Cardiovascular Considerations
Marc Childress
Jonathan A. Drezner
Ralph G. Oriscello
Francis G. O’Connor
INTRODUCTION
Exercise is clearly associated with improved cardiovascular health. In addition to a direct conditioning effect, physical activity is critical in the management and prevention of several chronic medical conditions that impact overall health (47).
However, vigorous exercise also can be a trigger for sudden cardiac arrest in individuals with underlying cardiovascular disease (43).
Sudden death in athletes is most often attributable to a cardiovascular disorder. Sudden cardiac death represents 75% of fatalities in National Collegiate Athletic Association (NCAA) athletes during training or competition, more than deaths related to blunt trauma, heat stroke, and sickle cell trait combined (1).
A high index of suspicion must be maintained during screening to detect conditions associated with sudden death, including appropriate individual assessments as well as reasonable measures to evaluate large populations.
When a serious cardiovascular condition is identified, appropriate treatment and activity modification may decrease the risk of sudden death.
CARDIOVASCULAR BENEFITS OF EXERCISE
The lack of regular physical activity has clearly been associated with an increase in coronary heart disease and the incidence of adverse cardiac events (4,34,41,48,49). Multiple studies have confirmed the benefit of aerobic exercise with a reduction in the number of cardiac events and a reduction in mortality (3,18,34,36,50). Although there is an increased risk for adverse cardiac events during activity, there is overwhelming evidence that the net benefits of consistent and regular physical exercise outweigh these risks in the primary prevention of cardiovascular disease (22,45).
THE ATHLETIC HEART SYNDROME
Vigorous athletic training is associated with specific physiologic and structural cardiovascular changes, so-called athletic heart syndrome (15,28). These changes represent normal adaptations to physical conditioning.
Studies demonstrate a constellation of morphologic changes that vary depending on the type of training (39).
In endurance-trained athletes, a chronic volume overload results in an increase in both left ventricular end-diastolic diameter and left ventricular wall thickness. This eccentric hypertrophy allows a larger stroke volume and thus a greater overall cardiac output at faster heart rates. Biatrial enlargement and right ventricular dilation also can be seen.
Strength-trained athletes develop a concentric hypertrophy with an increase in absolute and relative wall thickness without significant changes in end-diastolic diameter. Right-sided and atrial dimensions typically remain unchanged.
It is important to remember that the adaptive structural and physiologic response of the normal athletic heart does not rule out the presence of an underlying pathologic condition. In fact, it makes the task of diagnosing that condition more challenging for the primary care physician, sports medicine physician, and cardiologist (21). Criteria for distinguishing the characteristics of athletic heart syndrome from significant underlying pathology have been defined and, in some circumstances, may require detraining for 2-3 months (21). In benign cases, full resolution should be observed, whereas residual hypertrophic changes may suggest underlying concerns (38).
Physical Examination
The heart rate of well-conditioned athletes is usually between 40 and 60 bpm, secondary to enhanced vagal tone, decreased sympathetic tone, and a larger stroke volume. Thus, sinus bradycardia is a common finding, and sinus arrhythmia may be more noticeable.
The physiologic splitting of S2 may be slightly delayed during inspiration due to the larger stroke volume. An S3 may be noted in endurance-trained athletes secondary to the increased rate of left ventricular filling associated with the relative left ventricular dilatation (13,28).
Although an S4 may be noted in strength-trained athletes secondary to concentric hypertrophy, its presence always warrants clinical evaluation. Functional (flow) murmurs characterized by a soft 1-2/6 ejection murmur often present when supine and diminished with standing or Valsalva may be noted in 30%-50% of athletes on careful examination (15).
Table 27.1 Common ECG Findings in Athletic Heart Syndrome | ||||||||||||||||
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Electrocardiographic Changes
Several electrocardiographic changes can be seen in well-conditioned athletes. In most cases, these changes are benign reflections of structural and functional changes. However, some findings are abnormal and may suggest underlying pathology. It can be challenging to distinguish adaptive versus pathologic changes in trained athletes, and modern electrocardiogram (ECG) criteria should be used to assist in interpretation (8,9,14,15) (Tables 27.1 and 27.2).
ECG is helpful in the initial evaluation of cardiac conditions in athletes who present with cardiovascular symptoms or have abnormal findings on physical examination.
