Ventricular premature beats in triathletes: Still a physiological phenomenon?

Citation
P. Claessens et al., Ventricular premature beats in triathletes: Still a physiological phenomenon?, CARDIOLOGY, 92(1), 1999, pp. 28-38
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOLOGY
ISSN journal
00086312 → ACNP
Volume
92
Issue
1
Year of publication
1999
Pages
28 - 38
Database
ISI
SICI code
0008-6312(1999)92:1<28:VPBITS>2.0.ZU;2-2
Abstract
Sudden death is a tragic fact, unexpectedly arising in all age groups. Vent ricular arrhythmias are the main cause. At the end of a maximal exercise te st more ventricular premature beats were noted in a group of well trained t riathletes compared with a similar control group. The etiology is multifact orial. When these ventricular premature beats are associated with specific structural and functional heart adaptations, echocardiographically and elec trocardiographically well-documented, then those 'banal' ventricular premat ure beats cannot longer be considered as a physiological phenomenon. In the se circumstances the involved subject is a candidate for dangerous arrhythm ias and 'sudden cardiac death'. Purpose: The principal cause of 'Sudden car diac death' is ventricular arrhythmias. We explore the incidence of ventric ular premature beats (VPB) in triathletes, who engage in enforced endurance sports. Methods: Fifty-two triathletes were compared with twenty-two contr ol subjects with comparable anthropometric parameters in function of struct ural and functional cardiac adaptations. Maximal exercise tests were conduc ted on a stationary bicycle and a treadmill. During the last two minutes of each test, the VPB were registered. Results: Statistically significant dif ferences emerged in the cardiac structure and function between the triathle tes and the controls. There were signs of cardiac hypertrophy and arguments for a supernormally diastolic left ventricular function in the triathletes . The performance capacity was also significantly higher in the triathletes . The maximal heart rate was significantly higher in the control group. The number of VPB was significantly higher in the triathletes. The increased r isk of VPB in the triathlon group is caused by several factors: the degree of cardiac hypertrophy, the increased diastolic reserve, the duration of th e exercise, the existence of an aortic insufficiency jet and some specific electrocardiographic findings. Conclusions: The triathlete has an increased risk of VPB during maximal efforts. We doubt the traditionally accepted vi ew of the physiological nature of those VPB and suspect that the limit of p hysiological cardiac adaptations to sport efforts is exceeded with the appe arance of VPB. The triathlete with VPB and with specific electrocardiograph ic and echocardiographic findings is a candidate for 'sudden cardiac death' . Copyright (C) 2000 S. Karger AG, Basel.