Introduction Long-term Italian experience has provided evidence that preparticipation screening in competitive athletes with 12-lead ECG, history and physical examination is effective in identifying potentially lethal cardiovascular diseases. However, it is not being routinely practised in other countries.
Objectives To evaluate the usefulness of a preparticipation screening programme in a sample of players belonging to different disciplines.
Material and methods From September 2006 to June 2008, 1220 young athletes from different sports disciplines underwent a cardiovascular examination that included personal and family history, physical examination and a resting 12-lead ECG. Those with abnormal findings were referred for additional tests.
Results 1220 Athletes were screened: 96% males; mean age 23 (4) years. 90 (7.4%) players were referred for additional tests because of abnormal findings on baseline examination: 11 (0.9%) personal or family history, 4 (0.08%) physical examination and 75 (6.14%) 12-lead ECG. Echocardiographic assessment fulfilled left ventricular hypertrophy criteria in 8 of the 90 players. Of those, one case was considered an athlete's heart and one case was diagnosed with hypertrophic cardiomyopathy (septal thickness 23 mm). Further tests were needed in the remaining six, included in the “grey area”, with one additional case of hypertrophic cardiomyopathy (apical variant) suggested by cardiac MRI.
Conclusion Given the ability of 12-lead ECG to detect individuals with structural heart disease, we suggest its inclusion as a part of preparticipation screening programmes.
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Systematic preparticipation screening of competitive athletes was implemented by law in Italy in 1982, and it has been a routine practice in that country ever since. It includes a general medical and cardiovascular evaluation, with 12-lead resting ECG in addition to personal history and physical examination.1 For those elite athletes participating in national and international events, the evaluation requires an additional echocardiographic analysis. Although its proven efficacy in preventing sudden cardiac deaths related to sports, the Italian model is not being routinely practised in other countries. Furthermore, it has raised an open debate about the appropriate and effective preparticipation screening programme, with the role of ECG as the main point of controversy. The routine practice of a 12-lead ECG within the evaluation could lead to timely identification of individuals with several potentially lethal conditions such as hypertrophic cardiomyopathy (HCM), pre-excitation syndromes or long QT syndrome. The recognition of cardiovascular heart diseases may help to settle measures to prevent sudden cardiac death, an infrequent but tragic event that is the focus of preparticipation screening programmes.2 3
Our aim was to evaluate the usefulness of a preparticipation screening programme in a sample of players belonging to different disciplines. The primary goal was to determine the prevalence of abnormal findings during routine cardiovascular examination. In addition, ECG disturbances and their relationship with underlying cardiac diseases were studied.
From September 2006 to June 2008, we consecutively evaluated 1220 young amateur athletes from different sports disciplines: soccer players, soccer referees and a third group of different sports activities (including basketball, athletics and swimming). All of them were affiliated to the sports federation of our community, Asturias, which is located in Northwestern Spain. For our study, they all underwent a cardiovascular examination that included a personal and family history and a physical examination in addition to a resting 12-lead ECG. Evaluation was performed in our regional School of Sports Medicine by a licensed specialist in sports medicine. ECG was interpreted by a cardiologist. Those with ECG positive criteria defined by the European Society of Cardiology (2005)3 (table 1) or with abnormal physical examination were referred for additional tests such as echocardiography, 24-h ECG and/or exercise stress test.
Two-dimensional, M-mode and Doppler echo-cardiographic analyses were assessed by a cardiologist using a Sonos 5500 equipment (Philips, The Netherlands). End-diastolic and end-systolic left ventricular dimensions, septum and posterior free wall thickness were registered. Both systolic and diastolic functions (pulsed Doppler and tissue Doppler) were also measured. When necessary, exercise stress testing was performed on a cycloergometer following a protocol with 50-W increases every 2 min. Those athletes who fulfilled echocardiographic criteria for left ventricular hypertrophy (septal thickness >13 mm) were referred to our genetic division, where the MYBPC3 gene was studied. Cardiac magnetic resonance with a 1.5-T equipment (General Electric, UK) was practised if the aforementioned studies were non-conclusive and high suspicion of structural heart disease persisted. We report the results of this study.
A total of 1220 athletes were evaluated, with 825 soccer players, 226 soccer referees and 169 from different sports (including basketball, athletics and swimming). Ninety-six per cent were males, and mean age was 23±4 years (range 15–29). The average training time was 3 h per day, 3 days per week, over 10 years.
History: There were four cases with history of premature sudden death in a first-degree relative. Those deaths were not documented and therefore could not be attributed to cardiac cause. Three cases had effort syncope/near syncope and four cases had palpitations, with no associated clinical conditions and normal physical examination.
