion in resting RV ejecreduc-tion fracreduc-tion (47.15.9% vs. 51.1
3.7%). The authors hypothesize that extreme
endurance athletics is associated with repeated RV insult, injury, andfibrosis that can evolve late into a substrate for ventricular arrhythmia. It should be noted that this has not been documented as a cause of sports-related SCD on an epidemiological basis. From a public health perspective, we emphasize that although thesefindings raise some concerns about the benefits of endurance athletics at the high end, they do not undermine the substantial benefits of regular exercise on all-cause mortality in the vast majority of older athletes (Figure 5)(26).
CLINICAL APPROACH TO RISK STRATIFICATION FOR SCD IN
OLDER ATHLETES: GREATEST UTILITY IN THE SPORT-NAÏVE ATHLETE
The growing popularity of endurance athletics in an aging population will result in a larger pool of older
CENTRAL ILLUSTRATION The Balance Between Risk of Sudden Death and Benefits of Sports in the Older Athlete:
Tilted in Favor of Regular Sports Activity
MECHANISMS
• Coronary plaque rupture • Rare disorders • RV remodeling • Myocardial fibrosis 40-60% MORTALITY • Dose related • Any age
• Even moderate activity
HOW TO MITIGATE RISK • Gradual in activity • Aspirin Transient SCD Risk (Sports Paradox) Protective Effect of Regular Activity Sport-naïve athlete Habituated athlete For significant in activity level Older Athlete 3-STEP SCREENING • Patient questionnaire • Physician evaluation • Maximal stress testing
Chugh, S.S. et al. J Am Coll Cardiol. 2015; 65(5):493–502.
The consulting cardiologist can assist with stepwise screening, especially in the sport-naïve athlete, and encourage gradual increase in activity, both of which have the potential to further decrease risk. RV¼right ventricular; SCD¼sudden cardiac death.
athletes. This is, of course, very good news, because regular exercise has enormous proven potential to reduce cardiovascular morbidity and mortality. Therefore, there is a growing need to provide prac-tical, clinically relevant advice to minimize the asso-ciated risk. Among older athletes, the primary risk for sports-related SCD is CAD with acute plaque rupture. This risk is low for most endurance events, such as the marathon. Indeed, an epidemiological study has argued credibly that marathons reduce the death toll because the average number of race-associated SCDs is about one-half the number of deaths that would typically result from motor vehicle accidents if the race route were not closed to traffic (9). However, the risk associated with training is approximately 5-fold greater. Accordingly, we observe that cardiologists can intervene most effec-tively by advising noncompetitive or pre-competitive athletes. Because the most common substrate for risk is (by far) CAD, the main objective of
pre-participation screening of the older athlete is ruling out significant occult CAD. We considered 3 published documents for pre-participation screening of the older athlete in developing recommendations for risk stratification of the older athlete: 1) recom-mendations from a working group of the American Heart Association and allied organizations(3); 2) the American College of Sports Medicine guidelines(27); and 3) the European Association for Cardiovascular Prevention and Rehabilitation guidelines(28).
FIGURE 6 American Heart Association/American College of Sports Medicine Health/Fitness Facility Pre-Participation Screening Questionnaire
Assess your health needs by marking all true statements.
You should be able to exercise safely without consulting your healthcare provider in almost any facility that meets your exercise program needs. If you marked 2 or more of the statements in this section, consult your healthcare provider before engaging in exercise. You might benefit by
using a facility with a professionally qualified exercise staff to guide your exercise program.
If you marked any of the statements in this section, consult your healthcare provider before engaging in exercise. You may need to use a facility with a
medically qualified staff.
None of the above is true.
Other health issues:
You have musculoskeletal problems. You have concerns about the safety of exercise. You take prescription medication(s). You are pregnant.
History You have had:
A heart attack Heart surgery Cardiac catheterization Coronary angioplasty (PCTA) Heart valve disease Heart failure Heart transplantation Congenital heart disease
Pacemaker/implantable cardiac defibrillator/rhythm disturbance
Symptoms
You experience chest discomfort with exertion. You experience unreasonable breathlessness. You experience dizziness, fainting, blackouts. You take heart medications.
