Related Experiment Videos
Plaque disruption and thrombosis. Potential role of inflammation and infection
1Atherosclerosis Research Center, Burn and Allen Research Institute, Los Angeles, California, USA. Shahp@cshs.org
Insights
Atherosclerotic plaque rupture and thrombosis precipitate acute coronary syndromes. Plaque stabilization strategies may reduce the risk of these life-threatening events by targeting plaque vulnerability.
Area of Science:
- Cardiovascular Biology
- Vascular Medicine
- Atherosclerosis Research
Background:
- Acute coronary syndromes are often precipitated by atherosclerotic plaque disruption and subsequent thrombosis.
- Plaque characteristics like lipid core size, fibrous cap integrity, and inflammation influence vulnerability.
- Biomechanical forces and endothelial dysfunction can trigger plaque rupture.
Purpose of the Study:
- To explore the concept of plaque stabilization as a strategy to prevent acute coronary syndromes.
- To identify factors contributing to atherosclerotic plaque vulnerability.
Main Methods:
- Review of in vitro and in vivo vascular biology studies.
- Analysis of indirect evidence from clinical trials on lipid-lowering and lifestyle interventions.
Main Results:
- Evidence supports plaque disruption and thrombosis as key events in acute coronary syndromes.
- Specific plaque features and biomechanical stresses contribute to vulnerability.
- Endothelial dysfunction plays a role in plaque rupture and thrombosis.
Conclusions:
- Interventions focused on plaque stabilization may reduce acute coronary syndrome risk.
- Plaque stabilization represents a potential clinical strategy for managing coronary atherosclerosis.
- Further human validation is needed for plaque stabilization therapies.
Abstract:
Considerable data from in vitro and in vivo studies of vascular biology, together with indirect evidence from clinical trials of lipid-lowering or modifying and lifestyle or risk factor modifying interventions, provide strong support for the concept that disruption of atherosclerotic plaque and subsequent thrombosis is a key precipitant of potentially lethal, acute coronary syndromes. Certain characteristics of plaques, including the size and composition of the lipid core, the structure and composition of the fibrous cap, and the presence of a local inflammatory process, predispose the plaque to disruption. Stresses resulting from biomechanical and hemodynamic forces acting on plaques may then trigger disruption, releasing the thrombogenic contents of the lipid core. Alterations in endothelial function may also contribute to vulnerability of plaque rupture and thrombosis. Therefore, interventions aimed at decreasing plaque vulnerability to disruption--all based on the concept of plaque stabilization--may reduce the risk of acute coronary syndromes. Although not yet rigorously validated in humans, plaque stabilization may prove to be an important clinical strategy for preventing the lethal consequences of coronary atherosclerosis.