EDITORIAL COMMENT
Ventricular ectopy in athletes
Don’t worry ... more good news!*
Harold L. Kennedy, MD, MPH, FACC*,*
* Cardiovascular Division, Department of Medicine, University of South Florida, College of Medicine, Tampa, Florida, USA
* Reprint requests and correspondence: Dr. Harold L. Kennedy, Professor, University of South Florida, Chief, Department of Medicine, Director, Cardiovascular Research, Bay Pines VA Medical Center, Bay Pines, Florida 33744, USA.
Harold.Kennedy{at}med.va.gov
Ventricular ectopic beats (VEBs) have been described in approximately 1% of clinically normal persons as detected by standard electrocardiogram (ECG) (1), and in 40% to 75% of apparently healthy persons as detected by 24 to 48 h of continuous ambulatory (Holter) ECG (2–5). Both the incidence and the frequency of VEBs increase with age (2,5), and even frequent (>60/h or 1/min) and complex (involving multiform, alternating or repetitive patterns or R on T beats) VEBs occur in apparently healthy subjects (5–9). Such individuals constitute an estimated prevalence of 1% to 4% of the general population (6). Nevertheless, VEBs in apparently healthy persons have been the genesis of concern and anxiety to both patients and physicians ever since the earliest reports of an irregular pulse. This is particularly true when such ventricular ectopy is either frequent and/or complex, because the latter arrhythmias identify a subset of patients in cardiovascular disease populations at increased risk of death and sudden cardiac death (10–12). Never is physician concern more heightened as when these cardiac arrhythmias occur in young people engaged in strenuous activities such as competitive athletics (13). Whereas the risk of sudden cardiac death in high school athletes has been shown to be small (approximately one in 200,000 per year) and is usually due to underlying (and usually unsuspected) structural cardiovascular disease (14,15), nevertheless the detection of frequent and/or complex VEBs in a competitive athlete who appears to be apparently healthy engenders physician apprehension and a cautious attitude as to whether its occurrence is benign or potentially life-threatening.
Since 1985 it has been generally accepted that when frequent and/or complex VEBs are detected in apparently healthy persons who are thoroughly examined by modern noninvasive cardiologic diagnostic methods (i.e., history and physical examination, standard and ambulatory ECG, exercise stress testing and echocardiogram) and are found to have no evidence of structural heart disease, it is a benign condition with a favorable prognosis (6–9). This perspective was particularly germane in the 1980s when antiarrhythmic therapy was found to aggravate or provoke proarrhythmia (16), and the discovery that not infrequently antiarrhythmic medications prescribed to apparently healthy persons for VEBs was the etiologic agent of out-of-hospital sudden death (17). Subsequently, this evidence led to the clinical dictum that such persons should not be treated with antiarrhythmic medications. If subjects are symptomatic with minor palpitations, a recommendation to withdraw stimulants (caffeine, alcohol, smoking, etc.) is advised, and if symptoms continue to be worrisome to the patient, beta-blocker therapy is recommended (6). This viewpoint has on occasion been challenged (18), and when such reports are critically examined they seem to result from populations not thoroughly examined noninvasively to exclude structural cardiac disease (19).
