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Sudden cardiac death among the active populous: identifying risks, reasons and responses before it strikes.

Of the one million Americans who develop coronary artery disease (CAD) each year, between 25 and 50% will suffer sudden cardiac death (SCD). Frustratingly, the majority of these CAD cases are asymptomatic. Indeed, the Framingham study data show that, for some 60% of men and 45% of women, the first symptom of CAD is either SCD or myocardial infarction (MI). Additionally, the cases of SCD that occur without underlying CAD, while rare, are especially disconcerting and warrant our attention. We'll look at four major SCD case categories here, and attempt to place the problem in perspective--in terms of what we now know and what we still need to discover to identify and treat those at risk before a devastating cardiac event occurs.

At its simplest, the U.S. Centers for Disease Control and Prevention define SCD as death due to cardiac disease (or other heart abnormality) that occurs outside the hospital. But "sudden" cardiac death is something of a misnomer in that these deaths are without exception due to pathologies that progress over many years. In tandem with this important underlying perception of the problem, let's first address one potential stumbling block in patient thinking. Present research reveals that vigorous exercise is responsible for triggering up to 17% of SCDs. What does this really mean?

The Real Role of Exercise

To be sure, sudden death from cardiac causes occurs with unusually high frequency during or shortly after vigorous physical exertion. However, an essential point here is that the risk increases enormously in people who don't ordinarily exert themselves. In a widely-publicized 1993 study of Americans by Mittleman et al., the risk assessment score for SCD during exercise was 2.4 among those reporting regular vigorous exertion, and 107 among people who were habitually sedentary. This striking difference appears to be due in part to the effect regular exercise has on the sympathetic response, abolishing the "platelet hyperactivity" observed in sedentary people during exercise.

Sumeet Chugh, M.D., director of the Heart Rhythm Research Laboratory at Oregon Health & Science University in Portland, says, "Universally, I tell my patients that exercise is good. Is exercise ever bad? There's no indication of this for the athletic community." In short, patients may need reminding that a trigger is not a cause. On the contrary, where CAD is concerned, exercise is most certainly a preventive measure and, increasingly, a treatment.

And what about the non-athletic community? Exercise-based treatments for CAD differ depending on individual circumstances, but ultimately it is always a desirable modality. Charles Schulman, M.D., assistant clinical professor of Medicine at Harvard Medical School and current AMAA president, explains, "It just depends on whether you need drugs to lower cholesterol or blood pressure first. A stress test will never tell you, 'Don't exercise.' It may tell you to get treated with other modalities first, but it won't tell you not to begin exercise at all." Other treatments that may be appropriate before implementing an exercise regimen include angioplasty and bypass surgery, and ACE-inhibiting or beta-blocking medications. Patients may need careful monitoring during exercise, particularly those with known cardiac arrhythmias. Schulman adds, "The key is levels of exertion. Are you beginning a strenuous training regimen or are you starting the [ARA] Run-Walk program?"

Relative vs. Absolute Risk

While SCD risk may be higher during exercise than at other times, the absolute excess risk during any given bout is extremely low: 1 in 1.51 million. In a notable study of 133 men who died of cardiac arrest, the overall risk--i.e., both during and not during exercise--for those at the highest level of habitual activity was only 40% of the risk for the habitually sedentary men. Again, the trigger can make the treatment look a lot like the cause. As Chugh points out, "The trouble is, sudden cardiac death is a powerful event. Particularly when athletes drop, it's news. With people over age 65, it's way more frequent, but it's not news." But the strong cardioprotective effect of regular exercise clearly outweighs the transient risk of a cardiac event.

In marathoning, the risk of death from any cause--including hyponatremia or trauma, for example--is about one in every 50,000 finishers. While significantly higher than for road races between 10K and half-marathon distance (3.1 in a million), this risk is still extremely low (14 in a million). When one considers the number of deaths within the pool of total marathon participants, this risk is diminished further (possibly even eliminating the discrepancy between the marathon and shorter races).

Having established that exercise is not the cause of SCD, let's examine what is. What might be termed the four major categories of SCD cases undoubtedly have untold subdivisions and subtle differences within each. But it's helpful to start with these four broad distinctions. They are: 1.) patients with symptomatic CAD, a family history or any of the known risk factors as identified in the Framingham study; 2.) patients with symptomless or silent CAD; 3.) patients, often under age 35, without CAD but with another, frequently identifiable heart irregularity; and 4.) patients, often young, with concealed abnormalities about which little is known.

