Abstract 3391: Prevalence Of Hypertrophic Cardiomyopathy In Elite Athletes
Objectives: The prevalence of HCM in the general population is estimated to be around 1 in 500. The exact prevalence of HCM in athletes has never been reported and has important implications with regards to potential future national pre-participation screening programme in countries such as United Kingdom, where currently there is no such programme for junior athletes.
Methods: Between 1996 and 2006, 3500 asymptomatic and normotensive elite athletes (70% males) aged between 14–35 years (mean: 20.5±5.80) and a mean body surface area of 1.86±0.16 m2 (range1.36–2.29) underwent 12-lead EKG and 2D-echocardiography. Cardiac dimensions and function were measured using conventional methods.
Results: Of the 3500 athletes, 53 (2%) had maximal left ventricular wall thickness (LVWTd) > 12 mm (mean: 13.6 ± 0.9, range: 13–16). All 53 were male athletes and all except 3 of them had associated dilated LV cavity (58.5 ± 5.14 mm, range 52– 65) implying physiological left ventricular hypertrophy (LVH). This was also supported by normal indices of diastolic function and absence of family history of HCM or sudden cardiac death (SCD). However, there were 3 athletes with LVWT > 12mm who had a relatively non-dilated LV cavity (range:45– 46) and bizarre EKG changes (deep T-wave inversion) that that raised the suspicion of HCM. But none of them exhibited any other phenotypic feature of HCM on further testing with 48-hour EKG recording, cardiopulmonary exercise testing and assessment of their first-degree family members. Only one of the 3 athletes agreed to detrain for 12-weeks, which resulted in regression of LVH and complete resolution of EKG changes.
Conclusion: In our study, only 3 athletes had echocardiographic findings that could have been consisted with the diagnosis of HCM but further investigations failed to support the diagnosis. These results indicate that the prevalence of HCM in highly trained athletes is extremely rare. The structural and functional changes associated with HCM precludes generation of large amounts of cardiac output that are required during exercise selecting out most of these individuals from competitive sports. Our findings also questions the validity of previous data which proposes that HCM is the commonest cause of exercise related SCD in young athletes.