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- AMI, acute myocardial infarction
- CK, creatine kinase
- CITP, C-telopeptide for type-I collagen
- LV, left ventricular
- MMP, matrix metalloproteinase
- PICP, procollagen type-I carboxy-terminal propeptide
- PIIINP, procollagen type-III amino-terminal propeptide
- TIMP, tissue inhibitor of metalloproteinase
Ventricular remodelling following acute myocardial infarction (AMI) is a powerful adverse prognostic indicator, characterised by alterations to left ventricular (LV) size, shape, and function.1 Until recently, a clear distinction was made between the early changes of infarct expansion and LV dilatation and the later changes of fibrosis, scar formation, and continued alteration to LV geometry and function. However, it is increasingly recognised that remodelling is a continuum,2 starting during the acute event and progressing thereafter. The remodelling continuum is dependent on the balance between extracellular collagen degradation and synthesis,3 the extent of which can be examined biochemically.4 Procollagen type I carboxy-terminal propeptide (PICP) is cleaved from procollagen during the formation of type I collagen and is therefore a marker of collagen synthesis. Similarly, C-telopeptide for type I collagen (CITP) is released by endopeptidase cleavage by matrix metalloproteinases (MMP) during collagen degradation and is a marker of breakdown. Clearly, MMP activity must be tightly regulated and they are specifically inhibited by the tissue inhibitors of metalloproteinases (TIMPs). We examined plasma concentrations of PICP, CITP, and TIMP-1 as serological markers of collagen turnover in patients presenting with AMI.
We recruited 64 patients presenting with their first AMI, with electrocardiographic criteria for thrombolysis. Serial blood sampling was performed on admission, at 12 hours, 24 hours, 2 days, 3 days, 4 days, and 30 days for estimation of plasma PICP and CITP concentrations by radioimmunoassay (Orion Diagnostica, …