Collagen peptides, interstitial remodelling and sudden cardiac death in hypertrophic cardiomyopathy.

摘要

Hypertrophic cardiomyopathy (HCM) is characterised by inappropriate hypertrophy, small-vessel coronary artery disease, myocyte disarray and increased interstitial fibrosis (1). A continuous extracellular matrix turnover appears in HCM, leading to an increase of interstitial fibrosis due to the higher amount of collagen type I/III deposited. The presence of late gadolinium enhancement (LGE), assessed by cardiac magnetic resonance (MRI), seems to reflect an increase in myo-cardial fibrosis (2, 3). We have recently read the interesting study by Lin et al. (4), exploring the interstitial remodelling, by measuring the serum levels of type III aminoterminal pro-peptide of procollagen (PIUNP) in heart failure (HF) patients. In this study, PmNP is proposed as a serum bio-marker of cardiac autonomic control and risk of sudden cardiac death (SCD). Interestingly, a recent report by Ho et al. (5), also studied different biomarkers of fibrosis and interstitial remodelling and revealed that serum type I carboxy-terminal propeptide of procollagen (PICP) seems to indicate increased myocardial collagen synthesis in sarcomere-muta-tion carriers without overt disease. They proposed that this profibrotic state precede the development of left ventricular hypertrophy or fibrosis visible on MRI (5). Fibrosis may provide electrical heterogeneity and a substrate for arrhythmo-genicity, which may cause SCD, a feared first symptom that can appear at the onset of both pathologies (HF and HCM) (4, 6). The aim of the present study was to evaluate the collagen turnover in HCM by the serum collagen peptides and their relation with different clinical values of the severity of the disease.