Antonio Pelliccia

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.

Exercise and Acute Cardiovascular Events: Placing the Risks Into Perspective: A Scientific Statement From the American Heart Association Council on Nutrition, Physical Activity, and Metabolism and the Council on Clinical Cardiology

Habitual physical activity reduces coronary heart disease events, but vigorous activity can also acutely and transiently increase the risk of sudden cardiac death and acute myocardial infarction in susceptible persons. This scientific statement discusses the potential cardiovascular complications of exercise, their pathological substrate, and their incidence and suggests strategies to reduce these complications. Exercise-associated acute cardiac events generally occur in individuals with structural cardiac disease. Hereditary or congenital cardiovascular abnormalities are predominantly responsible for cardiac events among young individuals, whereas atherosclerotic disease is primarily responsible for these events in adults. The absolute rate of exercise-related sudden cardiac death varies with the prevalence of disease in the study population. The incidence of both acute myocardial infarction and sudden death is greatest in the habitually least physically active individuals. No strategies have been adequately studied to evaluate their ability to reduce exercise-related acute cardiovascular events. Maintaining physical fitness through regular physical activity may help to reduce events because a disproportionate number of events occur in least physically active subjects performing unaccustomed physical activity. Other strategies, such as screening patients before participation in exercise, excluding high-risk patients from certain activities, promptly evaluating possible prodromal symptoms, training fitness personnel for emergencies, and encouraging patients to avoid high-risk activities, appear prudent but have not been systematically evaluated.

Recommendations for interpretation of 12-lead electrocardiogram in the athlete.

Cardiovascular remodelling in the conditioned athlete is frequently associated with physiological ECG changes. Abnormalities, however, may be detected which represent expression of an underlying heart disease that puts the athlete at risk of arrhythmic cardiac arrest during sports. It is mandatory that ECG changes resulting from intensive physical training are distinguished from abnormalities which reflect a potential cardiac pathology. The present article represents the consensus statement of an international panel of cardiologists and sports medical physicians with expertise in the fields of electrocardiography, imaging, inherited cardiovascular disease, cardiovascular pathology, and management of young competitive athletes. The document provides cardiologists and sports medical physicians with a modern approach to correct interpretation of 12-lead ECG in the athlete and emerging understanding of incomplete penetrance of inherited cardiovascular disease. When the ECG of an athlete is examined, the main objective is to distinguish between physiological patterns that should cause no alarm and those that require action and/or additional testing to exclude (or confirm) the suspicion of an underlying cardiovascular condition carrying the risk of sudden death during sports. The aim of the present position paper is to provide a framework for this distinction. For every ECG abnormality, the document focuses on the ensuing clinical work-up required for differential diagnosis and clinical assessment. When appropriate the referral options for risk stratification and cardiovascular management of the athlete are briefly addressed.

The Heart of Trained Athletes Cardiac Remodeling and the Risks of Sports, Including Sudden Death

Young competitive athletes are widely regarded as a special subgroup of healthy individuals with a unique lifestyle who are seemingly invulnerable and often capable of extraordinary physical achievement.1–3 For more than 100 years, there has been considerable interest in the effects of intense athletic conditioning on the cardiovascular system.4–27 The advent of echocardiography more than 30 years ago provided a noninvasive quantitative assessment of cardiac remodeling associated with systematic training, and consequently, a vast body of literature has been assembled that is focused on the constellation of alterations known as “athlete’s heart.”4–27 Athlete’s heart is generally regarded as a benign increase in cardiac mass, with specific circulatory and cardiac morphological alterations, that represents a physiological adaptation to systematic training.1,6–27 However, the clinical profile of athlete’s heart has expanded considerably over the last several years as a result of greater accessibility to large populations of trained athletes studied systematically with echocardiography, ECG, cardiac magnetic resonance, and ambulatory Holter ECG monitoring. As a consequence, there is increasing recognition of the impact that prolonged conditioning has on cardiac remodeling, which may eventually mimic certain pathological conditions with the potential for sudden death or disease progression. Over the last several years, sudden deaths of trained athletes, usually associated with exercise, have become highly visible events fueled by news media reports and with substantial impact on both the physician and lay communities.1,28–36 Interest in these tragic events has accelerated owing to their increased recognition; awareness that underlying, clinically identifiable cardiovascular diseases are often responsible; and the availability of treatments to prevent sudden death for high-risk athlete-patients. In the present review, we offer a comprehensive assessment of many issues that target the interrelation of intense physical exertion with cardiac structure and function, as well as the rare, potentially adverse consequences of …

