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CURRENT Diagnosis & Treatment in Cardiology > Chapter 34. The Athlete’s Heart >

Essentials of Diagnosis

  • History of athletic training and performance.
  • Enhanced exercise ability (O 2max > 40 mL/kg/min).
  • Resting bradycardia.
  • Increased left ventricular mass by echocardiography.

General Considerations

The concept of the athlete’s heart is one that has been postulated for almost 100 years, promulgating the idea that myocardial hypertrophy could be a purely physiologic phenomenon. Media attention to the sudden deaths of widely known athletes has helped focus attention on the important distinction between pathologic cardiac hypertrophy and physiologic hypertrophy and the upper limits of the latter.

The adaptations of the human body to physical training involve (but are not confined to) the cardiovascular system. The exercise-related changes in other organ systems influence the cardiovascular response to exercise. It is important for the physician to be familiar with the physiologic responses to physical training in order to distinguish them from similar changes that can occur with cardiovascular disease.

Different forms of exercise produce a number of physiologic responses. Also, cardiovascular responses to short-term training and prolonged training differ. Exercise generally takes two basic physiologic forms—dynamic and static, or isometric, exercise—although most athletic activities are a variable combination of both forms of exercise. Dynamic exercise constitutes an alteration in the length of skeletal muscle with comparatively little change in muscle tension. Static exercise is essentially the reverse—that is, a marked alteration in skeletal muscle tension with little or no change in muscle length. Distance running is a classic example of dynamic exercise; weight lifting is a classic example of static exercise.

The morphologic and physiologic consequences of dynamic and isometric exercise are significant and may simulate changes associated with cardiac disease. The normal limits of changes that are due to athletic conditioning require careful identification. Awareness of these limits improves the physician’s ability to determine the end points at which normal anatomy and physiology become clinical disease.

Maron BJ et al. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. Circulation. 2006 Oct 10;114(15):1633–44. [PMID: 17030703]

Physiology of Exercise Training

The acute cardiovascular responses to exercise are specific and vary with different forms of exercise (Figure 34–1). There are also specific adaptive responses to exercise, particularly to dynamic exercise. In particular, the adaptive change in heart rate from an alteration in vagal parasympathetic tone defines the normal physiologic range; as noted earlier, this may be initially misinterpreted as representative of cardiovascular disease.

Figure 34–1.

Cardiovascular response to exercise. A: Response to dynamic exercise progressively increasing workload to maximal oxygen consumption. B: Response to static handgrip contraction at 30% maximal voluntary contraction. ABP, systolic, mean and diastolic arterial blood pressures; HR, heart rate; Q, cardiac output; SV, stroke volume; TPR, total peripheral resistance; O 2, oxygen consumption.

(Reprinted with permission from Mitchell JH, Raven PB. Cardiovascular adaption to physical activity. In: Bouchard C et al, editors. Physical Activity, Fitness and Health: International Proceedings and Consensus statement. Human Kinetics Publishers: Champain IL; 1994.)

Acute Responses to Exercise

Dynamic Exercise

Several acute cardiovascular responses to dynamic exercise are typical (Figure 34–1). As would be anticipated in meeting the demands of aerobic exercise, oxygen consumption increases because of an increase in both cardiac output and the arteriovenous oxygen difference. The increase in arteriovenous oxygen difference results from an increase in the oxygen extraction, or demand, by the exercising skeletal muscle and the increase in muscular capillary blood flow. Oxygen consumption is linearly related to the workload achieved during dynamic exercise. Maximal oxygen consumption (O  2max) is a highly reproducible measure of total aerobic capacity and thus dynamic exercise performance. Aerobic capacity varies with training, lean body mass, age, and gender and is significantly influenced by the individual’s genetic characteristics. In children, gender differences are seen only after puberty, when the aerobic capacity of girls and young women tends to be approximately 30% less than that of boys and young men of the same age. Although incompletely explained, these differences are believed to be multifactorial; females, for example, have a lower lean body mass and a lower hemoglobin level. Maximal oxygen consumption diminishes with increasing age, as a result of such factors as the gradual detraining effect of age, an alteration in cardiac stiffness, and a reduction in -adrenergic responsiveness that produces an attenuated heart rate response to exercise. Although it may be improved by dynamic training in older individuals, this improvement may well be due to an increased arteriovenous oxygen difference as much as to an increase in cardiac output and stroke volume. Furthermore, the improvement in O 2max is relative when the overall decline in fitness is taken into account.

