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Scarce information exist relative to the behavior of blood pressure during exercise in high-level athletes. We sought to define the upper limits of blood pressure response in elite athletes and describe clinical and morphologic characteristics of those with higher values. 1,140 athletes, divided

In recent years, there has been a major international focus on both the risks and benefits of exercise, as well as the relationship between physical activity and cardiovascular health at all ages.1–8 Based on more than 40 observational epidemiological studies, physical inactivity and sedentary lifestyle are recognized as major risk factors for the development of coronary heart disease, adverse cardiovascular events, and mortality.9–28 Regular aerobic exercise (occupational or leisure time) confers many health benefits, may reduce the risk for fatal and nonfatal myocardial infarction and other coronary events,1–28 and has been promoted as a national public health agenda in several countries for both primary and secondary prevention of cardiovascular disease.3–7,22,24,29,30 Conversely, acute vigorous physical exertion may trigger sudden death or myocardial infarction31–52 in the presence of underlying heart disease,48 particularly in individuals not accustomed to such activity or to regular exercise.31–33,35,41,51,52,52a,52b As sedentary individuals begin (or reinitiate) an exercise program, there is a period of increased risk during which exertion can provoke a cardiac event, whereas such risk associated with habitual exercise in active individuals is relatively low.31 Also, it is generally assumed that particularly strenuous exertion or sports competition may predispose athletes to greater cardiac risk than nonstrenuous physical activity. Nevertheless, there is widespread agreement that the overall benefits of exercise usually outweigh associated risks.1–30,35 Mechanisms by which exercise may protect patients from coronary events have also been proposed.53,54 Prior expert consensus documents have addressed the risk for sudden death associated with sports participation in competitive or recreational athletes with cardiovascular disease, including the criteria for disqualification and eligibility,49–51,55,56 and the screening of general populations for detection of cardiac abnormalities.47,50,51 These previous recommendations49,50,55–59 have focused largely on young competitive athletes or older athletes in recreational sports settings such as health and fitness facilities.51 Consequently, in the present scientific statement, the panel addressed issues relevant to competitive sports participants at the masters level primarily in midlife and beyond, cognizant of the unique psychological and physiological stresses that competition places on such athletes, particularly those with cardiovascular disease.22,52,60–74 It is believed that by offering prudent insights and advice to physicians concerning the screening and detection of cardiac disease, as well as recommendations for sports clearance and eligibility in such older athletes, this document may contribute to the prevention of cardiac catastrophes and events during exercise.

It is uncertain whether left ventricular (LV) shape is altered as a consequence of intensive athletic conditioning. We assessed LV dimensions and shape by Fourier analysis from digitized LV endocardial borders in 22 elite rowers and 14 untrained controls. Athletes had greatly increased LV cavity dimension, wall thickness, volume, and mass; however, LV shape was normal in athletes, and associated with normal ejection fraction and diastolic filling pattern.

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 P 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.

The field of sports cardiology has a long history within the European Society of Cardiology (ESC), being a topic of the first Working Group (WG1: Exercise physiology, physiopathology and stress testing). It was founded in 1982, the first chairmen being Bruno Caru from Italy and Henry Detry from Belgium, with the strong support of former ESC president Henry Denolin. With Italian colleagues, A. Venerando and V. Rulli, WG1 organized a meeting on sports cardiology for the first time in Fiuggi Terme (Italy) in 1984. From 1994, WG1 also included the WG of Rehabilitation, and kept an increasing interest in sports cardiology within the symposia organized in the annual spring meetings.

Two concepts from pathologic descriptions of myocardial hypertrophy in trained individuals merit consideration: (1) The heart of the trained athlete can be twice the normal size, but histologic structure remains intact, and (2) the weight of the trained heart does not usually surpass the limit of 500 g, defined as the critical heart weight. Even though this threshold cannot be accepted dogmatically, the concept of an upper limit for physiologic cardiac remodeling is nevertheless relevant to the clinical question of distinguishing extreme expressions of athlete's heart from primary pathologic conditions. This morphologic distinction depends on whether the magnitude of cardiac remodeling in athletes exceeds that expected as a result of athletic conditioning alone. There has also been a great interest in understanding the impact that types of athletic conditioning and gender have on defining the upper limits to which such physiologic hypertrophy may extend.

