Key result
Acute MI is linked to lower aortic wall collagen III expression compared to stable angina.
Why the study?
Extracellular matrix remodelling of the vessel wall is hypothesized to be important in atherosclerosis progression leading to myocardial infarction, but detailed understanding of ECM changes in IHD patients is needed.
Observational
p-value: p=<0.001
Lower aortic collagen III in acute MI patients suggests possible systemic ECM changes linked to plaque vulnerability; leaves open causal role in observational data.
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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Kong et al. (2012) conducted an observational in Ischaemic heart disease (acute myocardial infarction and stable angina). Acute myocardial infarction vs. Stable angina was evaluated on Aortic wall collagen III expression (p=<0.001). Patients with acute myocardial infarction had significantly lower aortic wall collagen III expression compared to patients with stable angina (P<0.001).
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