Oxygen consumption is also linearly related to cardiac output during dynamic exercise. The increase in cardiac output results principally from an increase in heart rate. Some increase in stroke volume takes place, resulting from the increase in venous return produced by the increasing skeletal muscle activity. The increase in left ventricular stroke volume during dynamic exercise is larger in an upright than in a supine position, but the absolute stroke volume at peak exercise is greatest in the supine position. Other hemodynamic responses contribute to the increased stroke volume. Intrathoracic pressure is reduced, left ventricular filling pressure rises, the mitral valve orifice enlarges, and the left ventricular end-diastolic volume increases. The net effect of these changes is activation of the Frank-Starling mechanism during the early initial and lower levels of dynamic exercise. Subsequently, at higher levels of exercise, sympathetic activation augments the Frank-Starling response in increasing stroke volume by increasing myocardial contractility and reducing end-systolic volume.

Resting heart rate is determined by vagal tone coupled with the level of sympathetic reflex activation. In the upright (versus supine) position, for example, resting heart rate is higher because of a mildly increased level of sympathetic activation. The initial increase in heart rate during exercise is due to a reduction in vagal tone, a central nervous system response mediated by stimulation of mechanoreceptors in the activated skeletal muscles. The heart rate increase is subsequently maintained by sympathetic activity and increased circulating catecholamines.

Systolic blood pressure increases during dynamic exercise, with a minimal increase in either diastolic or mean arterial pressure. The magnitude of the response is determined by the size of the activated muscle mass. Thus, the response during large muscle or leg exercise is greater than during small muscle or arm exercise. There is a greater increase in pulmonary arterial pressure than in systemic pressure during exercise because the change in vascular resistance is less in the pulmonary vasculature. This relative increase in pulmonary pressures is believed to augment pulmonary oxygen transport during exercise.

Static Exercise

In static exercise, intramuscular pressure increases dramatically, with a resultant reduction or obliteration of exercising skeletal muscle blood flow (Figure 34–1). Static exercise is sustained by anaerobic mechanisms, and the consequent increases in oxygen consumption and cardiac output are much less than during dynamic exercise. Furthermore, oxygen consumption and cardiac output increase after static exercise, presumably because of an immediate increase in blood flow to the involved muscles to rectify the oxygen debt acquired by anaerobic mechanisms during the static exercise.

The increase in cardiac output during static exercise is due mainly to the increase in heart rate; stroke volume remains almost unchanged. Systolic blood pressure increases significantly during static exercise. Because stroke volumes and systemic vascular resistance change only minimally, this increased arterial pressure is due to the effects of increased muscle contraction on arterial pressure waves. Although arteriovenous oxygen difference remains unchanged during static exercise, an increase does take place immediately following release as a result of increased blood flow to the muscle bed.

Effects of Systematic Exercise Training

As previously stated, O  2max is an accurate and reproducible measure of aerobic capacity and thus becomes an objective measure of dynamic fitness. In normal men, O 2max ranges from 25 mL/kg/min to 40 mL/kg/min, with the lower values occurring in the older individuals. More than 50 mL/kg/min is considered representative of an elite level of fitness (the level may go as high as 80 mL/kg/min), reflecting an increase in maximal cardiac output and arteriovenous oxygen difference.