Morphologic cardiac adaptation induced by athletic conditioning (athlete’s heart) has been recognized since the late century and to date, a large number of studies have described the morphologic features of the hearts of a variety of athletes engaged in different athletic disciplines [1–11]. However, some aspects of athlete’s heart are still topics of scientific interest, such as the physiological limits of morphological changes and the criteria of its differentiation from cardiovascular disease [12].

The Impact of Sports Cardiology on Clinical Practice.- Cardiovascular Response and Adaptation to Exercise.- Functional Evaluation in Sports Cardiology.- Cardiovascular Adjustments in Wheelchair Paraplegic Athletes (WPA).- Determinants and Physiological Limits of Cardiac Morphologic Adaptation in Elite Athletes.- Significance and Prognostic Evaluation of Bradyarrhythmias in Athletes.- Prognostic Evaluation of Supraventricular Arrhythmias in Athletes.- Prognostic Evaluation of Ventricular Arrhythmias in Athletes.- Radiofrequency Ablation in the Therapy of Wolff-Parkinson-White Syndrome.- The Long QT Syndrome.- Current Criteria for Evaluation of Athletes with Arrhythmias.- Congenital Heart Disease of Interest in Athletes.- Mitral Valve Prolapse: Criteria of Prognostic Evaluation in Athletes.- Cardiomyopathies, Myocarditis and Sport.- Pathology of Cardiac Diseases at Risk of Sudden Death in Athletes.- Methods for Distinguishing Athlete's Heart from Structural Heart Disease, with Emphasis on Hypertrophic Cardiomyopathy.- Sudden Cardiac Death in Competitive Athletes.- Physical Exercise and Ischemic Heart Disease.- Electrocardiographic Repolarization Abnormalities in Athletes.- Arterial Hypertension and Physical Activity.- Arterial and Venous Diseases in Athletes.- Noncardiac Diseases Mimicking and/or Affecting the Cardiovascular System.- IOC Banned Drugs and their Effects on the Cardiovascular System.- Legal Implications of the Cardiovascular Evaluation of Athletes.

OBJECTIVES; To define the expression of "athlete's heart" in women by determining the alterations in cardiac dimensions associated with long-term intense conditioning in elite female athletes. DESIGN; Prospective cardiovascular assessment conducted from 1986 through 1993. Subjects were evaluated using 2-dimensional, M-mode, and Doppler echo-cardiographic studies.Institute of Sports Science, Italian National Olympic Committee, Rome, Italy.A total of 600 elite female athletes (mean age, 21 years; range, 12-49 years) who had participated in vigorous training (mean duration, 9 years; range, 2-32 years) and had competed in 27 sports, including 211 athletes at the international level and 389 at the national level. A control group consisted of 65 sedentary volunteer women (mean age, 23.7 years; range, 14-41 years) who were free of cardiovascular disease and who did not participate in regular athletic training.Left ventricular end-diastolic cavity dimension and wall thickness.Athletes demonstrated larger left ventricular end-diastolic cavity dimension (mean +/- SD) (49 +/- 4 mm) and greater maximal wall thickness (8.2 +/- 0.9 mm) than controls (46 +/- 3 mm and 7.2 +/- 0.6 mm; P.001). These dimensions were 6% and 14% larger in athletes. Among athletes, left ventricular cavity dimension was 40 mm to 66 mm, exceeded normal limits (54 mm) in 47 women (8%), and was within the range consistent with primary dilated cardiomyopathy (or = 60 mm) in 4 athletes (1%). Training for endurance sports, such as cycling, cross-country skiing, and rowing had the greatest effect on cavity dimension. Left ventricular wall thickness was 6 mm to 12 mm in athletes and did not exceed normal limits or extend into the borderline gray zone with hypertrophic cardiomyopathy in any subject. Compared with data from 738 previously studied male athletes, female athletes showed significantly smaller left ventricular cavity dimension (11% less; P.001) and wall thickness (23% less; P.001).Highly trained women athletes frequently demonstrate cardiac dimensional changes as an adaptation to physical training, although absolute left ventricular cavity size exceeding normal limits was evident in a minority (8%) of women athletes and was rarely (1% of athletes) within the range of dilated cardiomyopathy. Athletic training was not a stimulus for substantial increases in absolute left ventricular wall thickness, which was within normal limits for all women athletes. These findings suggest that the clinical differentiation of athlete's heart and hypertrophic cardiomyopathy appears to be a diagnostic dilemma that is limited to male athletes.

