[Cardiac rhythm disturbance in athletes with cardiac connective tissue dysplasia syndrome]

ABSTRACT

Cardiac connective tissue dysplasia syndrome consists of mitral valve prolapse [MVP], anomalously located chordae tendinae of the left ventricle, or a combination of the two. MVP is marked by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. The nonclassic form of MVP carries a low risk of complications. Patients with severe classic MVP can suffer from mitral regurgitation [MR], infective endocarditis, and, infrequently, sudden death from cardiac arrest. Anomalously located left ventricular chordae tendinae are fibrous or fibromuscular bands that stretch across the left ventricle from the septum to the free wall. They have been associated with murmurs and arrhythmias. The purpose of this study is to assess the performance, as measured by the physical working capacity [PWC170] and maximal oxygen consumption [VO2 max], in athletes with cardiac connective tissue dysplasia syndrome. Of the 183 male athletes studied, 158 had cardiac connective tissue dysplasia syndrome and 25 were normal, healthy controls. Their mean age was 16.23 [ +/- 5.48] years and mean training time was 5.2 [ +/- - 4.6] years. Athletes with cardiac connective tissue dysplasia syndrome were divided to four groups. Group 1 consisted of those with MVP; Group 2 had patients with an additional cord in left ventricle; Group 3 was made up of athletes with a combination of MVP and additional cord; Group 4 contained athletes with a combination of MVP and MR. All sportsmen were studied by echocardiograph, veloergometer, and those with arrhythmias were studied and recorded using a Holter monitor. The most common form of this syndrome in our study groups was MVP. The PWC170and VO2 max among the athletes with the combination of MVP+MR [Group 4] was lower than that of athletes in other groups [P<0.05]. The most common arrhythmia among the athletes with anomalously located left ventricular chordae, Group 2, was Wolf-Parkinson-White [WPW] syndrome and early repolarization syndrome. The PWC170 and VO2 max in athletes with WPW syndrome, was lower than the other athletes who did not have WPW syndrome [P<0.05]. Conclusion: The lowest PWC170 and VO2 max were in those athletes with a progressive abnormality. However, the PWC170 and VO2 max among athletes with anomalously located left ventricular chordae was normal. Therefore, among athletes with a combination of anomalously located left ventricular chordae and disruption of rhythm, the PWC170 and VO2 max are lower than normal