Cardiovascular risk factors You are a man older than 45 years.
You smoke.
Your blood pressure is >140/90. You don’t know your blood pressure. You don’t know your cholesterol level.
You have a close blood relative who had a heart attack before age 55 (father or brother) or age 65 (mother or sister).
You are diabetic or take medicine to control your blood sugar. You are physically inactive (ie, you get <30 minutes of physical activity on atleast 3 days per week).
Your blood cholesterol level is >240 mg/dl.
You are >20 pounds overweight.
You are a woman older than 55 years or you have had a hysterectomy or you are postmenopausal.
PCTA¼percutaneous transluminal coronary angioplasty. Reproduced with permission from Balady et al.(29).
TABLE 2 Recommended Criteria for Identification of the
High-Risk Athlete During Evaluation by the Physician 10-year risk of coronary artery disease>5% (Framingham risk score) Total cholesterol level>320 mg/dl or low-density lipoprotein
cholesterol level>240 mg/dl Diabetes mellitus with microalbuminuria
Strong family history of sudden cardiac death or premature (age younger than 50 years) coronary artery disease in afirst-degree relative
AUTHORS’RECOMMENDATIONS FOR RISK STRATIFICATION IN THE ASYMPTOMATIC PATIENT
Because there is a significant amount of information common to the 3 guidelines and none of the
approaches have been tested prospectively, we sug-gest a succinct, 3-step process (Central Illustration): 1. Assess risk using the American Heart Association
pre-participation questionnaire (29) (Figure 6), which is a useful initial screening tool for com-pletion by the patient that is designed to elicit evidence of known risk factors. If any are detected, evaluation by a physician is recommended. If the patient is in the cardiologist’s office, then one could move directly to step 2.
2. Perform a physician-led evaluation comprising a careful clinical history (including family history that can uncover familial conditions, such as long QT syndrome), physical examination, and estima-tion of the absolute 10-year risk of CAD using the Framingham risk score(30). Any criterion lis-ted inTable 2indicates a high-risk profile. 3. Use maximal exercise stress testing as a
discrimi-nator when the risk profile is high and the gap between habitual physical activity and intended level of activity is large (Figure 7). If maximal exercise electrocardiography is unsuitable for a given patient, we suggest single-photon emission computed tomography or stress echocardiography as appropriate alternatives. This applies to sed-entary patients achieving <2 metabolic equiv-alents (MET)-h/week. For active patients already achieving >2 MET-h/week, low-intensity activity may be appropriate without this evaluation pro-cess. Routine use of stress testing in healthy, asymptomatic athletes is not recommended. Judi-cious use of resting 12-lead electrocardiogram and echocardiogram may be indicated and in some cases may result in diagnosis of previously unrecognized conditions, such as hypertrophic cardiomyopathy or arrhythmogenic RV dysplasia. Physical activity is important to manage, and potentially to restrict, in aspiring athletes, who may have conditions such as uncontrolled hyper-tension and active myocarditis.
PRE-PARTICIPATION SCREENING IN THE OLDER ATHLETE: FUTURE CONSIDERATIONS Stress testing is most likely to identify those with subocclusive CAD. However, plaque rupture, which is considered to be an important mechanism of SCD in the older athlete, can occur among coronary lesions that bring about mild to moderate coronary stenoses. Therefore, imaging of coronary plaque to identify lesions vulnerable to rupture has significant potential to enhance risk stratification. Although there is a conspicuous lack of studies that specifically evaluate
FIGURE 7 A Suggested 3-Step Screening Process for
Significant Occult Coronary Artery Disease in the Older Athlete
Assessment of Risk (self or by non-physician) Negative Negative Negative Positive Positive Positive Screening by Physician (History, Physical Exam, Risk factors, Resting ECG)
Maximal exercise testing Eligible for exercise training Further evaluation
Three levels are recommended for cardiovascular evaluation in older athletes, depending on the individual’s risk factors and intended physical activity. ECG¼electrocardiography. Modified from Borjesson et al.(28).