Athletes, however, constitute a different but apparently healthy population. Twenty-four-hour continuous ambulatory ECG studies have shown a higher prevalence of VEBs (70%) and frequent and/or complex forms (25% to 63%) in athletic populations (20). Moreover, top-level or highly trained athletes can show morphologic changes of the "athlete’s heart," which include increased left ventricular mass, wall thickness and cavity dimensions (21,22). These changes result as a consequence of several determinants, which include type of sport, gender and probable genetic factors (22,23). The extent of physiologic cardiac remodeling in some highly trained individuals may pose a physician dilemma of suspected structural cardiac disease, particularly when standard ECG abnormalities have been encountered in as many as 40% of one population of 1,005 elite athletes (22). Athletes may demonstrate a spectrum of ECG alterations that include increased R- or S-wave voltages, ST-segment or T-wave changes and deep Q waves suggestive of left ventricular hypertrophy or cardiomyopathy (22). A recent meta-analysis of 59 studies of 1,451 athletes showed that an athlete’s heart has divergent adaptation to dynamic and static sports with an endurance-trained heart (eccentric hypertrophy) and a strength-trained heart (concentric hypertrophy) not being an absolute and dichotomous concept (24,25). Subsequent ranking of sports was therefore based on the impact of training on left ventricular diastolic cavity dimension and left ventricular wall thickness (24,25). Prospective studies have further shown that detraining with a long-term deconditioning period (1 to 13 years; mean 5.6 years) results in left ventricular remodeling with significant reduction in cavity size and normalization of wall thickness (26). However, resolution of cavity enlargement is incomplete in most cases, and substantial chamber dilation can persist in more than 20% of athletes (26).
The report by Biffi et al. (27) in this issue of the Journal describes a selected population of 355 athletes encountered over a 15-year period (1984 to 1999) who were identified or referred because of the presence of >3 VEBs on a standard ECG or the complaint of palpitations, and who were subsequently examined by continuous ambulatory ECG. The cohort of 355 represented 2.3% of 15,889 athletes examined by the Institute of Sports Science of the Italian National Olympic Committee (27). Each of the 355 athletes (mean age 24.8 years; range 14 to 35 years) had previously received a cardiovascular evaluation consisting of history and physical examination, standard 12-lead ECG, echocardiogram, symptom-limited exercise test and chest X-ray. Based on clinical judgment and the degree of ventricular ectopy observed on ambulatory ECG, some athletes underwent further testing by magnetic resonance imaging (MRI) (n = 42), nuclear scintigraphy (n = 16), endomyocardial biopsy (n = 10) and electrophysiologic study with programmed ventricular stimulation (n = 24). Athletes were engaged in 18 different sports with training program durations of 1 to 13 years (median 4 years). Of the athletes, 70% (n = 245) had competed at the national level of competition, and 30% (n = 110) had achieved international recognition in World Championship and Olympic games (27).
Subsequent medical follow-up every 6 to 12 months was accomplished over a period of 2 to 15 years (mean 8.4 ± 6.3 years). Based on previous ambulatory ECG data of normal populations (5), the investigators (27) arbitrarily divided their data into groups A, 71 athletes with  2,000 VEBs and 1 episode of nonsustained ventricular tachycardia (NSVT)/24-h period; group B, 153 athletes with <2,000 but >100 VEBs without NSVT/24-h period; and group C, 131 athletes with <100 VEBs and without NSVT/24-h period. The latter group C athletes without complex forms or NSVT essentially demonstrated the same frequency of ventricular ectopy previously reported in normal population data (2–6). Overall examination disclosed that 93% (n = 329) of athletes demonstrated no evidence of structural cardiovascular abnormality, while 7% (n = 26) of athletes showed abnormalities of mitral valve prolapse with mitral regurgitation (n = 11), arrhythmogenic right ventricular cardiomyopathy (n = 7), myocarditis (n = 4) and dilated cardiomyopathy (n = 4). Whereas athletes with cardiovascular abnormalities were detected only in the presence of very frequent VEBs (groups A and B), their ventricular arrhythmias were not significantly different from other athletes in those groups without cardiovascular abnormalities. The VEB morphology of left bundle branch block pattern with inferior axis (i.e., right ventricular origin) previously described in normal populations was found dominant in all groups (65% to 78%), and the occurrence of right bundle branch block patterns suggesting left ventricular or septal origin did not significantly differ among the groups (27). Use of enhanced diagnostic methods (i.e., MRI, nuclear scintigraphy, myocardial biopsies and electrophysiologic study) contributed to the detection of cardiovascular abnormalities in 14 of the 26 subjects found to have abnormalities. All 71 athletes of group A were disqualified from competitive sports for a minimum of three months based on the Italian guidelines for determining eligibility (28), and during a mean follow-up of 8.4 years (range 2 to 15 years) only one athlete (who was previously disqualified) with arrhythmogenic right ventricular cardiomyopathy died suddenly while engaging (against medical advice) in a field-hockey game (27).
