Abstract

Objective: Studies of exercise induced left ventricular hypertrophy (LVH) in veteran athletes suggest the presence of abnormal diastolic filling and incomplete regression of LVH on cessation of exercise. We hypothesise that this is secondary to the presence of fibrosis. This study was therefore designed to document non-invasively the presence of fibrosis in veteran athletes with exercise induced LVH.

Design: Prospective case control study.

Setting: City centre district general hospital.

Participants: 45 normotensive elite veteran athletes and 45 normal sedentary subjects.

Interventions: Echocardiographic assessment was made of LV mass, LV systolic and LV diastolic function. Plasma carboxyterminal propeptide of collagen type I (PICP), carboxy-terminal telopeptide of collagen type I (CITP) and tissue inhibitor of matrix metalloproteinase Type I (TIMP-1) were measured as markers of collagen synthesis, degradation and inhibition of degradation respectively.

Results: Veteran athletes had significant elevation in LV dimensions and calculated LV mass index. Diastolic and systolic function was normal. Plasma PICP (259micrograms/l Vs 166micrograms/l p<0.001), CITP (5.4micrograms/l Vs 2.9micrograms/l p<0.001) and TIMP-1 (350nanograms/ml Vs 253 nanograms/ml p=0.01) were elevated in the cohort of athletes. There was a further elevation of TIMP-1 in athletes with echocardiographic LVH defined as a LVMI>130g/m2 (417nanograms/ml Vs 266 nanograms/ml p=0.02)

Conclusion: There is biochemical evidence of disruption of the collagen equilibrium favouring fibrosis in veteran athletes with LVH. This may suggest that fibrosis occurs as part of the hypertrophic process in veteran athletes.