Inflammatory biomarkers and coronary heart disease: from bench to bedside and back

Abstract

Inflammation plays a pivotal role in all stages of atherosclerosis from endothelial dysfunction and plaque formation to plaque destabilization and disruption. Inflammatory biomarkers, originally studied to better understand the pathophysiology of atherosclerosis, have generated increasing interest among clinicians, because of their utility in the challenging problems of diagnosis and risk assessment of patients with suspected or proved coronary heart disease. Moreover, in fascinating perspective, they could be used as therapeutic target, counteracting initiation, progression, and development of complications of atherosclerosis. In this review, we will provide an overview of the more promising inflammatory biomarkers, focusing on their utility and limitations in the clinical setting.

Circulating biomarkers with preventive, diagnostic and prognostic implications in cardiovascular diseases

“…Several subsequent prospective studies have consistently shown that baseline IL-6 levels are powerful predictor of cardiovascular events in apparently healthy subjects [69]. In the Framingham Heart Study patients without history of AMI or HF but with elevated IL-6, TNF-alpha and CRP levels had a markedly increased risk of developing HF.…”

“…More than 40 prospective studies among apparently healthy individuals have demonstrated that baseline CRP level is an independent predictor of future cardiovascular events, even beyond the Framingham risk score, and that it determines an improvement of the net reclassification index [15,69,83,84]. These studies included both men and women, European and American populations and both middle-aged and elderly patients.…”

Can YKL-40 be a new inflammatory biomarker in cardiovascular disease?

“…Inflammatory processes play a pivotal role in all stages of the development of both acute and chronic atherosclerosis, from the initial induction of endothelial dysfunction and plaque formation to plaque destabilization and disruption with superimposed thrombosis leading to acute MI or death (Biasillo et al 2010). During the entire process there is a contribution of activated inflammatory cells as neutrophils, lymphocytes, monocytes and resident macrophages, which are secreting pro-inflammatory cytokines.…”

The Role of Immune Inflammatory Reactions and Endothelial Dysfunction in Myocardial Remodeling and Progression of Ischemic Heart Disease

“…Представляются важными и данные о том, что повышенная экспрессия медиаторов воспаления (ФНО-α, ИЛ-1β, ИЛ-6, молекулы адгезии) наблюдается не только в крови, но и в миокарде [18,19,28]. Уси-ленная миокардиальная экспрессия цитокинов, обна-руживаемая при дисфункции миокарда, предполага-ет центральную роль цитокинов в развитии процессов ремоделирования миокарда и возникновении ХСН.…”