January 1, 2001Cardiology in Review104 citations
View Full PaperInflammation and Coronary Heart Disease: An Overview
Key Result
Elevated levels of C-reactive protein are associated with an increased risk of cardiovascular disease events and increased efficacy of lipid-lowering therapy with pravastatin.
Structured PICO
Do markers of inflammation like C-reactive protein predict cardiovascular risk and the efficacy of therapies such as pravastatin in patients with coronary heart disease?
P
Population
Patients with or at risk for coronary heart disease and myocardial infarction
I
Intervention
Therapies targeting vascular inflammation, including lipid-lowering therapy with pravastatin
Systemic markers of inflammation, particularly C-reactive protein, play a key role in atherosclerosis and can help predict cardiovascular risk as well as the efficacy of lipid-lowering therapies.
Abstract
About half of the patients presenting with myocardial infarction do not have the classic risk factors. This finding has stimulated a search for other factors that may be responsible and, when present, may help to predict which patients are at greatest risk for myocardial infarction and other cardiovascular events. With improved understanding of the pathogenesis of ischemic heart disease, new insights into potential markers of underlying atherosclerosis and cardiovascular risk have been gained. In recent years, data have accumulated demonstrating that certain markers of inflammation--both systemic and local--play a key role in the development of atherosclerosis. Specifically, elevated levels of one systemic marker of inflammation, C-reactive protein, are associated with an increased risk of cardiovascular disease events. Moreover, potentially important associations have been established between elevated markers of inflammation, such as C-reactive protein and increased efficacy of established therapies; and, in particular, lipid-lowering therapy with the hepatic hydroxymethylglutaryl coenzyme A reductase inhibitor pravastatin. This article discusses the pathogenesis of atherosclerosis, the role of endothelial dysfunction and plaque rupture, and evidence for the role of inflammation and reviews how therapy might reduce vascular inflammation.