What We Can Do

CAD and heart failure are the two leading causes of SCD in men age 45 and over and in women age 55 and older. Nearly 80% of SCD victims have some form of CAD. Within this first case category, much can be done to prevent these events. Noel Nequin, M.D., Chicago-based cardiologist, founding fellow of the American Association of Cardiovascular and Pulmonary Rehabilitation and immediate-past president of AMAA, feels that a simple baseline stress test truly is the test that could save your life. Nequin asserts, "This is especially important in individuals who have any or several of the major c.v. risk factors: smoking, hypertension, hyperlipidemia, physical inactivity, obesity or type-2 diabetes." Those with angina pectoris make obvious stress test candidates. But silent ischemic heart disease is a more rampant, and all the more thorny, problem. Nequin notes, somewhat alarmingly, "Some physicians still think that any adult who has no chest pain needs no further diagnostic evaluation." This does not preclude patients from membership in the second case category, those with silent CAD.

Still, there are signs that point to risk. While certain of the Framingham risk factors are not relevant to the physically active, many are. As Schulman puts it, "Runners are not automatically exempt from coronary heart disease." Age and family history are two additional factors in particular that deserve attention. Men 45 and older and women 55 and older should consider taking a stress test, especially if they are just beginning an exercise program. They certainly should if they also have high blood pressure or high cholesterol, or if a male relative under age 55 has heart disease, age 65 for female relatives. For Nequin, the "aura of invincibility" that too often surrounds athletes is a source of great frustration and needs immediate debunking.

He should know. In 1982, Nequin completed the first 50 miles of the Western States 100 without symptoms. The next month, he completed the entire 100 miles. Again, he showed no symptoms. The following month, a stress test showed marked ischemia--"only when my heart rate was 150 beats per minute [bpm] and higher"--but still, no chest pain. An angiogram revealed that his proximal right coronary artery had a 90% blockage, which was later found with PTCA scanning to be in actuality 99% blocked. Nequin concludes, "The ability to do hard work, run a marathon, et cetera, does not guarantee the coronary arteries are clean. People run with silent ischemia all the time."

The Limitations of Screening

The above call for cardiac workups among a certain active demographic stems from the well-founded belief that screening can greatly reduce incidents of SCD within the first two case categories. The third case category for SCD is far more difficult to recognize and treat before it's too late. These are patients, usually under age 35, with compromised arterial physiology or hypertrophic cardiomyopathy. The latter, a congenital condition in which the walls of the heart are excessively thick, is the most common cause of SCD in adolescents. A third type of known irregularity is arrhythmogenic right ventricular dysplasia (ARVD), in which fatty tissue has replaced normal heart muscle.

These cases illustrate the problem inherent in screening. There is no comprehensive way to screen for everything. Sixty-year-old runners are easier to test because to the extent they may be at risk for SCD, they almost certainly have CAD. That is, it's easy to match a test with this type of patient. A doctor should first screen for CAD in an older person, because profiling has taught us that CAD, symptomless or not, is the heart complication he or she is most likely at risk of harboring. Patients like this acquire common types of diseases. In younger people, SCD is much harder to predict. Though a relatively common condition such as a mitrovalve prolapse is unlikely to be a stand-alone SCD cause, other heart anomalies, like certain arrhythmias, can of themselves be warning signs. But available screening techniques are too often imprecise.

In a tragic case study recently published in Medical Science Sports & Exercise, a 14-year-old boy collapsed during soccer practice. He was given an extensive cardiac workup, including a transthoracic ECG and a stress ECG at 200 bpm peak heart rate; the tests revealed no abnormalities. The boy suffered cardiac arrest and died during a warm-up jog two weeks later. Only upon autopsy did it become clear that he had an acute angle take-off of the left main coronary artery. This condition is difficult if not impossible to diagnose during life. Coronary angiography can sometimes identify when an artery originates from an inappropriate sinus, but it isn't useful in detecting acute angle take-off.

Presently, clinicians are urged to look for the following warning signs that may point to a hidden heart abnormality in an athlete: palpitations, chest pain, dizziness, passing out or a change in the athlete's exercise capacity. For example, they run 18 miles on one day of a typical training week and suddenly find they are only able to go four on a given day in the next week. Once more, family history serves as another red flag. It's been documented that SCD occurrence in a parent results in an up to 1.8-fold SCD risk increase in their offspring, even after controlling for conventional risk factors like smoking. Chugh's recently published study found that one SCD victim merely had a family member with a history of dizziness.

A test developed in July of 2002 can detect the hormone BNP in the bloodstream, which serves as an indicator of heart disease in that the body produces the hormone when its ventricles are strained. This test, with results in 15 minutes, represents a step toward the kind of surefire lab testing that many view as the future of CAD and SCD-risk screening. Unidentifiable, subclinical risks, whether inherited or acquired, remain the daunting frontier researchers must conquer if they are to prevent shockingly sad cases like that of the 14-year-old soccer player. There is, however, reason for hope in the form of genetic research that has made great strides in recent years.

