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Circulating levels of procollagen type I carboxy‐terminal propeptide reflect myocardial fibrosis

Myocardial fibrosis is a consequence of a profound change in the architecture and composition of the cardiac extra-cellular matrix affecting the structure and function of the heart. Non-specific insults to the cardiovascular system (e.g. hypertension, diabetes, ageing, ischaemia, genetic alterations) may dysregulate various cell types and signalling pathways, ultimately resulting in myocardial fibrosis.1,2 Once established, myocardial fibrosis is strongly associated with a poor prognosis, including in patients with idiopathic dilated cardiomyopathy (DCM).3,4 Despite the sound pathophysiological background and prognostic impact of myocardial fibrosis, its assessment remains challenging in clinical practice. Circulating markers reflecting collagen synthesis are under investigation as potential means for evaluating myocardial fibrosis non-invasively. In this regard, procollagen type I carboxy-terminal propeptide (PICP) may directly reflect the synthesis of collagen type 1 because it is produced during the conversion of procollagen type I to collagen type I in a 1:1 ratio.1 Furthermore, serum PICP levels have been correlated with total myocardial collagen volume fraction (CVF) (assessed in myocardial samples with collagen-specific staining) in patients with hypertension, heart failure and DCM.4,5 Another potential marker of collagen synthesis is N-terminal propeptide of type III collagen (PIIINP). PIIINP is generated from the conversion of procollagen type III into collagen type III and has been correlated with the amount of collagen type III fibres in the myocardium of heart failure patients, but it