Physical examination: A systolic murmur >II/VI was found in four cases, which were referred for echocardiographic assessment. There were no cases of diastolic murmur, delayed femoral pulses or stigmata suggestive of Marfan syndrome.
ECG findings: Twelve-lead ECG was considered positive in the presence of one or more of the findings reported in table 1. According to these criteria, 75 players (6.14%) showed a positive ECG. The most common findings were repolarisation abnormalities (ST-segment depression or T-wave flattering or inversion in two or more leads), which constituted more than a half of the ECG disturbances reported (3.27% of the initial sample). Complete right bundle-branch block (0.73%) and right axis deviation (0.65%) were frequent abnormalities encountered. Five cases fulfilled voltage criteria for left ventricular hypertrophy and two showed left axis deviation, with two more cases of pathologic Q wave. Mean PR duration was 141 ms, with an SD of 30.2.
In four cases, a short PR interval was followed by a delta wave (two right posteroseptal morphology, two left lateral ones). None of them had family history of arrhythmia, nor had they ever had palpitations, syncope or any symptom suggestive of a pre-excitation syndrome. Mean QT duration was 383 ms (SD 24.6), with one case in the upper limit of normality (440 ms). Personal and family histories were both negative for rhythm disturbances. Other abnormalities related with conduction disorders were premature ventricular beats, which were found in four cases; no supraventricular tachycardia, atrial flutter or atrial fibrillation was encountered; nor were there pathologic sinus bradycardia or atrioventricular blocks.
Echocardiographic findings: Ninety players were referred for echocardiographic assessment because of abnormal preparticipation screening findings (table 2). The mean ventricular septal thickness was 11 (2) mm (8–23 mm), with eight cases fulfilling criteria of left ventricular hypertrophy (septal thickness >13 mm), one case of athlete's heart (enlarged ventricular dimensions, normal diastolic, systolic and right ventricular function, septal thickness 13–15 mm) and one case of HCM (case 1) (septal thickness 23 mm, diastolic dysfunction, without mitral regurgitation, systolic anterior movement of mitral valve or subaortic gradient). However, six cases remained in a blurred group called the “grey area” because echocardiographic findings were not sufficient to confirm or exclude diagnosis of cardiomyopathy (13–15 mm septal thickness, non-dilated left ventricle, with normal systolic and diastolic function). Further evaluation was required.
Additional tests: An exercise test was performed in five cases because of ECG abnormalities suggestive of rhythm disorders. Four players showed short PR interval followed by delta wave on baseline ECG, raising suspicion of pre-excitation syndrome. The pre-excitation disappeared suddenly with exercise, thus revealing that the accessory pathway had a relatively long refractory period and was unlikely to precipitate arrhythmias. The fifth case was a player with QT duration in the upper limit of the normality, where physical activity showed its progressive shortening within normal values. The five players underwent a 24-h ECG with normal results. According to the low-risk findings on non-invasive assessment, these asymptomatic players were allowed to participate in competitive sports. They received counselling, and no further examination (electrophysiological study) was practised.
The six cases included in the “grey area” underwent a genetic test with sequentiation of myosin binding protein (MYBPC), with negative results. These findings excluded HCM related to MYBPC but could not rule out other mutations that have been described in association with this form of disease. MRI in one of those cases confirmed an apical variety (type VI) of HCM (case 2), according to the degree and distribution of hypertrophy. A detraining period has been recommended in the remaining five individuals in the “grey area” and may help to better classify them as having athlete's heart or a pathological form of cardiac hypertrophy. Diagnosis of athlete's heart would be favoured by involution of ECG abnormalities and/or reduced cardiac mass with detraining. The exactly duration for the deconditioning period remains unclear. On the basis of previous data,4 we established a period of at least 3 months, with clinical re-evaluation and serial echocardiographic assessment.
Familial screening with genetic analysis and echocardiographic evaluation were performed in first-degree relatives of the two cases with a diagnosis of HCM.
Case 1: Genetic analysis revealed a mutation for MYBPC3 (Arg 495 Trp in 18 exon), which was present in the index case, his mother and his grandfather. The latter also showed echocardiographic criteria for HCM.
Case 2: Both genetic test and echocardiographic assessment were negative in the relatives studied.
