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Published on: February 3, 2021
Therapeutic approaches to the control of coronary atherosclerosis
1Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Vic., Australia.
Insights
Atherosclerosis involves plaque buildup and rupture. Therapies targeting cholesterol and blood pressure, like calcium antagonists, can help manage this complex cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Pathology
- Pharmacology
Background:
- Atherosclerosis is a complex, multifactorial disease characterized by plaque formation and rupture.
- Early lesion development involves lipid accumulation, monocyte infiltration, and smooth muscle cell proliferation.
- Young, fragile atherosclerotic lesions are prone to rupture, leading to hemorrhage and thrombosis.
Purpose of the Study:
- To outline the key events in atherosclerotic lesion formation and rupture.
- To discuss therapeutic strategies for managing atherosclerosis, focusing on risk factor reduction and interfering with lesion development.
Main Methods:
- Review of the pathological cascade of atherosclerosis.
- Analysis of therapeutic interventions, including lipid-lowering agents and calcium antagonists.
Main Results:
- Identification of key cellular and molecular events in early and late lesion development.
- Highlighting the role of hypertension and hypercholesterolemia as risk factors.
- Demonstrating the dual action of calcium antagonists in lowering blood pressure and impacting metabolic events.
Conclusions:
- Therapeutic interventions targeting risk factors like hypertension and hypercholesterolemia are crucial.
- Pharmacological agents, such as calcium antagonists, offer a dual approach by managing blood pressure and directly influencing atherosclerotic processes.
Abstract:
Atherosclerosis is a multifactorial disease which culminates in the ruptured plaque seen at autopsy. Hypercholesterolaemia, subintimal accumulation of lipid, monocyte adhesion followed by penetration across the endothelium, the conversion of monocytes to macrophages and smooth muscle cell proliferation and migration are some of the events involved in the early stages of lesion formation. Late events include the formation of excess ground substance and collagen, and the formation of the fibrotic cap. Young lesions tend to be more fragile than "old" calcified lesions, and it is these young lesions which rupture, haemorrhage and provide anchor points for platelets. Therapeutic interventions aimed at controlling lesion formation include those which reduce risk factors, including hypertension as well as those which interfere with the cascade of events involved in lesion formation. Agents which lower plasma cholesterol provide one approach. Another approach is to use calcium antagonists which not only lower blood pressure, but also directly interfere with some of the metabolic events involved in lesion formation.
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