The longitudinal data of Biffi et al. (27) represent the largest cohort of apparently healthy persons (including athletes) identified with frequent and/or complex VEBs who have been followed prospectively for clinical outcomes (2–9). The Biffi et al. (27) data confirm the clinical axiom that frequent and/or complex occurrence of VEBs in apparently healthy subjects does not confer an ominous prognosis in the absence of structural heart disease (6–9); their findings extend that observation to athletes subjected to the unique environmental conditions and stress of intense exercise training and competition (with neurohumoral alterations in blood volume, electrolytes and the autonomic nervous system). A minority of the cohort (eight with detected cardiovascular abnormalities) received drug therapy, which was predominantly beta-blocker therapy. Surprisingly, the population identified by Biffi et al. (27) did not identify individuals with hypertrophic cardiomyopathy or coronary anomalies thought to be the most common cardiovascular abnormalities associated with sudden death in athletes (14,15). Whether such persons were selected out by family history or echocardiography, went undetected or did not enter the cohort because of a lack of frequent VEBs is a matter of speculation. Nevertheless, the presence of frequent and/or complex VEBs did not indicate an adverse prognosis in the athletes without cardiovascular structural abnormalities. A limitation of the current report encountered in all long-term investigations is the inability to apply emerging methods and science currently available to the investigation of their subjects. Still, the omission of concurrent data of the standard ECG abnormalities encountered, which may have defined the presence or lack of "athlete’s heart" patterns or repolarization abnormalities associated with the frequent and/or complex VEBs measured, is a limitation.
The report, however, does focus attention on the changing medical concept of without structural cardiac abnormalities, which has evolved over time with emerging medical technology and scientific discovery. Biffi et al. (27) did not examine all subjects with extensive noninvasive or invasive methods, but they selected clinically those subjects of greatest concern to utilize MRI, nuclear scintigraphy, myocardial biopsy or electrophysiologic testing. Although the pathogenesis of frequent and/or complex VEBs in apparently healthy subjects continues to be confounded by multiple mechanisms, early studies have defined subtle abnormalities of ventricular contractility by cineangiography (29), evidence of lymphocytic or old myocarditis (30,31), the presence of left ventricular false tendons (32) or adrenergic innervation abnormalities (33) as possible causative mechanisms of the VEBs. More recent MRI and cine-MRI investigations have called attention to detection of right ventricular outflow tract enlargement in the transverse and anteroposterior axis diameter, and anterior/lateral wall motion abnormalities with or without bulging in the right ventricular outflow tract of subjects with frequent and/or complex VEBs (34). Finally, the presence of focal ventricular Purkinje abnormalities as a triggering etiology of frequent VEBs has been demonstrated by electrophysiologic study and radiofrequency catheter ablation studies of patients with severely symptomatic VEBs (35–38), although such treatment has been viewed with editorial concern (39,40). One can speculate that in the present study ventricular dilation and/or hypertrophy defined in previous investigations of the "athlete’s heart" was a contributing factor to the genesis of the frequent VEBs found.
In future studies of both athletic and apparently healthy populations with frequent and/or complex VEBs, it is to be hoped that an algorithm resulting from the findings of the conventional diagnostic examinations will define more clearly when utilization of extended diagnostic methods are indicated. Utilization of MRI and cine-MRI, endomyocardial biopsies and genetic studies probably can identify the small subset of subjects with covert cardiac disorders who warrant physician concern. In the meantime, practicing physicians can continue to take solace in the good news that the subject with frequent and/or complex VEBs, who is thoroughly examined with conventional noninvasive cardiovascular diagnostic methods and found to have no evidence of structural cardiac disease, is at low risk of sudden cardiac death ... even if he or she is an athlete engaged in competitive sports.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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