Why the study?
It has not been fully explained why some coronary artery plaques remain quiescent while others evolve to high-risk, vulnerable plaques predisposing to cardiac events, with many patients developing acute coronary syndromes without prior symptoms or angiographically evident disease.
This review highlights the critical role of local hemodynamic forces, particularly endothelial shear stress and dysfunction, in driving coronary plaque progression and destabilization.
Highlights hemodynamic assessment in coronary plaque evaluation; leaves open whether modulating forces alters outcomes.
Coronary artery disease is the leading cause of morbidity and mortality worldwide, especially in developed countries, with an increasing incidence in developing countries. Despite the advances in cardiology, there are yet many unanswered questions about the natural history of coronary atherosclerosis. However, it has not been fully explained why some coronary artery plaques remain quiescent over time, whereas others evolve to a high-risk, "vulnerable" plaque with a predisposition to destabilize and induce a cardiac event. Furthermore, approximately half of the patients with acute coronary syndromes demonstrate no prior symptoms of ischemia or angiographically evident disease. Recent findings have indicated that apart from cardiovascular risk factors, genetics, and other unknown factors, local hemodynamic forces, such as endothelial shear stress, blood flow patterns, and endothelial dysfunction of the epicardial and microvascular coronary arteries, are associated with the progression of coronary plaque and the development of cardiovascular complications with complex interactions. In this review article, we summarize the mechanisms that affect coronary artery plaque progression, indicating the importance of endothelial shear stress, endothelial dysfunction of epicardial and microvascular vessels, inflammation, and their complex associations, underlying in parallel the clinical perspectives of these findings.
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Siasos et al. (2023) studied this question.
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