Dynamic Exercise Training

This type of training decreases resting heart rate because of an adaptive increase in vagal tone; it also decreases the heart rate response at any level of exercise. The heart rate response to maximal exercise, however, is identical in both the trained and untrained individual. Therefore, the increase in maximum cardiac output associated with dynamic training is due to increased stroke volume. It should also be noted that these physiologic adaptive changes to dynamic training occur in association with morphologic and physiologic changes in the heart.

Static Exercise Training

This type of training does not produce the same degree of O 2max as does dynamic training. It is probable that the use of anaerobic rather than aerobic mechanisms to generate muscle energy requires a lower increase in cardiac output. Although morphologic changes do occur, the hemodynamic response to static exercise is similar in trained and untrained individuals.

Cross Training

Dynamic training improves the response to static exercise in that the increased stroke volume at a lower heart rate allows the subject to sustain a greater cardiac pressure load and thus improve isometric performance. Static exercise training does not improve dynamic performance, however, except in areas or activities where greater strength or power is required (eg, pole vaulting).

Cardiovascular Response

The frequency, intensity, and duration of exercise all affect the cardiovascular response. To obtain a significant training effect requires 30 minutes of dynamic exercise at 60–80% of maximal O 2 three times per week. Little effect is seen unless rates of more than 130 bpm are achieved for prolonged periods. Although lower levels and less frequent episodes of training may create a training effect, cessation of exercise produces a rapid detraining effect—which is complete within 3 weeks.

Measurement of the heart rate provides a good index of training. As discussed earlier, the alteration in resting heart rate is said to be due to an increase in vagal parasympathetic tone rather than a decrease in sympathetic tone or lower circulating catecholamine levels. In trained athletes, circulating levels of both epinephrine and norepinephrine are lower during dynamic and static exercise, with a lower heart rate response to the relative intensity of both forms of exercise.

Systematic training has some effects on other organ systems. Total blood and plasma volumes increase with dynamic training; these changes are thought to be related to increases in renin activity and serum albumin levels. Higher hemoglobin levels lead to an increase in both maximal oxygen consumption and endurance. Well-trained athletes use oxygen more efficiently, and the vascular conductance of skeletal muscle changes, resulting in a greater arteriovenous oxygen difference during dynamic exercise. Dynamic exercise training also increases high-density lipoprotein levels and decreases low-density lipoprotein and very-low-density lipoprotein levels, as well as body weight.

Morphologic Responses to Training

Physiologic hypertrophy is a prominent feature of the athlete’s heart. The morphologic adaptations to the increased stroke volume induced by exercise conform to the principles of Laplace law, which relates the wall tension to intracavitary size and pressure. The increase in wall thickness in the setting of volume and pressure overload tends to normalize wall stress in both dynamic and isometric exercise (Figure 34–2).

Figure 34–2.

Distribution of cardiac dimensions in large populations of highly trained male and female athletes. Top: Left ventricular end-diastolic dimension. Middle: Transverse left atrial dimension. Bottom: Maximal left ventricular wall thickness.

(Reprinted with permission from Pelliccia A et al. Ann Intern Med. 1999;130:23 and Pelliccia A et al. J Am Coll Cardiol. 2005;46:690 and Pelliccia A et al. N Engl J Med. 1991;3324:295.)

The availability of two-dimensional and Doppler echocardiography and radionuclide ventriculography has allowed for the assessment of the mechanics of systolic and diastolic function in the trained athlete. The value of these technologies, although substantial, is limited by the inability to directly measure changes in intracardiac pressures, making absolute conclusions regarding detailed adaptive changes more difficult. Nevertheless, when compared with matched controls (age, gender, and body surface area), any relative changes in parameters of systolic or diastolic function are valid. It is also evident that the functional changes are consequences of the adaptive morphologic changes of the dynamically and isometrically trained athlete. Noninvasive parameters of systolic function in trained athletes usually fall within accepted normal limits. The occasional abnormal findings may be satisfactorily explained as secondary to the adaptive morphologic changes associated with the different types of training. Similarly, noninvasive parameters of diastolic function usually fall within a normal range of values at rest, irrespective of the type of training.