Recommendations for Physical Activity and Recreational Sports Participation for Young Patients With Genetic Cardiovascular Diseases

A group of relatively uncommon but important genetic cardiovascular diseases (GCVDs) are associated with increased risk for sudden cardiac death during exercise, including hypertrophic cardiomyopathy, long-QT syndrome, Marfan syndrome, and arrhythmogenic right ventricular cardiomyopathy. These conditions, characterized by diverse phenotypic expression and genetic substrates, account for a substantial proportion of unexpected and usually arrhythmia-based fatal events during adolescence and young adulthood. Guidelines are in place governing eligibility and disqualification criteria for competitive athletes with these GCVDs (eg, Bethesda Conference No. 26 and its update as Bethesda Conference No. 36 in 2005). However, similar systematic recommendations for the much larger population of patients with GCVD who are not trained athletes, but nevertheless wish to participate in any of a variety of recreational physical activities and sports, have not been available. The practicing clinician is frequently confronted with the dilemma of designing noncompetitive exercise programs for athletes with GCVD after disqualification from competition, as well as for those patients with such conditions who do not aspire to organized sports. Indeed, many asymptomatic (or mildly symptomatic) patients with GCVD desire a physically active lifestyle with participation in recreational and leisure-time activities to take advantage of the many documented benefits of exercise. However, to date, no reference document has been available for ascertaining which types of physical activity could be regarded as either prudent or inadvisable in these subgroups of patients. Therefore, given this clear and present need, this American Heart Association consensus document was constituted, based largely on the experience and insights of the expert panel, to offer recommendations governing recreational exercise for patients with known GCVDs.

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.

