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Inflammation, infection and acute coronary plaque events

J.C. Kaski* and E.G. Zouridakis

Coronary Artery Disease Research Unit, Cardiological Sciences, St. George's Hospital Medical School, London, U.K.

* Correspondence: Professor Juan Carlos Kaski, MD, FRCP, FESC, FACC, Coronary Artery Disease Research Unit, Cardiological Sciences, St. George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, U.K.

Abstract

Aims In recent years it has become apparent that inflammatory and immune mechanisms are involved not only in the initiation and progression of atherosclerosis but also in the pathophysiology of atheromatous plaque disruption and the development of acute coronary syndromes. Fissuring and rupture of the fibrous cap that overlies the lipid-rich core of an atherosclerotic lesion has been recognized as the most common cause of acute coronary thrombosis and acute coronary events. Hence, the integrity of the fibrous cap is a crucial determinant of plaque stability.

Methods and results This overview examines inflammatory and infectious factors that affect the integrity of the fibrous cap and hence the likelihood of acute coronary plaque events. Inflammatory cells such as activated macrophages within atherosclerotic lesions can express metalloproteinases — enzymes responsible for the degradation of collagen in the fibrous cap — while activated lymphocytes can suppress collagen synthesis. The result is a weakening of the fibrous cap, which can lead to the transformation of a lesion from ‘stable’ to ‘unstable’, and hence prone to rupture and thrombosis. Pro- and anti inflammatory cytokines control the complex interactions that take place between the different components of the inflammatory process. A number of recent studies have also provided increasing evidence that chronic infections by bacteria or viruses may play a contributory role in the inflammation that underlies active atherosclerotic lesions and the development of acute coronary syndromes.

Conclusion Despite the recognition of the major role of inflammation in atherogenesis and acute plaque events, the effects of anti-inflammatory treatments in primary and secondary prevention are still largely unknown. The emergence of novel agents with both anti-inflammatory and anti-platelet properties may help in the future to reduce the incidence of serious coronary events in high-risk patients.

Key Words: Acute coronary syndromes • atherosclerosis • anti-inflammatory • anti-platelet • unstable atheromatous plaques

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