FIGURE 8 A Graded Approach to Exercise Conditioning in the Older Athlete
3/week <3 METS, 50-70% Max predicted HR 3-6 METS, 50-70% Max predicted HR >6 METS, 70-85% Max predicted HR 5/week 3→5/week
Balancing the risk of sudden cardiac death with the protective effect of regular activity can be addressed through screening of the older athlete and by emphasis on the frequency, rather than the intensity, of the activity level, which should be increased gradually. HR¼ heart rate; METS¼metabolic equivalents.
SCD as an outcome, plaque characteristics clearly determine the risk of acute coronary syndrome and major adverse cardiovascular events (31). Increased coronary artery calcification, as measured by com-puted tomography, is a strong predictor of incident CAD beyond standard risk factors, with a 10-fold increased risk in those with coronary calcium scores
>300(32). However, any additions to the risk strati-fication armamentarium of the older athlete should require assessment of SCD as the outcome and careful consideration of cost versus benefit.
STRATEGIES TO MITIGATE RISK IN THE SPORT-NAÏVE ATHLETE: AUTHORS’ SUGGESTIONS
We propose that gradually increasing the level of habitual activity has the greatest potential to render exercise safe while improving all-cause mortality. The increased risk associated with a sedentary life-style identifies this group as high risk, and graded training can in theory reduce the risk of sports-related SCD by a factor of 10 to 50(7,10). Although specific, universally applicable recommendations for reducing risk through graded conditioning are difficult to pro-vide, we propose a few principles. First, frequency of physical activity (rather than intensity) should be emphasized at the outset. Exercise intensity is usu-ally defined by either METs or heart rate in relation to the maximum predicted heart rate and the number of sessions per week (Figure 8). An initial period of low-intensity exercise (<3 METs, or increase in heart rate to 50% to 70% of maximum predicted) performed 3 times a week attenuates the risk and may render moderate or higher intensity exercise safer (Figure 8). Each stage should ideally be covered in 6 to 8 weeks or longer, on the basis of the patient’s overall fi t-ness and conditioning level. This graded approach obviates the risk of high-intensity exercise performed by poorly conditioned athletes.
In our opinion, the decision regarding cholesterol-lowering therapy, such as statins, should be driven by standard recommendations (33). For many, life-style alterations associated with sports activity may obviate the need for such drugs. Statins may, in the-ory, contribute to coronary plaque“stabilization,”but any modest beneficial effects could be offset by the
statin-induced muscle fatigue or myopathy reported among 10% to 25% of patients in clinical practice(34), which is particularly relevant during exercise training adaptation (35). Low-dose aspirin (75–100 mg) may have a modest contribution to primary prevention of cardiovascular disease(36), but we propose that the overall mortality benefit is likely to exceed the risk in asymptomatic middle-aged and older athletes. CONCLUSIONS
The increased risk of sports-related SCD in older athletes is real, but it is balanced by the benefits of fitness. However, as the population ages and endurance athletics gain in popularity, the popula-tion at risk is growing. Unlike in younger athletes, CAD is the predominant cause of SCD in older ath-letes. On a population basis, the risk associated with sporting events is much lower than the risk associated with training or leisure athletics. In mul-tiple studies, low levels of habitual exercise are a very strong risk factor for sports-related SCD. Therefore, cardiologists should advise appropriately graded athletic training as the safest, most effective
course. Both American and European societies
recommend screening for occult CAD by question-naire along with risk stratification on the basis of CAD risk profiles. Maximal stress testing for a high-risk subset may be beneficial in appropriate pa-tients. However, a negative stress test may not identify all patients at risk for SCD. In the future, imaging of the coronary plaque may enhance pre-participation screening for occult CAD. It is impor-tant to remember that reductions in cardiovascular and all-cause mortality associated with moderate-intensity exercise performed$3 times per week are in the range of 40% to 60%. On balance, the health benefits of regular exercise heavily outweigh the risks of SCD in older athletes, especially in those who train appropriately.
REPRINT REQUESTS AND CORRESPONDENCE: Dr. Sumeet S. Chugh, Cedars-Sinai Medical Center, Advanced Health Sciences Pavilion, Suite A3100, 127 South Vicente Boulevard, Los Angeles, Califor-nia 90048. E-mail:sumeet.chugh@cshs.org.
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KEY WORDS athletics, endurance, exercise, risk stratification
