MYOCARDIAL FIBROSIS ASSESSED BY C-TERMINAL PROPEPTIDE OF PROCOLLAGEN TYPE I RELATES TO SYSTOLIC AND DIASTOLIC FUNCTION, BUT NOT TO DYSSYNCHRONY IN SYSTOLIC HEART FAILURE: PP.1.03

Abstract

Objective: Hypertensive left ventricular hypertrophy, an important factor for future development of heart failure, is associated with cardiomyocyte hypertrophy and excess in myocardial collagen. Myocardial fibrosis may also be involved in cardiac remodelling in heart failure. Circulating levels of C-terminal propeptide of procollagen type I (PICP), an index of collagen type I synthesis, has been shown to correlate with the extent of myocardial fibrosis. We examined the associations between PICP and brain natriuretic peptide (BNP), echocardiographic, and clinical findings in heart failure patients. Design and Methods: 132 patients >60 years old with systolic heart failure (NYHA II-IV and an ejection fraction <45% by echocardiography) were studied. Mean age was 75 years, blood pressure 134/80 mm Hg, ejection fraction 34%, BNP 312 pg/ml, and atrial fibrillation was present in 55 % (n = 72). Results: PICP was higher in patients with atrial fibrillation (86 ± 43 vs 73 ± 27 μg/l, p = 0.039). In heart failure patients, PICP related to left ventricular end diastolic diameter (LVEDD; r = 0.29, p = 0.002), relative wall thickness (r = -0.22, p = 0.024), AV-plane displacement (r = -0.29, p = 0.003), E-deceleration time (r = -0.25, p = 0.003), intraventricular relaxation time (IVRT; r = -0.34, p <0.001), and BNP (r = 0.37, p < 0.001). Weak trends were found between PICP and echocardiographic measures of dyssynchrony (left ventricular filling time/RR interval, r = -0.16, p = 0.083, aortic preejection time/RR interval, r = 0.13, p = 0.127), but no associations with age, blood pressure, or QRS duration. Multivariate analyses confirmed (R2 = 0.30, p < 0.001) an inverse association between PICP and IVRT (p = 0.002), and positive associations with LVEDD (p = 0.018), and BNP (p = 0.026). Conclusions: PICP is independently associated with signs of systolic and diastolic dysfunction, but not to indices of dyssynchrony. Thus, myocardial fibrosis may be part of cardiac functional remodelling in heart failure.