Key result
Cardiovascular risk factors converge on endothelial dysfunction and inflammation to drive coronary atherosclerosis.
Why the study?
Vessel wall inflammation and an inflammatory-fibroproliferative response to endothelial-cell injury constitute major factors in the development of atherosclerosis, atheroma instability, plaque disruption, and subsequent local thrombosis underlying acute coronary syndromes.
Highlights the role of endothelial-cell injury and the subsequent inflammatory-fibroproliferative response in the development of atherosclerotic plaques.
Following Russel Ross [1], there is now general agreement that vessel wall inflammation constitutes a major factor in the development of atherosclerosis, atheroma instability and plaque disruption followed by local thrombosis, that underlies the clinical presentation of acute coronary syndromes [2-4].Endothelial-cell injury is the main stimulus for development of the atherosclerotic plaque: an inflammatory-fibroproliferative response results from various forms of insult to the endothelium.
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Raúl Altman (2003) conducted a review in Coronary atherosclerosis. Cardiovascular risk factors (dyslipidemia, diabetes, hypertension, obesity, immunity, infection, hyperhomocysteinemia, smoking) was evaluated on Athero-inflammation and endothelial dysfunction. Cardiovascular risk factors including diabetes, dyslipidemia, obesity, infection, and smoking converge on endothelial dysfunction and arterial inflammation to promote coronary atherosclerosis.
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