Physiologic Left Ventricular Cavity Dilatation in Elite Athletes

Long-term athletic training is associated with cardiac morphologic changes, including increased left ventricular cavity dimension, wall thickness, and calculated mass, that are commonly described as athletes heart (1-4). These changes seem to represent adaptations to the hemodynamic load produced by long-term, frequent, intensive exercise programs (5-7). The extent to which absolute left ventricular cavity dimension is increased by systematic training is modest in most athletes (3) but may be more substantial in others, raising the clinical dilemma of distinguishing athletes heart from structural heart disease (8). This differential diagnosis has particularly important implications because the identification of certain cardiovascular diseases may constitute the basis for disqualifying an athlete from competition in an effort to minimize the risk for sudden cardiac death or disease progression (9). These considerations prompted us to use echocardiography to systematically evaluate the morphologic characteristics and physiologic limits of left ventricular cavity enlargement associated with intensive and long-term athletic conditioning in a large sample of highly trained athletes. Methods Study Sample The Institute of Sports Science, Rome, Italy, is a medical division of the Italian National Olympic Committee and is responsible for the physiologic and medical evaluation of competitive athletes who form the Italian national teams from which Olympic athletes are selected every 4 years. Since 1963, in accordance with the statutes of the Italian National Olympic Committee, it has been mandatory for all junior and senior national team members to undergo a preparticipation medical evaluation, usually on an annual basis (10). This program has routinely included a cardiovascular evaluation with history, physical examination, 12-lead and exercise electrocardiography, chest radiography, and (since 1985) echocardiography. Between January 1992 and December 1993, 1313 apparently healthy athletes were routinely evaluated as part of this program. Four of these athletes were subsequently excluded from the study sample because of cardiac abnormalities that could alter left ventricular cavity dimensions (bicuspid aortic valve with regurgitation in 3 athletes and mitral valve prolapse with regurgitation in 1 athlete). Thus, the final study sample comprised 1309 athletes who were judged to be free of structural cardiovascular or systemic disease. Blood pressure was consistently or predominantly less than 140/90 mm Hg in all participants. Athletes participated in 38 different sports (Table 1). Their ages ranged from 13 to 59 years (mean age, 24.3 6.0 years); 957 (73%) were male. Physical characteristics were as follows: body weight, 33 to 135 kg (mean, 71.6 14.9 kg); height, 139 to 214 cm (mean, 175.9 11.1 cm); and body surface area, 1.13 to 2.67 m2 (mean, 1.86 0.25 m2). Selected data from 267 of these athletes, all women, were presented as part of a previous analysis (11). Table 1. Demographic and Morphologic Characteristics of 1309 Athletes according to the Sports in Which They Participated All athletes had participated in vigorous training programs for substantial periods ranging from 2 to 34 years (mean, 7 years). Of the 1309 athletes, 340 (26%) had achieved international recognition in the Olympics or world championships; the remaining 969 competed at the national level. Echocardiography Two-dimensional and Doppler echocardiographic studies were performed by using a commercially available Hewlett-Packard (Andover, Massachusetts) instrument (Sonos 1500) with a 3.5-MHz transducer. Images of the heart were obtained in multiple cross-sectional planes by using standard transducer positions (12). M-mode echocardiograms were derived from two-dimensional images under direct anatomic visualization and were recorded at 100 mm/s. Measurements of end-diastolic and end-systolic left ventricular cavity dimensions, as well as anterior ventricular septal and posterior free-wall thicknesses, were obtained from the M-mode echocardiogram, in accordance with recommendations of the American Society of Echocardiography (13). To increase the accuracy of these measurements by reducing the possibility of erroneous inclusion of trabeculations or other overlying structures within the septal or free-wall thicknesses, measurements obtained from the M-mode echocardiogram were verified with the two-dimensional images. Posterior ventricular septal and anterolateral free-wall thicknesses were assessed from two-dimensional stop-frame images, as described elsewhere (14). Left ventricular mass was calculated from end-diastolic wall thicknesses and cavity dimension by using the formula proposed by Devereux (15). Left ventricular cavity dimension was normalized to body surface area and height, as suggested by de Simone and colleagues (16). Relative wall thickness was calculated as the ratio of the average of ventricular septal and posterior free-wall thicknesses to the radius of the internal ventricular cavity (17). Characteristics of left ventricular filling were obtained by using pulsed Doppler echocardiography, as described elsewhere (18, 19). Because the focus of this study was to determine the frequency with which athletes show left ventricular cavity enlargement in a range compatible with pathologic conditions, we relied primarily on absolute cavity dimensions (rather than values normalized to body surface area or other variables [16, 20, 21]) and arbitrarily chose a cut-off value of 60 mm for end-diastolic cavity dimension. This value exceeds the 95% prediction limits for normal left ventricular cavity dimension independent of the age, sex, height, or body surface area of most normal persons (21-23) and has been used clinically as a partition value for the detection of left ventricular cavity enlargement and hypertrophy (24, 25). Echocardiograms were obtained in each athlete during periods of intense training; however, because of unavoidable practical considerations, echocardiography could not always be performed when athletes were at the peak of their conditioning. When serial studies were available from the same athlete, the echocardiogram obtained at peak conditioning was used. Interobserver variability in measurements of left-ventricular end-diastolic cavity dimension was assessed in a subset of 35 athletes randomly selected from our study participants. Measurements were made by two of the authors independently and without knowledge of the identity of the participants. Concordance between the two observers was assessed by using the unpaired Student t-test and intraclass correlation. Statistical Analysis Data are expressed as the mean SD. Differences between means were assessed by using unpaired or paired Student t-tests where appropriate. A two-tailed P value less than 0.05 was considered statistically significant. We used multiple regression to analyze several continuous variables (height, weight, body surface area, age, systolic and diastolic blood pressure, and heart rate). Only continuous variables that significantly correlated with left ventricular cavity dimension were subsequently used in the covariance analysis, together with sex and type of sport (categorical variables). These two categorical variables were coded by using a series of (N 1) binary dummy variables, and their effect on left ventricular cavity dimension (that is, regression coefficients) was assessed after removing the effect of the continuous covariates. To evaluate the effect of type of sport and sex, we selected table tennis as the reference sport (because table tennis players had the smallest left ventricular cavity dimension) and female as the reference sex. We then calculated the regression coefficients for type of sport and both sexes. Subsequently, we assessed the relative effect of each type of sport on left ventricular cavity dimension by modifying the coefficients (impact factors) by the formula (I j I ref), where I j is the impact factor of the jth sport and I ref is the impact factor of the reference sport. These impact factors were presented in rank order from the lowest, set as zero (table tennis), to the highest (cycling). In addition, we clustered individual sports into three subgroups with high ( 4.4), medium (4.3 to 2.0), and low (<2.0) impact on the basis of the relative sport impact factors. Likewise, patients were divided into three subgroups for each sex according to body surface area: low ( 1.80 m2), medium (1.81 to 2.00 m2), and high (>2.00 m2) in men and low ( 1.50 m2), medium (1.51 to 1.70 m2), and high (>1.70 m2) in women. Mean values and SDs for left ventricular cavity dimension were stratified according to these subgroups of sport impact and body surface area in male and female athletes. To reduce the potential for false-positive results due to the large number of sport types, we assessed the significance of differences in mean left ventricular cavity dimensions in the different sports by using Bonferroni and Tukey multiple tests (26, 27). Finally, we assessed the significance of each variable in the covariance analysis by using the Wald test (26). Role of Study Sponsor This study was supported by the Italian National Olympic Committee and the Minneapolis Heart Institute Foundation. The funding sources had no impact on the gathering and interpretation of the results or on whether the report would be published. Results Cardiac Dimensions Left Ventricular Cavity In 725 of the 1309 participants (55%), the left ventricular cavity dimension was within generally accepted normal limits ( 54 mm) (21, 24). However, it exceeded the upper normal limits ( 55 mm) in the other 584 athletes (45%) and was substantially enlarged ( 60 mm) in 185 athletes (14% of the overall group). The end-diastolic left ventricular cavity dimension ranged from 38 to 66 mm (mean, 48.4 4.2 mm; 95th percentile value, 56 mm) in women and 43 to 70 mm (mean, 55.5 4.3 mm; 95th percentile val