Echocardiography allows cardiac anatomy to be detailed in a noninvasive serial manner; it is particularly useful in finding and documenting changes in cardiac morphology in athletes. Changes in cavity sizes, left ventricular wall thickness, and left ventricular mass have been documented in a number of studies of athletes undergoing both dynamic and static exercise training (Figure 34–2).

Left Ventricular Cavity

A consistent finding in dynamically trained athletes is an increased left ventricular end-diastolic dimension, which is present irrespective of body surface area, height, or gender. Compared with sedentary control subjects, the left ventricular end-diastolic dimension is increased by approximately 10% in the trained athlete, which represents an increase in end-diastolic volume of approximately 33%. Most dynamically trained athletes have an end-diastolic dimension of 60 mm or less. In contrast, left ventricular end-diastolic dimension is not altered with static exercise training, whether expressed in absolute values, or normalized by body surface area, weight, or lean body mass. This difference is believed to reflect the pressure, rather than volume load, on the left ventricle that is created by isometric training. The end-systolic dimension and volume remain within normal limits in the endurance athlete, producing the increase in stroke dimension and volume associated with dynamic exercise training.

Left Ventricular Wall Thickness

Concomitant with the increase in left ventricular cavity size in the dynamically trained athlete, left ventricular posterior wall and interventricular septal thickness increase. The increase (compared with sedentary controls) in left ventricular posterior wall thickness is as high as 19%; in the same study, 98% had a left ventricular posterior wall thickness of 12 mm or less. Isometric exercise produces septal wall thicknesses of up to 16 mm. These increased values fall within an acceptable range when normalized for body surface area, weight, or lean body mass.

Although septal hypertrophy is a characteristic of hypertrophic cardiomyopathy, the increase in septal thickness in athletes is rarely above 16 mm and the septal-posterior wall thickness ratio does not increase above 1.2:1. Furthermore, there is no evidence in the literature that primary hypertrophic cardiomyopathy may develop with training.

Left Ventricular Mass

Estimates of left ventricular mass incorporate measurements of intraventricular septum and posterior wall thickness, both of which increase significantly in trained athletes. It is therefore reasonable to expect a significant increase in left ventricular mass in both dynamically and isometrically trained athletes. An increase of as much as 45% is found, even after normalization for body surface area.

Right Ventricular Cavity

Increases of up to 24% in right ventricular cavity dimensions may be seen in trained athletes.

Left Atrial Cavity

Increases in left atrial cavity size are also found in trained athletes and appear to be related to both the intensity and duration of the exercise.

Electrocardiography

Any type of athletic training in any form can alter the electrocardiogram (ECG) (Table 34–1). In a recent survey of 1005 trained athletes, 40% of ECGs were abnormal. It is important to know the effects of normal training on the ECG as well as the ECG abnormalities that warrant further investigation. Alterations on the ECG also depend on the nature, intensity, and level of training. The ECG reflects the morphologic adaptive changes of the heart—sinus bradycardia and voltage criteria for left ventricular hypertrophy (LVH)—that are due to the nature of the training. In the dynamically trained athlete in particular, the sinus bradycardia, which can be profound, reflects the adaptive increase in left ventricular cavity size that delivers large stroke volumes at rest and during exercise. Sinus bradycardia is usually due to high vagal tone, which may also be associated with sinus arrhythmia, sinoatrial block, multifocal atrial rhythms, junction rhythms, first-degree atrioventricular block, and Mobitz I second-degree atrioventricular block. All these abnormalities disappear during exercise. The P wave of the ECG may be notched and increased in amplitude. Interventricular conduction abnormalities are common in athletes. The ST segment may be elevated and the T wave increased in amplitude. Occasionally in trained athletes, the ST segment may be depressed and the T wave biphasic or inverted, all of which correct during exercise. These latter findings at rest are characteristic of ischemic heart disease, however, and their existence in the athlete warrants further investigation.

