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Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,6
Online ISSN 1827-1898
Avanzas P. 1*, Arroyo-Espliguero R. 2*, Garcia-Moll X. 3, Kaski J. C. 4
1 Department of invasive Cardiology, Hospital Universitario Central de Asturias, Oviedo, Spain.
2 Department of Cardiology Hospital Universitario Guadalajara, Guadalajara, Spain.
3 Department of Cardiology
4 Coronary Artery Disease Research Unit Department of Cardiological Sciences St. George´s Hospital Medical School, London, UK
In the last decade, compelling evidence has evolved at both the basic science and clinical level for the implication of inflammation in the pathogenesis of atherosclerosis and its complications. The composition of the atherosclerotic plaque, rather than the degree of stenosis, is now recognized as a pivotal feature in determining plaque vulnerability and hence the risk of acute coronary ischaemic events. Current evidence supports a key role for inflammation in all phases of the atherosclerotic process, from plaque formation through to progression and, ultimately, the thrombotic complications of atherosclerosis. The growing appreciation of the role of inflammation in atherogenesis has focused attention on whether circulating levels of inflammatory biomarkers may help to identify those at risk of future cardiovascular events. In addition, the protective effects of a variety of interventions, such as statins, aspirin, and fibrates, are often associated with the evidence of reduced inflammation, further strengthening the notion that inflammation and the acute complications of atherosclerosis are causally related. The present review describes the pathophysiology of atheromatous plaque vulnerability and discusses the clinical use of inflammatory biomarkers for prognostic stratification of patients with acute coronary syndromes.