Long-term Italian experience has provided evidence that systematic preparticipation screening with 12-lead ECG, history and physical examination is effective in identifying athletes with potentially lethal cardiovascular disease and actually saves lives. However, concerns have been raised about the cost-effectiveness of screening because of the high level of false-positive results from the ECG. Pelliccia and colleagues analysed the prevalence of ECG abnormalities in different groups of athletes with an important contribution to our understanding of the athlete's ECG. An early study on the evaluation of 1005 trained athletes by ECG showed that 17% of men and 8% of women had distinctly abnormal ECGs and a further 28% of men and 14% of women had mildly abnormal ECGs.5 Later on, they analysed a large, unselected population of 32 652 Italian amateur athletes. 12-lead ECG patterns were considered normal in 28 799 of the 32 652 athletes (88.2%) and abnormal in 3853 (11.8%). Only a minority of screened individuals (∼5.0%) showed ECG abnormalities, such as inverted T waves, intraventricular conduction disturbances, ventricular pre-excitation and prolonged QTc interval, which required additional testing to exclude an underlying cardiovascular condition at risk of sudden cardiac death during sports.5 The rate of abnormal ECGs in our study is low (6.14%) and similar to the previously reported. The main ECG alterations were those found in repolarisation, which accounted for 53.3% of all the electrocardiographic disturbances. This was the main reason for indicating additional tests (3.27%) and the constant disturbance present in those who finally showed structural heart disease. Abnormal repolarisation patterns have previously been reported to occur in 2–4% of large populations of trained athletes who are young adults (aged 18–35 years).5 7 The vast majority of such ECGs have been largely interpreted only as extreme manifestations of physiological athlete's heart if structural heart disease was ruled out with additional tests. In these sense, we found 33 players with marked repolarisation abnormalities in the absence of cardiac disease (one case considered athlete's heart: septal thickness 13 mm; enlarged cavity dimensions; normal transmitral flow pattern and tissue Doppler velocities). Although the relative good prognosis attributed to them, a recent study suggested that it could represent the initial expression of underlying cardiomyopathies that may be not evident until many years and that may be ultimately associated with adverse outcomes.8 In our sample, 2 athletes out of 1220 (approximately 1 in 600) were diagnosed with HCM. This is consistent with the prevalence of HCM in the general population (about 1 in 500). In addition, the precise ECG abnormalities in both athletes identified HCM. These observations underscore the importance of greater diagnostic scrutiny and continued clinical surveillance of trained athletes who present with such distinctly abnormal ECGs. Conversely, the finding of a normal ECG during preparticipation screening can be regarded as reasonably reliable evidence to exclude the presence of potentially lethal cardiac disease and can serve as a source of reassurance to young athletes. 93.8% (1145 athletes) of our sample had no major ECG disturbances. Some of them required additional tests because of abnormal findings on medical history or physical examination. In this sense, none of the 15 cases with a positive criteria on history or physical examination had structural cardiac disease on echocardiogram, which comprises a 1.2% of false positives from the initial sample. On the other hand, neither history nor physical examination had raised suspicion in any of the eight cases with left ventricular hypertrophy confirmed by echocardiogram. The value of these measures alone is questionable. First, the accuracy of some responses elicited by history-taking from young sports participants may depend on a level of personal compliance and their depth of medical knowledge; parental verification of the responses for high school and middle school students is recommended, but not compulsory.9 Second, screening should be done by a physician trained in this activity. Whereas the Italian model uses licensed sports medicine physicians, other healthcare workers are accepted in many other countries. Their experience and level of training are somewhat uncertain and might not have enough sensitivity to rule out cardiovascular abnormalities.10 These results emphasise the necessity of additional non-invasive tools to enhance sensitivity for detecting problems that could lead to sudden cardiac death. On the basis of our data and the previous literature, it seems reasonable that 12-lead ECG may be a feasible and useful technique for identifying athletes with suspected underlying heart disease. Given the potential for mortality reduction, we suggest that the cost of routine ECG should not represent an obstacle for implementation of large-scale preparticipation screening in young athletes.
First, we aimed to report the descriptive results of a cross-sectional study, without providing follow-up data on clinical end points. Second, there is uncertainty on the prevalence of cardiovascular abnormalities in the group of athletes without abnormal findings in the first step of evaluation. Additional tests in this group would have provided information on the prevalence of false-negative results of the screening method proposed. Finally, our sample represents a selected population mainly represented by male white athletes and therefore the results should not be extrapolated to other sex or ethnic groups.
The authors would like to express their thanks to the School of Sports Medicine (Escuela de Medicina del Deporte), Oviedo, and the Real Grupo Cultura Covadonga, Gijón.
Competing interests None.
Patient consent Not obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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