What We Can't Do--Yet

The fourth case category consists of people with no obvious heart condition. Sometimes these patients fall victim to an unusual combination of factors that contribute to an SCD event. Perhaps a concealed genetic abnormality in concert with a marathon on an unseasonably warm day triggers the unthinkable. These are the patients about whom we know far too little. Schulman likens their cases to airline crashes. "It's hard to draw conclusions from rare events," he says.

Chugh, who lectured at AMAA's Boston Marathon symposium this year, explains, "There is a list of known risk factors. The list is not comprehensive." Assessments by phenotype are inadequate measures of who is predisposed to potentially life-threatening arrhythmias. Research efforts next need to focus on genotype; we must discover which genes are responsible. Chugh sees that this research has untold merits across all case categories. As he notes in a recent review, the predictive power of lipid levels, hypertension, smoking and diabetes in subclinical heart disease is "quite low." Furthermore, advancements in the electrophysiology lab such as arrhythmia inducibility can't be feasibly applied to the asymptomatic population, "where SCD prevalence is in fact the highest."

The recent completion of the Human Genome Project is analogous to discovering all of the cities in the United States. Chugh says, "What we now need is to find out who lives at each address, and what they do for a living." High-density gene mapping and examination of functional pathways and genomic structures are the best ways to identify genetic susceptibilities to lethal arrhythmias. To the extent that therapeutic modalities like defibrillators and antiarrhythmic drugs are effective, they nearly always come after the fact. Chugh and his colleagues are bent on preventing SCD and MI before they happen. "What I do is put portable defibrillators in people," he says. "All of these people have had a cardiac event. I'd like to put them in people who've never had an event." Similarly, gene screening will allow antiarrhythmic drug treatment to begin before a cardiac event occurs. Researchers at Oregon Health & Science University are at work presently identifying more and more culprit genes.

Of the SCD cases Chugh has researched, 4.4% of the patients had a structurally normal heart. On top of that, many structural problems, as we have seen, cannot be screened and are detected only during autopsy. Chugh mentions that several specific genes that increase the risk of SCD have been identified. The eventual goal, then, is to identify all the candidate genes that put patients at risk of SCD, and develop tests to comprehensively screen for them. One such gene is KCNH2. Some people in whom Chugh found the KCNH2 gene defect lacked a family history in both SCD and CAD. On occasion, apparently minor variations in gene sequences may combine with drugs, even certain antiarrhythmic drugs (e.g., sotalol and quinidine), to increase the risk of SCD.


Incidents of SCD among the active populus are rare. Nevertheless, exercise can trigger SCD if there is pre-existing cardiac disease and/or a heart abnormality. Though regular exercise is of great benefit in both the prevention and treatment of CAD, athletes are not automatically exempt from CAD; nor are they exempt from SCD. While present screening measures are surely effective in identifying many patients at risk of SCD, the measures are in many ways inadequate.

Chugh and his colleagues have calculated that approximately 5% of the middle-aged U.S. population has a "presently indeterminable but significant predisposition" to SCD. There is optimism embedded in that statement, however, with the operative word being "presently." Genetic scanning technologies will continue to both improve and decrease in cost. This vital research will eventually enable us to identify all of the problematic genes, and develop tests to detect them in people. Beyond that, there is hope that gene mapping will lead to new, better-targeted treatments, including, but by no means limited to, novel drug therapies.


Arking DE, et al. Genomics in Sudden Cardiac Death. Circulation Research 2004; 94(6): 712-723.

Chugh SS, et al. Postmortem Molecular Screening in Unexplained Sudden Death. Journ. Am. College Cardiology 2004; 43(9): 1625-1629.

Frere JA, et al. The Risk of Death in Running Road Races: Does Race Length Matter? Phys. & Sportsmed. 2004; 32(4):33-40.

Hardman AE, Stensel DJ. Physical Activity and Health: The Evidence Explained, Routledge, London, pp. 229-251, 2003.

Iskandar EG, Thompson PD. Exercise-Related Sudden Death Due to an Unusual Coronary Artery Anomaly. Med. Sci. Sports & Exerc. 2004; 36(2):180-182.

Personal corresp., Sumeet Chugh, M.D., Noel Nequin. M.D. and Charles Schulman, M.D.

Jeff Venables is the editor of Running & FitNews, the publication of the American Running Association.
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Author:Venables, Jeff
Publication:AMAA Journal
Geographic Code:1USA
Date:Jun 22, 2004
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