Abstract
The development and progression of coronary artery disease depend on both incorporation of lipid and deposition of fibrin and platelets into the arterial wall, with subsequent growth of fibroblasts and smooth muscle cells, as recently reviewed.1,2 Lipid incorporation contributes to luminal narrowing and appears to predispose the vascular wall to vasoconstriction and injury and subsequent thrombus formation. Variable degrees of vascular injury and mural thrombosis lead to repeated subclinical and periodic acute events in the progression of atherosclerosis (Figure 2.1). Most of the arterial changes are subclinical without symptoms, but others are clinical and include the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death.
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Meyer, B.J., Badimon, L., Chesebro, J.H. (1999). Syndromes of Accelerated Atherosclerosis. In: Contemporary Concepts in Cardiology. Developments in Cardiovascular Medicine, vol 217. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5007-5_2
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DOI: https://doi.org/10.1007/978-1-4615-5007-5_2
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