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Updated: Aug 10, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Pathophysiology and clinical significance of atherosclerotic plaque rupture
1Cardiovascular Institute, Mount Sinai Medical Center, New York, NY 10029-6574, USA.
Insights
Atherosclerotic plaque rupture causes acute coronary syndromes, including myocardial infarction (MI). Despite advances, event rates remain high, necessitating improved treatment strategies for coronary artery disease.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Medical Research
Background:
- Acute coronary syndromes (ACS) like myocardial infarction (MI) and unstable angina are primarily caused by atherosclerotic plaque rupture and thrombosis.
- Sudden cardiac death is also frequently linked to atherosclerotic plaque disruption.
- Despite significant advancements in understanding atherosclerosis, patient outcomes after ACS remain suboptimal.
Purpose of the Study:
- To review the pathophysiology of atherosclerotic plaque development and rupture.
- To discuss the consequences of coronary plaque rupture.
- To examine current therapeutic strategies for acute coronary syndromes.
Main Methods:
- Literature review focusing on atherosclerotic plaque development and rupture.
- Analysis of the pathophysiology of acute coronary syndromes.
- Evaluation of existing treatments for ACS.
Main Results:
- Atherosclerotic plaque rupture is the key event leading to intracoronary thrombosis and ACS.
- Current understanding of plaque development and disruption has grown substantially.
- High event rates post-ACS indicate a need for more effective interventions.
Conclusions:
- Improved understanding of atherosclerotic plaque pathophysiology is crucial for advancing ACS treatment.
- Further research into plaque development and rupture mechanisms may lead to novel therapeutic targets.
- Enhanced treatment strategies are needed to reduce the high incidence of adverse events following acute coronary syndromes.
Abstract:
Atherosclerotic plaque rupture and resulting intracoronary thrombosis are thought to account for most acute coronary syndromes. These syndromes include unstable angina, non-Q-wave myocardial infarction (MI) and Q-wave MI. In addition, many cases of sudden cardiac death may be attributable to atherosclerotic plaque disruption and its immediate complications. Our understanding of the atherosclerotic process and the pathophysiology of plaque disruption has advanced remarkably. Despite these advances, event rates after acute coronary syndromes remain unacceptably high. This review will focus on the pathophysiology underlying atherosclerotic plaque development, the sequellae of coronary plaque rupture, and current therapies designed to treat the acute coronary syndromes. It is hoped that as our understanding of the atherosclerotic plaque improves, treatment strategies for the acute coronary syndromes will advance.
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