Background: Studies on 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.
Hypothesis: Myocardial fibrosis occurs in exercise induced LVH in veteran athletes.
Aim: To document non-invasively the presence of fibrosis in veteran athletes
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), carboxyterminal 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 (LVMI). Diastolic and systolic function was normal. Plasma PICP (259 vs 166 μg/l, p<0.001), CITP (5.4 vs 2.9 μg/l, p<0.001) and TIMP-1 (350 vs 253 ng/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 an LVMI >130 g/m2 (417 vs 266 ng/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.
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- CITP, carboxyterminal telopeptide of collagen type I
- IVSd-1, interventricular septal thickness in diastole
- LPWd, left posterior wall thickness in diastole
- LV, left ventricular
- LVH, left ventricular hypertrophy
- LVIDd, left ventricular internal dimension in diastole
- LVMI, left ventricular mass index
- PICP, plasma carboxyterminal propeptide of collagen type I
- RWT, relative wall thickness
- TIMP-1, tissue inhibitor of matrix metalloproteinase type I
Published Online First 20 February 2007
Competing interests: None declared.
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