Abstract
Acute myocardial infarction (AMI) is often underdiagnosed in women. It is therefore of interest to identify biomarkers that indicate increased risk of AMI and thereby help clinicians to have additional focus on the difficult AMI diagnosis. Type I Collagen, a component of the cardiac extracellular matrix, is cleaved by matrix metalloproteinases (MMPs) generating the neo-epitope C1M. We investigated the association between serum-C1M and AMI and evaluated whether C1M is a prognostic marker for outcome following AMI. This study is based on The Prospective Epidemiological Risk Factor (PERF) Study including postmenopausal women. 316 out of 5,450 women developed AMI within the follow-up period (14 years, median). A multivariate Cox analysis assessed association between serum-C1M and AMI, and re-infaction or death subsequent to AMI. The risk of AMI increased by 18% (p = 0.03) when serum-C1M was doubled and women in the highest quartile had a 33% increased risk compared to those in the low quartiles (p = 0.025). Serum-C1M was, however not related to reinfarction or death subsequent to AMI. In this study C1M was be an independent risk factor for AMI. Measuring MMP degraded type I collagen could be useful for prediction of increased risk of AMI if replicated in other cohorts.
Highlights
Atherosclerosis is an inflammatory process characterized by accumulation of plaques and plaque calcification
Cavusoglu et al.[4] report elevated matrix metalloproteinases (MMPs)-3 levels in plasma to be associated with five-year-risk of AMI in men
This study is based on data from the Prospective Epidemiological Risk Factor (PERF) study including Danish postmenopausal women and assessed whether serum-C1M is associated to risk of AMI
Summary
Atherosclerosis is an inflammatory process characterized by accumulation of plaques and plaque calcification. Plaque rupture is the most common cause of AMI by triggering the coagulation cascade whereby the risk of thrombosis is accelerated. A ruptured plaque has a necrotic core with an overlying thin fibrous cap infiltrated by inflammatory cells[4,6] and expression of macrophage-released matrix metalloproteinases (MMPs) affects plaque stability[7]. Plaque rupture, which will trigger the thrombotic cascade leading to AMI4,8–11 and detection of plaque instability is of interest. Dragsbaek et al.[12] demonstrated the MMP-2, −9, and −13 generated type I collagen degradation fragment (C1M) to be associated with cardiovascular mortality. C1M data presented by Dragsbaek et al.[12] were further analysed to evaluate (i) association between serum-C1M and AMI in postmenopausal women and (ii) baseline serum-C1M as a biomarker for short-term prognosis following AMI
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