Abstract

Objectives: Beta-blocker therapy inhibits LV remodeling, and improves not only LV systolic function but also LV diastolic function, and improves prognosis of heart failure patients. But it is unknown why beta-blocker therapy improves LV function. Recently, serum collagen markers such as Procollagen type I C-terminal propeptide (PICP) and collagen type I C-terminal telopeptide (CITP), are useful as index of myocardium collagen synthesis and degradation. We investigate correlation between collagen turnover and LV function following induction of beta-blocker therapy with systolic heart failure patients. Methods: Study population consisted of 46 patients with systolic heart failure. Patients were clinically stable within 1 month and on stable medical therapy, including ACEI or ARB and diuretics, and no beta-blocker therapy. We started beta-blocker therapy, initiated at a target dose of from 5 to 10mg/day. Echocardiography was performed before, 2, 6, and 12 months after the initiation of beta-blocker therapy. LV systolic function was estimated using the LV ejection fraction by Simpson biplane method. Peak systolic strain in the radial direction was measured at the anterior and posterior walls in the short-axis view. We measured E- and A-wave peak velocities and deceleration time (DcT) form the mitral inflow profile, and tissue Doppler early diastolic mitral annular velocity (E'). Serum PICP and CITP were determined. Results (table): A total of 46 patients were enrolled. The median age of all patients was 56±14 years. 15 patients were women and 31 patients were men. EF, DcT and E' were improved after induction of beta-blocker therapy. PICP was not changed, but CITP was decreased from 8.9±7.8 to 6.1±1.7ng/ml at 12 months after treatment. The lower %changes in CITP was associated with the higher %changes in DcT (r=0.21, p<0.05), EF (r=0.29, p<0.01) and radial systolic strain (r=0.26, p<0.05), but not E'. The %changes in PICP were not related %changes in DcT and E'. Conclusions: The improvement in LV systolic function as indexes in EF and radial systolic strain and LV diastolic stiffness as indexes in DcT, correlated with inhibition of collagen degradation in patients with LV systolic function.

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