The aim of this study was to assess the prevalence and the prognostic value of ventricular late potentials in apparently healthy top-level athletes with ventricular arrhythmias, and the effect of physiological myocardial hypertrophy (athlete's heart) on the electrogenesis of the signal-averaged electrocardiogram (ECG). Two groups of asymptomatic athletes without underlying heart disease were studied: group A consisted of 35 athletes without arrhythmias and group B of 25 athletes with frequent and complex ventricu lar arrhythmias (ventricular ectopic beats >5000. 24 h−1 and ventricular couplets >15 . 24 h−1). Late potentials were present if athletes had significantly prolonged filtered QRS and low amplitude signal duration and low root mean square voltages at both 25–250 Hz and 40–250 Hz filters. While late potentials were absent in all normal athletes of group A, they were present in seven of 25 (28%) athletes with arrhythmias of group B ( P 350 g), and it is correlated to a non-sustained ventricular response during an electrophysiological study.

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)

Category: 27. Clinical Electrophysiology—Ventricular ArrhythmiasSession-Poster Board Number: 1057-382 Authors: Luisa Verdile, Emanuele Guerra, Elvira De Blasiis, Roberto Ciardo, Filippo Quattrini, Fernando M. Di Paolo, Cataldo Pisicchio, Barbara Di Giacinto, Alessandro Biffi, Antonio Pelliccia, Institute of Sport Medicine and Science, Roma, Italy Background: Sudden death in athletes is presumably related to life-threatening ventricular arrhythmias occuring during sport activities. There are few data on clinical significance and risk for ventricular arrhythmias induced by exercise in athletes without apparent structural heart disease. To assess long-term clinical significance of exercise-induced tachyarrhythmias in athletes.Methods: We selected 12 athletes without cardiovascular abnormalities and frequent and/or complex ventricular arrhythmias. Selection criteria were the occurrence of ≥10 premature ventricular depolarization (PVDs) and/or ≥ 1 couplet induced by exercise test.The follow-up period was 9,18 ± 4,66 years during which the athletes underwent clinical evaluations, ECG and color-doppler echocardiography, 24-hours Holter monitoring and selectively, electrophysiologic study and cardiac magnetic resonance with late enhancement.Results: During the follow-up no athlete developed symptoms, events or evidence of cardiomyopathies. In 6 athletes (50%) the arrhythmias disappeared (in 2 athletes) or was substantially reduced (in 4).In 3 athletes arrhythmia was unchanged and in 2 worsened. These latter athletes underwent successfull radio-frequency ablation to allow resumption of athletic activity. A right ventricular outflow tract PVDs morphology was documented in 8 athletes (67%).Conclusions: Exercise induced ventricular arrhythmias in athletes without evidence of structural heart disease are associated with a good clinical outcome and with a trend of reduction over 9 years of follow-up.

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 athlete's 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; p0.001), as was the calculated LV mass index (96 +/- 12 vs 81 +/- 8 g/m2; p0.001); LV end-diastolic cavity dimension was similar in athletes and controls (55 +/- 4 and 54 +/- 3, respectively; p0.05). 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).