Table 34–1. Effects of Dynamic and Isometric Exercise and Training on the Electrocardiogram.

Notched P waves
Voltage criteria for LVH
Interventricular conduction abnormalities
Symmetric peaked T waves
Sinus bradycardia
Sinus arrhythmia
Sinoatrial block
Multifocal atrial rhythm
Junctional rhythm
First-degree AV block
Mobitz I second-degree AV block

AV, atrioventricular; LVH, left ventricular hypertrophy.

Distinguishing between physiologic and pathologic LVH by ECG may not be possible, particularly in a young athlete. The adaptive development of LVH and sinus bradycardia is characteristic of the trained athlete, as is the loss of these adaptive characteristics as a detraining effect. In the older athlete, where the prevalence of ischemic heart disease is much higher, voltage criteria for LVH, ST- and T-wave abnormalities, and repolarization abnormalities of the QRS complex are more common. The threshold for pursuing further investigation of abnormal ECG findings should be much lower in these older athletes.

Racial Differences in Response to Training

No detailed studies addressing the adaptive responses to training in the black athlete have yet been completed. Circumstantial evidence, however, would suggest that these responses may differ in black athletes. It is known that LVH is more prevalent in a black hypertensive population than in a white population, given similar levels of blood pressure elevation. Because a racial difference appears to exist in the blood pressure response to both dynamic and isometric exercise, the potential for an increased prevalence and greater degree of LVH appears to exist among black athletes. A study of black collegiate athletes showed that more than 30% had an interventricular septal thickness of more than 13 mm; a separate study of white athletes found only 3% with similar increases in thickness. These factors, coupled with the occurrence of sudden death in athletes—including black athletes—clearly indicate the need for studies of trained black athletes as well as comparative studies of black and white athletes.

Detraining

The adaptive responses to both dynamic and isometric exercise training persist only if the training continues with sufficient duration and intensity. Cessation of the training activity results in a temporal regression of these adaptive changes: the detraining effect. Although this effect is consistent despite age, gender, or the overall duration or type of training, the time course appears to be influenced by these factors. Following cessation of training, a regression of physiologic hypertrophy of up to 60% takes place within 7 days, so-called left ventricular remodeling. Both posterior left ventricular wall thickness and interventricular septal thickness regress equally, and the septal-posterior wall thickness ratio remains unchanged. The left ventricular end-diastolic dimension decreases within 7 days, with little change thereafter. The detraining effect is also associated with a reduction in O  2max. After 12 weeks of inactivity (cessation of training), O 2max decreases up to 16%, with half of this loss occurring in the first 3 weeks. Maximal cardiac output during exercise is also reduced by up to 8% in the first 3 weeks of detraining.

Germann CA et al. Sudden cardiac death in athletes: a guide for emergency physicians. Am J Emerg Med. 2005 Jul;23(4):504–9. [PMID: 16032621]

Pellicia A et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation. 2000 Jul 18;102(3):278–84. [PMID: 10899089]

Pelliccia A et al. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation. 2002 Feb 26;105(8):944–9. [PMID: 11864923]

Sharma S et al. Physiologic limits of left ventricular hypertrophy in elite junior athletes: relevant to differential diagnosis of athlete’s heart and hypertrophic cardiomyopathy. J Am Coll Cardiol. 2002 Oct 16;40(8):1431–6. [PMID: 12392833]

Sudden Death in Athletes

The publicity attached to the sudden deaths of high-profile collegiate and professional athletes has raised the general awareness of sudden death in young athletes and led to a reappraisal of the validity and extent of a preparticipatory medical examination. It should be noted, however, that despite the publicity, the incidence of sudden death in athletes is very low, irrespective of age. In young athletes, it is rare. The incidence increases with age and an increased prevalence of coronary atherosclerosis; however, it remains very low. Little data exist on the incidence of sudden death in female athletes. Further studies have shown that while sports activities may be associated with sudden death, the individual sports were the trigger rather than the cause in athletes with cardiovascular disease.