The role of ECG in the preparticipation screening of athletes is controversial. Opponents of ECG screening are concerned about false-positive results, cost effectiveness, and unnecessary disqualifications in athletes (46). Proponents of ECG screening recognize that the sensitivity of a history and physical examination alone to detect potentially lethal cardiovascular disorders in athletes is very low, that the addition of an ECG greatly increases the sensitivity, and that it can be accomplished with a low and acceptable false-positive rate when performed by experienced physicians guided by modern ECG criteria (11,35).
SUDDEN CARDIAC DEATH IN EXERCISE
The overall risk of sudden death during exercise varies depending on age, gender, and sport. Estimates from studies in runners range from 1:15,000 joggers per year to 1:50,000 marathon participants per race (24,43). For high school and college-aged athletes, the range is 1:45,000 to 1:160,000 per year, and sudden deaths occur disproportionally more often in males, African Americans, and basketball and football players (1,23).
The specific etiologies contributing to sudden cardiac death are strongly related to age. For sudden death in persons over age 35, more than 75% are associated with coronary artery disease. This association increases with age, consistent with the rising prevalence of atherosclerosis (18).
Table 27.2 Classification of Abnormalities of the Athlete’s Electrocardiogram
Group 1: Common and Training-Related ECG Changes
Sinus bradycardia
First-degree AV block
Incomplete RBBB
Early repolarization
Isolated QRS voltage criteria for left ventricular hypertrophy
Group 2: Uncommon and Training-Unrelated ECG Changes
T-wave inversion
ST-segment depression
Pathologic Q waves
Left atrial enlargement
Left axis deviation/left anterior hemiblock
Right axis deviation/left posterior hemiblock
Right ventricular hypertrophy
Ventricular pre-excitation
Complete LBBB or RBBB
Long- or short-QT interval
Brugada-like early repolarization
AV, atrioventricular; ECG, electrocardiogram; LBBB, left bundle branch block; RBBB, right bundle branch block.
SOURCE: Reproduced with permission from Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J. 2010;31:243-59.
In younger athletes, sudden cardiac death is most often the result of intrinsic structural or electrical abnormalities. Hypertrophic cardiomyopathy (HCM) is the most common cause of sudden cardiac death, followed by coronary artery anomalies, myocarditis, and arrhythmogenic right ventricular cardiomyopathy (ARVC). Other etiologies include genetic conductive system abnormalities such as ion channel disorders (long QT syndrome), aortic rupture from Marfan syndrome, premature coronary artery disease, idiopathic left ventricular hypertrophy, substance abuse (cocaine or steroids), aortic stenosis, mitral valve prolapse, sickle cell trait, and blunt chest trauma (commotio cordis). This list reflects cases of sudden death in athletes over the past two decades in the United States (23). It is important to note that the relative prevalence of many of these conditions is variable, based on regional and ethnic differences. For example, ARVC is the leading cause of sudden cardiac death in the Veneto region of Italy (12).
Screening for Sudden Death
The American Heart Association (AHA) Science and Advisory Committee published consensus guidelines for preparticipation cardiovascular screening for high school and college athletes in 1996 and reaffirmed their recommendations in 2007 (25,26). A complete personal and family history and
physical examination should be done for all athletes. It should focus on identifying those cardiovascular conditions known to cause sudden death. The recommended interval for evaluation begins in middle school and is repeated every 2 years with an interim history between examinations (Table 27.3).
Family history should include a specific inquiry for a family history of premature coronary artery disease, diabetes mellitus, hypertension, sudden death, syncope, death or significant disability from cardiovascular disease in relatives younger than age 50, or the presence of inherited cardiac disorders such as HCM, ARVC, Marfan syndrome, and long QT syndrome.
Personal past history should include specific inquiries on the detection of a heart murmur; risk factors for coronary artery disease such as diabetes mellitus, hypertension, hyperlipidemia, and smoking; and a history of syncope, near syncope, exercise intolerance, exertional chest pain, dyspnea, or excessive fatigue.
Table 27.3 The 12-Element AHA Recommendations for Preparticipation Cardiovascular Screening of Competitive Athletes
Medical History*
Personal History
1.
Exertional chest pain/discomfort
2.
Unexplained syncope/near syncope**
3.
Excessive exertional and unexplained dyspnea/fatigue, associated with exercise
4.
Prior recognition of a heart murmur
5.
Elevated systemic blood pressure
Family History
6.
Premature death (sudden and unexpected, or otherwise) before age 50 years due to heart disease, in ≥ 1 relative
7.
Disability from heart disease in a close relative < 50 years of age
8.
Specific knowledge of certain cardiac conditions in family members: HCM, long QT syndrome, or other ion channelopathies, Marfan syndrome, or clinically important arrhythmias
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