4.6 Review

Plaque Structural Stress: Detection, Determinants and Role in Atherosclerotic Plaque Rupture and Progression

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fcvm.2022.875413

关键词

plaque structural stress; atherosclerosis; plaque rupture; computational modeling; intravascular imaging

资金

  1. British Heart Foundation (BHF) [FS/19/66/34658, PG/16/24/32090, RG71070, RG84554]
  2. National Institute of Health Research Cambridge Biomedical Research Center
  3. BHF Center for Research Excellence

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Atherosclerosis is a major cause of death globally, with myocardial infarctions often resulting from rupture or erosion of coronary plaques. Imaging modalities alone have limited ability to accurately assess plaque risk, necessitating the use of additional biomarkers. Plaque structural stress (PSS), which incorporates various variables, has been shown to be correlated with acute coronary syndrome, plaque rupture, and major adverse cardiovascular events, offering valuable prognostic information beyond imaging. This review explores the methods for calculating PSS, the imaging modalities used for modeling PSS, and the potential for refining treatment options and predicting future events based on PSS.
Atherosclerosis remains a major cause of death worldwide, with most myocardial infarctions being due to rupture or erosion of coronary plaques. Although several imaging modalities can identify features that confer risk, major adverse cardiovascular event (MACE) rates attributable to each plaque are low, such that additional biomarkers are required to improve risk stratification at plaque and patient level. Coronary arteries are exposed to continual mechanical forces, and plaque rupture occurs when plaque structural stress (PSS) exceeds its mechanical strength. Prospective studies have shown that peak PSS is correlated with acute coronary syndrome (ACS) presentation, plaque rupture, and MACE, and provides additional prognostic information to imaging. In addition, PSS incorporates multiple variables, including plaque architecture, plaque material properties, and haemodynamic data into a defined solution, providing a more detailed overview of higher-risk lesions. We review the methods for calculation and determinants of PSS, imaging modalities used for modeling PSS, and idealized models that explore structural and geometric components that affect PSS. We also discuss current experimental and clinical data linking PSS to the natural history of coronary artery disease, and explore potential for refining treatment options and predicting future events.

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