The causes of sudden death in athletes appear to be related to age and the nature of the trained athlete population. Athletes younger than 35 years are likely to die of hypertrophic cardiomyopathy (about 50%) or coronary artery anomalies (Table 34–2). In hypertrophic cardiomyopathy, sudden deaths occur during exercise rather than at rest and are thought to be due to ventricular arrhythmias, particularly in individuals with ventricular arrhythmias documented prior to death. One study has shown exercise-induced ischemia as a prodromal feature of sudden death in hypertrophic cardiomyopathy, although a direct cause-and-effect relationship has not been established. It should be noted, however, that the prevalence of hypertrophic cardiomyopathy in young athletes is very low and has been shown not to warrant routine Doppler echocardiographic surveys. The prevalence increases in individuals with symptoms of exertional or postexertional syncope or arrhythmias, or with a family history of similar symptoms or sudden death. Furthermore, the magnitude of LVH appears to be directly related to the risk of sudden death. A variant of hypertrophic cardiomyopathy as a cause of sudden death is idiopathic LVH. These individuals have normal myocardial histology and LVH and thus have changes consistent with the training activity of the individual.

Table 34–2. Causes of Sudden Death in Athletes under 35 Years.

Hypertrophic cardiomyopathy
Aberrant coronary arteries
Premature atherosclerosis
Arrhythmogenic right ventricular dysplasia
Marfan syndrome
Idiopathic left ventricular hypertrophy
Mitral valve prolapse syndrome
Wolff-Parkinson-White syndrome
Prolonged QT syndrome
Myocarditis
Coronary artery vasospasm
Blunt chest trauma
Kawasaki disease
Heat stroke

Among athletes older than 35 years, the most common cause of sudden death is coronary atherosclerosis (Figure 34–3 and Table 34–3). Furthermore, older athletes tend to jog rather than engage in group sports activities. Risk factors for cardiovascular disease are usually present in those older than 35 years who have exercise-related sudden death; they also may show prodromal features of angina or unusual fatigue. Retrospective reviews of these individuals often show a history of hypertension, cigarette smoking, and hyperlipidemia, and a family history of ischemic heart disease.

Figure 34–3.

Distinction between hypertrophic cardiomyopathy (HCM) and the athlete’s heart, when there is a “gray zone” of morphologic overlap. LVH, left ventricular hypertrophy; LA, left atrial; ECG, electrocardiogram; O 2, oxygen consumption.

(Reprinted with permission from Maron BJ et al. Circulation. 1995;91:1596.)

Table 34–3. Causes of Sudden Death in Athletes over 35 Years.

Coronary atherosclerosis
Hypertrophic cardiomyopathy
Aberrant coronary arteries
Premature atherosclerosis
Right ventricular dysplasia
Marfan syndrome
Idiopathic left ventricular hypertrophy
Mitral valve prolapse syndrome
Wolff-Parkinson-White syndrome
Prolonged QT syndrome
Myocarditis
Coronary artery vasospasm

The second most common cause of sudden death in athletes younger than 35 years is a coronary artery anomaly, which invariably precipitates death during exercise (all coronary anomalies may predispose to sudden death). Both angina and syncope have retrospectively been identified as prodromal features of this condition; these symptoms should prompt an immediate evaluation of a young athlete. Right ventricular dysplasia and Uhl anomaly are rare causes of sudden death in young athletes, who may have a history of syncope, palpitations, or ventricular tachycardia.

There is a paucity of literature of sudden death following anabolic steroid use, usually in weight lifters. Accelerated atherosclerosis in young subjects has been reported at autopsy in these individuals.

