Antonio Spataro

The Upper Limit of Physiologic Cardiac Hypertrophy in Highly Trained Elite Athletes

BACKGROUND In some highly trained athletes, the thickness of the left ventricular wall may increase as a consequence of exercise training and resemble that found in cardiac diseases associated with left ventricular hypertrophy, such as hypertrophic cardiomyopathy. In these athletes, the differential diagnosis between physiologic and pathologic hypertrophy may be difficult. METHODS To address this issue, we measured left ventricular dimensions with echocardiography in 947 elite, highly trained athletes who participated in a wide variety of sports. RESULTS The thickest left ventricular wall among the athletes measured 16 mm. Wall thicknesses within a range compatible with the diagnosis of hypertrophic cardiomyopathy (greater than or equal to 13 mm) were identified in only 16 of the 947 athletes (1.7 percent); 15 were rowers or canoeists, and 1 was a cyclist. Therefore, the wall was greater than or equal to 13 mm thick in 7 percent of 219 rowers, canoeists, and cyclists but in none of 728 participants in 22 other sports. All athletes with walls greater than or equal to 13 mm thick also had enlarged left ventricular end-diastolic cavities (dimensions, 55 to 63 mm). CONCLUSIONS On the basis of these data, a left-ventricular-wall thickness of greater than or equal to 13 mm is very uncommon in highly trained athletes, virtually confined to athletes training in rowing sports, and associated with an enlarged left ventricular cavity. In addition, the upper limit to which the thickness of the left ventricular wall may be increased by athletic training appears to be 16 mm. Therefore, athletes with a wall thickness of more than 16 mm and a nondilated left ventricular cavity are likely to have primary forms of pathologic hypertrophy, such as hypertrophic cardiomyopathy.

Clinical Significance of Abnormal Electrocardiographic Patterns in Trained Athletes

BACKGROUND-The prevalence, clinical significance, and determinants of abnormal ECG patterns in trained athletes remain largely unresolved. METHODS AND RESULTS-We compared ECG patterns with cardiac morphology (as assessed by echocardiography) in 1005 consecutive athletes (aged 24+/-6 years; 75% male) who were participating in 38 sporting disciplines. ECG patterns were distinctly abnormal in 145 athletes (14%), mildly abnormal in 257 (26%), and normal or with minor alterations in 603 (60%). Structural cardiovascular abnormalities were identified in only 53 athletes (5%). Larger cardiac dimensions were associated with abnormal ECG patterns: left ventricular end-diastolic cavity dimensions were 56. 0+/-5.6, 55.4+/-5.7, and 53.7+/-5.7 mm (P<0.001) and maximum wall thicknesses were 10.1+/-1.4, 9.8+/-1.3, and 9.3+/-1.4 mm (P<0.001) in distinctly abnormal, mildly abnormal, and normal ECGs, respectively. Abnormal ECGs were also most associated with male sex, younger age (<20 years), and endurance sports (cycling, rowing/canoeing, and cross-country skiing). A subset of athletes (5% of the 1005) showed particularly abnormal or bizarre ECG patterns, but no evidence of structural cardiovascular abnormalities or an increase in cardiac dimensions. CONCLUSIONS-Most athletes (60%) in this large cohort had ECGs that were completely normal or showed only minor alterations. A variety of abnormal ECG patterns occurred in 40%; this was usually indicative of physiological cardiac remodeling. A small but important subgroup of athletes without cardiac morphological changes showed striking ECG abnormalities that suggested cardiovascular disease; however, these changes were likely an innocent consequence of long-term, intense athletic training and, therefore, another component of athlete heart syndrome. Such false-positive ECGs represent a potential limitation to routine ECG testing as part of preparticipation screening.

