Elite athletes with mitral or aortic regurgitation and their cardiopulmonary capability

Aortic or mitral valvular regurgitation (left cardiac valvular regurgitation, LCVR) of less than second-degree (< degree II) occasionally found in competitive athletes is of questionable relevance. Precisely detectable by echocardiography there is scarce published data that clarifies cardiopulmonary capacity or any limitations LCVR < degree ll may cause.

In this single-centre study we consecutively recruited highly trained athletes (n= 14) with LCVR < degree ll detected in 2D echo. Not included were athletes with multi- or right-cardiac valvular dysfunction and structural heart disease other than bicuspid aortic valve or mitral valve prolaps. Target parameters were determined by 2D echo and spiroergometry.

There were no significant differences with regard to age and body mass index. Echocardiographically determined muscle mass index was increased in both groups (134 14.7 vs 129.6+/-27.5; P=0.69), whereas the left-ventricular end-diastolic diameter index was significant higher in the LCVR < degree II group (27.3 +/- 1.3 vs 25.2 +/- 2.4; P = 0.04). However, there were no significant differences with regard to (oxygen uptake) V02, at baseline (athletes with LCVR < degree II 5.7 +/- 0.9 vs controls 5 +/- 0.96, P= 0.06), at the anaerobic threshold (athletes with LCVR < degree II 47.3 +/-8.4 vs controls 47.4 +/- 5, P= 0.97) and maximally (VO2max; athletes with LCVR < degree II 57.7 6.3 vs controls 57.1 +/- 5.1, P= 0.81). Neither levels of lactate nor of brain natriuretic peptide differed significantly.

High level athletes presenting with aortic or mitral regurgitation < degree II in are not disadvantaged with regard to their cardiopulmonary capability.