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$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

Mandatory electrocardiographic screening of athletes would detect heart problems and save lives, argue Antonio Pelliccia and Domenico Corrado, but Roald Bahr (doi:10.1136/bmj.c4914) claims that the diagnostic accuracy is questionable

Regular aerobic exercise at moderate intensities and an increased physical fitness are associated with a reduced risk of fatal and nonfatal coronary events in middle-aged individuals. In contrast, moderate and vigorous physical exertion is associated with an increased risk for cardiac events, including sudden cardiac death in individuals harbouring cardiovascular disease. The risk-benefit ratio may differ in relation to the individual’s age, fitness level, and presence of cardiovascular disease; sedentary individuals with underlying coronary artery disease are at greatest risk. The intention of the present position stand of the European Association of Cardiovascular Prevention and Rehabilitation is to encourage individuals to participate in regular physical activity and derive the benefits of physical exercise while minimizing the risk of cardiovascular adverse events. Therefore, the aim is to establish the most practical method of cardiovascular evaluation in middle-age/senior individuals, who are contemplating exercise or who are already engaged in nonprofessional competitive or recreational leisure sporting activity. These recommendations rely on existing scientific evidence, and in the absence of such, on expert consensus. The methodology of how middle-aged and older individuals should be evaluated appropriately before engaging in regular physical activity is both complex and controversial. On practical grounds the consensus panel recommend that such evaluation should vary according to the individual’s cardiac risk profile and the intended level of physical activity. Self assessment of the habitual physical activity level and of the risk factors, are recommended for screening of large populations. Individuals deemed to be at risk require further evaluation by a qualified physician. In senior/adult individuals with an increased risk for coronary events, maximal exercise testing (and possibly further evaluations) is advocated. Hopefully, the recommendations in this paper provide a practical solution for facilitating safe exercise prescription in senior/adults.

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.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.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).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.

Absolute left ventricular cavity dimension may be substantially increased in some highly trained athletes. This raises questions about the differential diagnosis between athlete's heart and dilated cardiomyopathy as well as possible disqualification from competitive sports.To evaluate the morphologic characteristics and physiologic limits of left ventricular cavity enlargement associated with intensive, long-term athletic conditioning.Evaluation of left ventricular cavity dimension in a large sample of highly trained athletes.Institute of Sports Science, Rome, Italy.1309 elite Italian athletes (957 men and 352 women), 13 to 59 years of age (mean, 24 years), participating in 38 different sports.Echocardiographic assessment of left ventricular cavity dimension and multivariate statistical analysis of the determinants.Left ventricular end-diastolic cavity dimensions varied widely (38 to 66 mm [mean, 48 mm] in women and 43 to 70 mm [mean, 55 mm] in men) and was within generally accepted normal limits for most participants (or = 54 mm in 725 athletes [55%]). According to an arbitrary clinical cut-point of 60 mm, the left ventricular cavity was substantially enlarged in 185 participants (14%). These athletes had global left ventricular systolic function within normal limits and no regional wall-motion abnormalities; participants remained free of cardiac symptoms and impaired performance over 1 to 12 years (mean, 4.7 years). The major determinants of cavity dimension were greater body surface area and participation in certain endurance sports (cycling, cross-country skiing, and canoeing).In a sample of highly trained athletes, left ventricular cavity dimension varied widely but was strikingly increased to a degree compatible with primary dilated cardiomyopathy in almost 15% of participants. In the absence of systolic dysfunction, this cavity dilatation is most likely an extreme physiologic adaptation to intensive athletic conditioning. The long-term consequences and significance of this marked left ventricular remodeling of the athlete's heart is not known.