Morphology of the “athlete's heart” assessed by echocardiography in 947 elite athletes representing 27 sports

In the present study, we used echocardiography to investigate the morphologic adaptations of the heart to athletic training in 947 elite athletes representing 27 sports who achieved national or international levels of competition. Cardiac morphology was compared for these sports, using multivariate statistical models. Left ventricular (LV) diastolic cavity dimension above normal (> 54 mm, ranging up to 66 mm) was identified in 362 (38%) of the 947 athletes. LV wall thickness above normal (> 12 mm, ranging up to 16 mm) was identified in only 16 (1.7%) of the athletes. Athletes training in the sports examined showed considerable differences with regard to cardiac dimensions. Endurance cyclists, rowers, and swimmers had the largest LV diastolic cavity dimensions and wall thickness. Athletes training in sports such as track sprinting, field weight events, and diving were at the lower end of the spectrum of cardiac adaptations to athletic training. Athletes training in sports associated with larger LV diastolic cavity dimensions also had higher values for wall thickness. Athletes training in isometric sports, such as weightlifting and wrestling, had high values for wall thickness relative to cavity dimension, but their absolute wall thickness remained within normal limits. Analysis of gender-related differences in cardiac dimensions showed that female athletes had smaller LV diastolic cavity dimension (average 2 mm) and smaller wall thickness (average 0.9 mm) than males of the same age and body size who were training in the same sport.(ABSTRACT TRUNCATED AT 250 WORDS)

Outcomes in athletes with marked ECG repolarization abnormalities.

BACKGROUND Young, trained athletes may have abnormal 12-lead electrocardiograms (ECGs) without evidence of structural cardiac disease. Whether such ECG patterns represent the initial expression of underlying cardiac disease with potential long-term adverse consequences remains unresolved. We assessed long-term clinical outcomes in athletes with ECGs characterized by marked repolarization abnormalities. METHODS From a database of 12,550 trained athletes, we identified 81 with diffusely distributed and deeply inverted T waves (> or = 2 mm in at least three leads) who had no apparent cardiac disease and who had undergone serial clinical, ECG, and echocardiographic studies for a mean (+/-SD) of 9+/-7 years (range, 1 to 27). Comparisons were made with 229 matched control athletes with normal ECGs from the same database. RESULTS Of the 81 athletes with abnormal ECGs, 5 (6%) ultimately proved to have cardiomyopathies, including one who died suddenly at the age of 24 years from clinically undetected arrhythmogenic right ventricular cardiomyopathy. Of the 80 surviving athletes, clinical and phenotypic features of hypertrophic cardiomyopathy developed in 3 after 12+/-5 years (at the ages of 27, 32, and 50 years), including 1 who had an aborted cardiac arrest. The fifth athlete demonstrated dilated cardiomyopathy after 9 years of follow-up. In contrast, none of the 229 athletes with normal ECGs had a cardiac event or received a diagnosis of cardiomyopathy 9+/-3 years after initial evaluation (P=0.001). CONCLUSIONS Markedly abnormal ECGs in young and apparently healthy athletes may represent the initial expression of underlying cardiomyopathies that may not be evident until many years later and that may ultimately be associated with adverse outcomes. Athletes with such ECG patterns merit continued clinical surveillance.

Conversion From Vagal to Sympathetic Predominance With Strenuous Training in High-Performance World Class Athletes

Background—Benefits of moderate endurance training include increases in parasympathetic activity and baroreflex sensitivity (BRS) and a relative decrease in sympathetic tone. However, the effect of very intensive training load on neural cardiovascular regulation is not known. We tested the hypothesis that strenuous endurance training, like in high-performance athletes, would enhance sympathetic activation and reduce vagal inhibition. Methods and Results—We studied the entire Italian junior national team of rowing (n=7) at increasing training loads up to 75% and 100% of maximum, the latter ∼20 days before the Rowing World Championship. Autoregressive power spectral analysis was used to investigate RR interval and blood pressure (BP) variabilities. BRS was assessed by the sequences method. Increasing training load up to 75% of maximum was associated with a progressive resting bradycardia and increased indexes of cardiac vagal modulation and BRS. However, at 100% training load these effects were reversed, with increases in resting heart rate, diastolic BP, low-frequency RR interval, and BP variabilities and decreases in high-frequency RR variability and BRS. Three athletes later won medals in the World Championship. Conclusions—This study indicates that very intensive endurance training shifted the cardiovascular autonomic modulation from a parasympathetic toward a sympathetic predominance. This finding should be interpreted within the context of the substantial role played by the sympathetic nervous system in increasing cardiovascular performance at peak training. Whether the altered BP and autonomic function shown in this study might be in time hazardous to human cardiovascular system remains to be established.

