Significance of Intraplaque Hemorrhage for the Development of High-Risk Vulnerable Plaque: Current Understanding from Basic to Clinical Points of View

Acute coronary syndromes due to atherosclerotic coronary artery disease are a leading cause of morbidity and mortality worldwide. Intraplaque hemorrhage (IPH), caused by disruption of Intraplaque leaky microvessels, is one of the major contributors of plaque progression, causing a sudden increase in plaque volume and eventually plaque destabilization. IPH and its healing processes are highly complex biological events that involve interactions between multiple types of cells in the plaque, including erythrocyte, macrophages, vascular endothelial cells and vascular smooth muscle cells. Recent investigations have unveiled detailed molecular mechanisms by which IPH leads the development of high-risk vulnerable plaque. Current advances in clinical diagnostic imaging modalities, such as magnetic resonance image and intra-coronary optical coherence tomography, increasingly allow us to identify IPH in vivo. To date, retrospective and prospective clinical trials have revealed the significance of IPH as detected by various imaging modalities as a reliable prognostic indicator of high-risk plaque. In this review article, we discuss recent advances in our understanding for the significance of IPH on the development of high-risk plaque from basic to clinical points of view.

Automated summary

Acute coronary syndromes due to atherosclerotic coronary artery disease are a leading cause of morbidity and mortality worldwide. Intraplaque hemorrhage (IPH) is a major contributor to plaque progression, causing sudden plaque volume increase and destabilization. Recent studies have revealed the intricate cellular interactions and molecular mechanisms involved in IPH. Advances in diagnostic imaging modalities have allowed for in vivo identification of IPH, which has been shown to be a reliable prognostic indicator of high-risk plaque. This review discusses the significance of IPH on the development of high-risk plaque from both basic and clinical perspectives.