Arrythmogenic right ventricular (RV) cardiomyopathy (ARVC) is a cardiomyopathy characterized pathologically by fibrofatty replacement primarily of the RV and clinically by life-threatening ventricular arrhythmias in apparently healthy young people. The prevalence of the disease has been estimated at 1 in 5,000 individuals, although this estimate will likely increase as awareness of the condition increases among physicians. Arrythmogenic RV cardiomyopathy is recognized as a cause of sudden death during athletic activity because of its association with ventricular arrhythmias that are provoked by exercise-induced catecholamine discharge. Diagnosis may be difficult because many of the electrocardiographic abnormalities mimic patterns seen in normal children, and the disease often involves only patchy areas of the RV. For this reason, international diagnostic criteria for ARVC were proposed by an expert consensus panel in 1996. Treatment is directed to preventing life-threatening cardiac arrhythmias with medications and the use of implantable defibrillators. This article will present in detail the etiology, clinical presentation, diagnosis and management of this condition.

ObjectivesThe aim of this study was to clarify the clinical relevance of ventricular tachyarrhythmias assessed by 24-h ambulatory electrocardiograms (ECG) in a large, unique, and prospectively evaluated athletic population.BackgroundFor athletes with ventricular tachyarrhythmias, the risk of sudden cardiac death associated with participation in competitive sports is unresolved.MethodsWe assessed 355 competitive athletes with ventricular arrhythmias (VAs) on a 24-h ambulatory (Holter) ECG that was obtained because of either palpitations, the presence of ≥3 premature ventricular depolarizations (PVDs) on resting 12-lead ECG, or both.ResultsAthletes were segregated into three groups: Group A with ≥2,000 PVDs/24 h (n = 71); Group B with ≥100

ObjectivesThe purpose of this research was to evaluate the impact of athletic training and, in particular, physical deconditioning, on frequent and/or complex ventricular tachyarrhythmias assessed by 24-h ambulatory (Holter) electrocardiogram (ECG).BackgroundSudden deaths in athletes are usually mediated by ventricular tachyarrhythmias.MethodsTwenty-four hour ambulatory ECGs were recorded at peak training and after a deconditioning period of 19 ± 6 weeks (range, 12 to 24 weeks) in a population of 70 trained athletes selected on the basis of frequent and/or complex ventricular tachyarrhythmias (i.e., ≥2,000 premature ventricular depolarization [PVD] and/or ≥1 burst of non-sustained ventricular tachycardia [NSVT]/24 h).ResultsA significant decrease in the frequency and complexity of ventricular arrhythmias was evident after deconditioning: PVDs/24 h: 10,611 ± 10,078 to 2,165 ± 4,877 (80% reduction; p < 0.001) and NSVT/24 h: 6 ± 22 to 0.5 ± 2, (90% reduction; p = 0.04). In 50 of the 70 athletes (71%), ventricular arrhythmias decreased substantially after detraining (to

Antimitochondrial autoantibodies (AMA) were tested by indirect immunofluorescence in three groups of subjects with different types of myocardial hypertrophy: 35 patients affected with hypertrophic cardiomyopathy (HC), 20 patients with cardiac hypertrophy secondary to essential hypertension, and 35 active endurance athletes with exercise-induced left ventricular hypertrophy. Forty-two healthy subjects served as a control group. Left ventricular hypertrophy was considered a left ventricular mass (LVM) echocardiographically calculated (Devereux formula), exceeding 244 gm or a LVM index exceeding 122 gm/m2 (greater than 2 SD from a previously studied normal population). AMA were found in 15 of 35 (43%) patients with HC and in 6 of 20 (30%) patients with hypertensive heart disease (p less than 0.01); in contrast, AMA were not present in the sera of athletes or in the sera of controls. Although the significance of AMA in subjects with pathologic myocardial hypertrophy has not yet been established, their absence in the sera of athletes strengthens the opinion that cellular changes, as a compensatory response of the myocardium to a work overload, have a physiologic fashion in these cases. Moreover, identification of AMA in the sera of athletes with disproportionate severe left ventricular hypertrophy of uncertain origin may be helpful to ensure a single diagnosis.