Reduction in left ventricular wall thickness after deconditioning in highly trained Olympic athletes.

BACKGROUND--Clinical distinction between athletes heart and hypertrophic cardiomyopathy in a trained athlete is often difficult. In an effort to identify variables that may aid in this differential diagnosis, the effects of deconditioning on left ventricular wall thickness were assessed in six highly trained elite athletes who had competed in rowing or canoeing at the 1988 Seoul Olympic Games. Each of these athletes showed substantial ventricular septal thickening associated with training (13-15 mm) which resembled that of hypertrophic cardiomyopathy. METHODS--The athletes voluntarily reduced their training substantially for 6-34 weeks (mean 13) after the Olympic competition. Echocardiography was performed at peak training and also after deconditioning, and cardiac dimensions were assessed blindly. RESULTS--Maximum ventricular septal thickness was 13.8 (0.9) mm in the trained state and 10.5 (0.5) in the deconditioned state (p < 0.005) (change 15-33%). CONCLUSIONS--The finding that deconditioning may be associated with a considerable reduction in ventricular septal thickness in elite athletes over short periods strongly suggests that these athletes had a physiological form of left ventricular hypertrophy induced by training. Such a reduction in wall thickness with deconditioning may help to distinguish between the physiological hypertrophy of athletes heart and primary pathological hypertrophy (for example, hypertrophic cardiomyopathy) in selected athletes with increased left ventricular wall thickness.

Absence of left ventricular wall thickening in athletes engaged in intense power training

There is a widely held perception that power training increases left ventricular (LV) wall thickness. Consequently, in individual power-trained athletes, confusion may legitimately occur with regard to the differential diagnosis of athletes heart and nonobstructive hypertrophic cardiomyopathy. To investigate the effects of systematic strength training on cardiac dimensions (particularly absolute LV wall thickness), 100 relatively young and highly conditioned athletes participating in weight and power lifting, wrestling, bobsledding and weight-throwing events for 3 to 24 years (mean 7) were studied by echocardiography. No athlete showed a maximal absolute LV wall thickness that exceeded the generally accepted upper limits of normal (i.e., 12 mm; range 8 to 12). When compared with 26 normal, sedentary control subjects of similar age and body surface area, maximal septal thickness was mildly but significantly greater in athletes (9.6 +/- 0.8 vs 9.0 +/- 0.5 mm; p < 0.001), as was the calculated LV mass index (96 +/- 12 vs 81 +/- 8 g/m2; p < 0.001); LV end-diastolic cavity dimension was similar in athletes and controls (55 +/- 4 and 54 +/- 3, respectively; p > 0.05). Consequently, echocardiographic data in this selected group of purely strength-trained athletes show that whereas this form of conditioning is associated with increased LV mass and a disproportionate increase in wall thickness in relation to cavity dimension, only modest alterations in absolute wall thickness occur (which do not exceed upper normal limits). Therefore, in highly conditioned, strength-trained, competitive athletes, the presence of substantial LV wall thickening (> 13 mm) should suggest alternative explanations, such as the diagnosis of pathologic hypertrophy (i.e., hypertrophic cardiomyopathy).