Corrado D et al. Does sports activity enhance the risk of sudden death in adolescents and young adults? J Am Coll Cardiol. 2003 Dec 3;42(11):1959–63. [PMID: 14662259]

Germann CA et al. Sudden cardiac death in athletes: a guide for emergency physicians. Am J Emerg Med. 2005 Jul;23(4):504–9. [PMID: 16032621]

The Preparticipation Physical Examination

The identification of sudden death in athletes by the media has stressed the importance of establishing guidelines and internationally accepted levels of practice to evaluate any type of athlete prior to their partication in their athletic endeavor. Although standard levels of care have not yet been substantiated by evidence-based measures, many reputed societies have begun to introduce certain expected predictors of cardiovascular disease and sudden death for further evaluation. All athletes of any age should undergo a preparticipation cardiac examination and subsequent regular periodic examinations. These should be done in a closed setting, providing time for a detailed history and physical examination, rather than in an assembly-line atmosphere. Knowledge of the subject and the subject’s family history are essential. The history should detail any information regarding congenital heart disease in the subject or family members as well as sudden death of any family members. Symptoms such as exercise intolerance, syncope at rest or during exercise, dyspnea, angina or its equivalents, and palpitations need to be recorded. In older athletes, close attention should be paid to the existence of cardiovascular risk factors as well as the symptoms and manifestations of coronary artery disease.

Physical examinations should exclude Marfan syndrome. Arterial blood pressure should be measured accurately. Auscultation of the heart should be comprehensive, keeping in mind that both S3 and S4 sounds are common in athletes, as are pulmonary arterial flow murmurs in young athletes and aortic valve flow murmurs in older athletes. The cardiac examination should include the upright position to lessen innocent murmurs and intensify the murmur from hypertrophic cardiomyopathy. Because of the significance of hypertrophic cardiomyopathy, when a systolic murmur is auscultated, its features during squatting and during and after the Valsalva maneuver should be characterized.

Further testing is not routinely required, unless warranted by an abnormal feature of the history or physical examination. Furthermore, should a cardiovascular test be carried out, the limitations of the procedure as well as the altered normal ranges of parameters evaluated by the procedure must be kept in mind. The extent of any evaluation beyond the history and physical examination depends on any abnormality that emerges. The routine use of electrocardiography, exercise testing, and echocardiography is precluded on a cost-benefit basis as a population-based screening tool because of the very low prevalence of sudden death in the trained athlete population. It is possible that the threshold for a diagnostic echocardiogram may be lower for an older or masters athlete, again emphasizing its indication is provided by any potential abnormality emerging from the detailed history and physical examination, and previously substantiated cardiovascular risk factors.

There are other relevant reasons for forgoing expensive cardiovascular tests. The morphologic changes produced by the various forms of athletic training often produce changes in certain tests (particularly the echocardiogram) that would be abnormal in a normal, sedentary, age-matched population. It must be remembered that the normal range of values for athletes varies considerably from the accepted normal ranges of left ventricular cavity size, posterior wall and interventricular septal thickness, and left ventricular wall mass. The same applies to routine ECGs in this population, in that abnormal ECG findings may be normal variants in a group of trained athletes. In addition, the incidence of false-positive exercise stress tests appears to be higher in a population of trained athletes. Although these observations do not completely preclude the use of cardiovascular tests, they reinforce the conclusion that they need not be done routinely.

Corrado D et al. Does sports activity enhance the risk of sudden death in adolescents and young adults? J Am Coll Cardiol. 2003 Dec 3;42(11):1959–63. [PMID: 14662259]

Corrado D et al; Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus statement of the Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005 Mar;26(5):516–24. [PMID: 15689345]

Maron BJ et al. 36th Bethesda Conference. Introduction: eligibility recommendations for competitive athletes with cardiovascular abnormalities—general considerations. J Am Coll Cardiol. 2005 Apr 19;45(8):1318–21. [PMID: 15837280]

Pelliccia A et al; Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Recommendations for competitive sports participation in athletes with cardiovascular disease: a consensus document for the Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005 Jul;26(14):1422–45. [PMID: 15923204]

Pfister GC et al. Preparticipation cardiovascular screening for US collegiate student-athletes. JAMA. 2000 Mar 22–29;283(12): 1597–9. [PMID: 10735397]

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