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)

Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’

Sudden cardiac death (SCD) is the leading cause of death in athletes during sport. Whether obtained for screening or diagnostic purposes, an ECG increases the ability to detect underlying cardiovascular conditions that may increase the risk for SCD. In most countries, there is a shortage of physician expertise in the interpretation of an athletes ECG. A critical need exists for physician education in modern ECG interpretation that distinguishes normal physiological adaptations in athletes from abnormal findings suggestive of pathology. On 13–14 February 2012, an international group of experts in sports cardiology and sports medicine convened in Seattle, Washington, to define contemporary standards for ECG interpretation in athletes. The objective of the meeting was to develop a comprehensive training resource to help physicians distinguish normal ECG alterations in athletes from abnormal ECG findings that require additional evaluation for conditions associated with SCD.

Bethesda Conference #36 and the European Society of Cardiology Consensus Recommendations Revisited: A Comparison of U.S. and European Criteria for Eligibility and Disqualification of Competitive Athletes With Cardiovascular Abnormalities

Aspiration to reduce the risks of athletic field deaths prompted the American Heart Association and European Society of Cardiology (ESC) to establish consensus guidelines for eligibility/disqualification decisions in competitive athletes with cardiovascular abnormalities. Since 2005, the Bethesda Conference #36 and the ESC consensus documents have been relied upon by physicians from different parts of the world. The 2 consensus documents emanate from largely different cultural, social, and legal backgrounds existing in the U.S. and Europe and, although several recommendations are similar, in some instances the Bethesda Conference #36 and the ESC consensus documents suggest different approaches to disqualification decisions and implications for clinical practice, raising the possibility that confusion and discrepancies will contaminate the management of competitive athletes with cardiovascular disease. In the present article, the differences between the 2 documents are critically viewed, with special attention to genetic cardiovascular diseases relevant to sudden death in young athletes, through the prism of different cultural backgrounds, societal attitudes, and also perceptions regarding exposure to legal liability in the U.S. and Europe. In conclusion, it seems appropriate at some time to consider assembling updated recommendations for sports eligibility/disqualification that assimilate both the U.S. and European perspectives, with the aspiration of creating a unique and authoritative document applicable to the global sports medicine community.