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Characteristics of aortic wall extracellular matrix in patients with acute myocardial infarction: tissue microarray detection of collagen I, collagen III and elastin levels. | LitMetric

AI Article Synopsis

  • The study examines the role of extracellular matrix (ECM) remodeling in the progression of atherosclerosis, linking it to serious heart conditions like myocardial infarction (MI).
  • Researchers analyzed tissue samples from patients with acute MI and stable angina to assess the levels of collagen I, collagen III, and elastin in the aortic wall.
  • Results indicated significantly lower collagen III levels in MI patients, suggesting that this decrease may contribute to plaque instability and highlight potential markers for predicting cardiovascular events.

Article Abstract

Objectives: Extracellular matrix (ECM) remodelling of the vessel wall is hypothesized to be an important step in atherosclerosis. Changes of the ECM are associated with the gradual progression of an atherosclerotic lesion from a lipid streak to complicated unstable plaque, leading to a complete vessel occlusion and eventually myocardial infarction (MI). Understanding of this process is critical in the treatment and prevention of ischaemic heart disease (IHD).

Methods: We investigated the histopathological characteristics of aortic wall ECM in IHD patients. Collagen I, collagen III and elastin were assessed immunohistochemically in patients with acute MI and those with stable angina, using aortic punch tissues obtained from coronary artery bypass graft surgery. Fluorescence tissue images were analysed using the tissue microarray technique.

Results: The results showed that collagen III expression was found to be significantly lower in the acute MI group (P < 0.001). As a result of this change, the patients with MI also revealed a significant reduction in the collagen III/collagen I ratio. The elastin/collagen III ratio was significantly higher in the MI group (P < 0.001).

Conclusions: Our study provided evidence of a decrease in collagen III content in patients with MI, which could possibly explain the mechanism of plaque vulnerability and weakening of the plaque cap. A reduction in collagen III content, particularly away from the atherosclerotic lesions, might be explained by the systemic vascular changes in patients with MI, and inflammation and immune responses could be potential causes of these systemic transformations. The biochemical mechanisms and factors regulating collagen III production might be potential markers to predict possible cardiovascular events.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523627PMC
http://dx.doi.org/10.1093/icvts/ivs421DOI Listing

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