Prospective echocardiographic screening for coronary artery anomalies in 1,360 elite competitive athletes

A nomalous origin of the left main coronary artery (LMCA) from the anterior (right) sinus of Valsalva, as well as other congenital coronary anomalies, have been incriminated as causes of sudden death in asymptomatic persons,‘” including competitive athletes.4 We previously reported that it is possible to identify such malformations prospectively, using conventional transthoracic echocardiography, and have suggested the possible role of echocardiography in the detection of anomalous origin of the LMCA in screening young athletes for cardiovascular disease.5 Therefore, the present investigation was undertaken to assess the efficacy of this diagnostic approach and the prevalence of such coronary anomalies in a surviving athletic population. Between January 1990 and August 1991, 1,360 athletes were evaluated consecutively at the Institute of Sports Science (Rome, Italy) and routinely subjected to an echocardiographic assessment that included examination of the ostia of the right and left coronary arteries, using cross-sectional views of the aorta from the parasternal and apical windows.6 In each of these athletes particular care was taken, in a prospective fashion, to achieve the optimal dejnition of the coronary ostia. Of the 1,360 athletes, 87 (6%) were excluded because of technically unsatisfactory echocardiograms, in which the origin of neither the left or the right coronary artery (RCA) could be imaged from d@erent acoustic windows. Thus, the @al study population comprised 1,273 athletes. All were asymptomatic and judged to be free of systemic or cardiovascular disease. Athletes were 13 to 49 years of age (mean 22); 828 were male (65%). Each was an elite athlete, having participated in vigorous training programs and competition for periods of 3 to 20 years. They were engaged in a wide range of 25 di

RELATION BETWEEN TRAINING-INDUCED LEFT VENTRICULAR HYPERTROPHY AND RISK FOR VENTRICULAR TACHYARRHYTHMIAS IN ELITE ATHLETES

erent sports and about one third had achieved an international level of competition. In 1,257 of the 1,273 athletes (9X7%), the ostium of the LMCA was visualized with its origin in the normal position (at, or about, 5 o’clock in the short-axis view of the aortic root) (Figure 1). In only 16 athletes was the ostium of LMCA not visualized; however; in these 16, the RCA was identijied in its proper position and there was no evidence of the LMCA emanating from the right sinus of Valsalva. Therefore, in the 1,273 athletes studied, an anomalous origin or course of the LMCA could be excluded. In 225 of the 1,257 athletes in whom the LMCA was visualized, the course of the LMCA could be followed to its btjia-cation for 3 to 20 mm (average 11); in 87 of these 225 athletes the proximal portions of the left anterior descending and the left cir-

Patterns of ventricular tachyarrhythmias associated with training, deconditioning and retraining in elite athletes without cardiovascular abnormalities.

The aim of this study was to analyze the relation between the magnitude of training-induced left ventricular (LV) hypertrophy and the frequency and complexity of ventricular tachyarrhythmias in a large population of elite athletes without cardiovascular abnormalities. Ventricular tachyarrhythmias are a common finding in athletes, but it is unresolved as to whether the presence or magnitude of LV hypertrophy is a determinant of these arrhythmias in athletes without cardiovascular abnormalities. From 738 athletes examined at a national center for the evaluation of elite Italian athletes, 175 consecutive elite athletes with 24-hour ambulatory (Holter) electrocardiographic recordings (but without cardiovascular abnormalities and symptoms) were selected for the study group. Echocardiographic studies were performed during periods of peak training. Athletes were arbitrarily divided into 4 groups according to the frequency and complexity of ventricular arrhythmias during Holter electrocardiographic monitoring. No statistically significant relation was evident between LV mass (or mass index) and the grade or frequency of ventricular tachyarrhythmias. In addition, a trend was noted in those athletes with the most frequent and complex ventricular ectopy toward lower calculated LV mass. In conclusion, ventricular ectopy in elite athletes is not directly related to the magnitude of physiologic LV hypertrophy. These data offer a measure of clinical reassurance regarding the benign nature of ventricular tachyarrhythmias in elite athletes and the expression of athletes heart.