BJSM of a cardiomyopathy.39 40 Such abnormal ECGs raise the question of differentiating between the initial, subtle expression of cardiac disease or the extreme but innocent ECG expression of the ‘athlete’s heart’.26 41 42 Investigators researched the clinical outcomes of 81 athletes presenting initially with markedly abnormal repolarisation patterns in the absence of detectable cardiac abnormalities.43 After an average 9-year follow-up, a new diagnosis of cardiomyopathy was made in five athletes (6%), including three with HCM, one with ARVC and one with DCM.43 Two athletes experienced adverse events (0.3% per year), including one cardiac arrest from HCM and one sudden death related to ARVC.43 Figure 9. ECG (left panel) and cardiac MRI (right panel) of apical hypertrophic cardiomyopathy. Deep T wave inversions across the precordial leads are a characteristic ECG finding. The region of hypertrophy (red arrow) is isolated to the left ventricular (LV) apex, which can be challenging to detect by echocardiography. Markedly abnormal ECGs, therefore, may represent insufficient to assess all myocardial segments or when myocardial hypertrophy falls into the ‘grey zone’ between 1.2 and 1.5 cm. Cardiac MRI is recommended for markedly abnormal ECGs suggestive of apical HCM, specifically ECGs with deep TWI and/or ST depression in the inferolateral leads (V4–V6, I, aVL, II and aVF), in which echocardiography often does not provide an adequate assessment of the LV apex or inferior septum (figures 1–3). A common clinical dilemma is the detection of myocardial hypertrophy in an athlete in which the hypertrophy may be due to physiological adaptation to exercise. Differentiating athlete’s heart from HCM requires careful clinical evaluation by an experienced provider.36–38 Cardiac MRI, cardiopulmonary exercise testing and Holter monitoring should be considered. Findings suggestive of HCM include the presence of unusual patterns of hypertrophy with substantial differences in wall thickness of the LV segments, normal or reduced LV cavity size, extreme LAE, diastolic dysfunction, family history of HCM or SCD, below normal peak oxygen consumption (peak VO2), and the presence of ventricular arrhythmias. When diagnostic uncertainty remains, genetic testing and/or a period of deconditioning followed by reassessment to document regression (or lack thereof) of exercise-induced LVH may be considered. Long-term follow-up of markedly abnormal ECGs Highly trained athletes occasionally present markedly abnormal ECG patterns instinctively suggesting the presence 32 Sport & Geneeskunde | juli 2013 | nummer 3 the initial expression of cardiomyopathy, preceding by many years the phenotypic or morphological expression of structural heart disease. Athletes presenting with distinctly abnormal ECGs (ie, deep TWI in the lateral leads) and no evidence of structural heart disease after a thorough work-up may be permitted to participate in competitive athletics. However, these athletes should undergo serial clinical evaluation on an annual basis, even in the absence of symptoms, including repeat imaging tests such as echocardiography and/or cardiac MRI to evaluate for the development of cardiomyopathy. Competing interests None. Provenance and peer review Commissioned; internally peer reviewed. References 1 Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006. Circulation 2009;119:1085–92. 2 Maron BJ. Sudden death in young athletes. N Engl J Med 2003;349:1064– 75. 3 Corrado D, Basso C, Schiavon M, et al. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med 1998;339:364–9. 4 Corrado D, Biffi A, Basso C, et al. 12-Lead ECG in the athlete: physiological versus pathological abnormalities. Br J Sports Med 2009;43:669–76. 5 Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243–59. 6 Uberoi A, Stein R, Perez MV, et al. Interpretation of the electrocardiogram of young athletes. Circulation 2011;124:746–57. Pagina 31
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