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Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
Published on: August 18, 2016
[Acute coronary thrombosis]
1INSERM U 541 Hôpital Lariboisière 75475 Paris. ziad.mallat@larib.inserm.fr
Insights
Atherosclerosis involves arterial wall inflammation. Inflammatory and apoptotic processes destabilize plaques, leading to thrombus formation and ischemic events.
Area of Science:
- Cardiovascular Biology
- Inflammation Research
- Pathology
Context:
- Atherosclerosis is a chronic inflammatory arterial disease.
- Ischemic events stem from thrombus formation on unstable atherosclerotic plaques.
- Plaque instability is linked to inflammatory and apoptotic processes.
Purpose:
- To elucidate the roles of inflammation and apoptosis in atherosclerotic plaque instability.
- To understand the mechanisms driving fibrous cap rupture and plaque thrombogenicity.
Summary:
- Inflammatory mediators contribute to smooth muscle cell loss and collagen degradation, causing fibrous cap rupture.
- Apoptosis is a key determinant of plaque thrombogenicity.
- Plaque erosion (40%) and rupture (60%) lead to thrombus formation.
Impact:
- Highlights the critical involvement of inflammatory and apoptotic pathways in atherothrombosis.
- Provides insights into mechanisms underlying plaque destabilization and ischemic complications.
- Informs potential therapeutic strategies targeting inflammation and apoptosis in atherosclerosis.
Abstract:
Atherosclerosis is an inflammatory disease of the arterial wall. Ischaemic manifestations of atherosclerosis are mainly due to thrombus formation upon a superficially eroded (denudation of luminal endothelium, 40% of cases) or deeply ruptured (fibrous cap rupture, 60% of cases) plaques. Recent studies have unraveled potentially critical roles for both inflammatory and apoptotic processes in plaque unstability leading to thrombus formation. Pro-inflammatory mediators have been particularly implicated in the loss of smooth muscle cells and the promotion of collagen degradation that are responsible for fibrous cap rupture, whereas apoptosis has been identified as one of the major determinants of plaque thrombogenicity.
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