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Coronary artery disease: pathogenesis and acute coronary syndromes
S G Worthley1, J I Osende, G Helft
1Cardiovascular Biology Research Laboratory, Zena and Michael A. Weiner Cardiovascular Institute, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029-6574, USA.
Insights
Atherosclerotic plaques can become fatal when disrupted and thrombosed, leading to acute coronary syndromes. Current therapies target these thrombotic complications to reduce cardiovascular disease mortality.
Area of Science:
- Cardiovascular Medicine
- Pathology
Background:
- Atherosclerotic diseases and thrombotic complications are leading causes of mortality and morbidity.
- Cardiovascular disease accounts for significant mortality in the United States.
- Plaque disruption is a critical step in converting silent atherosclerotic lesions into life-threatening conditions.
Purpose of the Study:
- To review current theories of atherogenesis.
- To explore how these theories impact the understanding of acute coronary syndromes.
Main Methods:
- Review of clinical, experimental, and postmortem evidence.
- Focus on the role of plaque disruption and thrombosis in acute coronary syndromes.
Main Results:
- Plaque disruption followed by acute thrombosis is central to acute coronary syndromes.
- Therapeutic strategies primarily aim to reduce thrombotic complications.
Conclusions:
- Understanding atherogenesis is key to comprehending acute coronary syndromes.
- Targeting thrombosis in atherosclerotic plaques is crucial for reducing mortality.
Abstract:
Atherosclerotic diseases and their thrombotic complications remain the leading causes of mortality and morbidity in Western society. In the United States, cardiovascular disease is responsible for one in every 2.4 (41.4%) deaths and is the leading single cause of mortality. Furthermore, the presence of atherosclerotic disease (defined as thickening of the arterial wall through the accumulation of lipids, macrophages, T-lymphocytes, smooth muscle cells, extracellular matrix, calcium and necrotic debris) is more prevalent, but by itself rarely fatal. The crucial, final common process for the conversion of a nonocclusive, often clinically silent atherosclerotic lesion to a potentially fatal condition is often plaque disruption. The mortality associated with atherosclerotic disease relates to the acute coronary syndromes, including acute myocardial infarction, unstable angina pectoris and sudden cardiac death. Substantial clinical, experimental and postmortem evidence demonstrates the central role that a superimposed acute thrombosis on a disrupted atherosclerotic plaque plays in the onset of acute coronary syndromes. Therefore, therapeutic approaches to date have focused on reducing such thrombotic complications of atherosclerotic plaques (i.e., antiplatelet, anticoagulant and thrombolytic therapies) to reduce the resulting morbidity and mortality. In this review, we will focus on the current theories of atherogenesis and how they impact on our understanding of acute coronary syndromes.