Systemic and local inflammation in patients with unstable atherosclerotic plaques.
The response to injury in the vasculature and the heart is inflammation. Atherosclerosis is often the result of injury followed by inflammation and atherosclerosis. Vascular and myocardial infections from various pathogens, including viruses, bacteria, chlamydia, and other infections result in vascular inflammation and almost certainly play a role in the development of atherosclerosis and acute coronary heart disease syndromes in at least some patients. Current evidence favors prior exposure to multiple pathogens as most likely playing a role in initiating inflammation and contributing to atherosclerosis. Genetic predisposition is almost certainly an important factor in the development of inflammation, impaired endothelial vascular repair, vascular infection, thrombosis, and atherosclerosis. The aging process itself is most likely associated with altered vascular and myocardial defense mechanisms predisposing to inflammation. The oxidation of cholesterol and low-density lipoprotein (LDL) leads to the production of oxidized radicals that promote vascular inflammation. Interventional injury, including angioplasty and stenting, causes endothelial inflammation, thrombosis, and fibroproliferation. Systemic evidence of inflammation identifies patients at high risk of future coronary events, including those who appear to be healthy initially as well as those with stable and unstable coronary heart disease syndromes. Increases in serum C-reactive protein (CRP) identify individuals at risk for future vascular events, including unstable angina, acute myocardial infarction, acute cerebrovascular accident, and sudden death. Similarly, systemic elevations in serum troponin 1, serum amyloid-like protein, fibrinogen, and interleukins-1, 2, 6, 8, and 18 identify patients with unstable angina and non-Q-wave myocardial infarction at increased risk for future coronary events. The presence of vascular inflammation may be detected by identifying temperature heterogeneity within plaques that demonstrate inflammation. In the future, the local evaluation of atherosclerotic plaques to detect the presence of inflammation coupled to measurements of systemic markers of inflammation, such as C-reactive protein, may help identify patients at increased risk and allow both local and systemic therapies that reduce their risk and prevent the development of acute coronary syndromes in at least some patients.
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