Authors: Rossella R. Cacciola,; Francesca Guarino,; Riccardo Polosa,

Source: Current Medicinal Chemistry, Volume 14, Number 17, July 2007 , pp. 1887-1892(6)

Publisher: Bentham Science Publishers

Abstract:

Cigarette smoking plays a major role in the development of atherosclerosis and is associated with increased morbidity and mortality for coronary heart disease, stroke and peripheral vascular disease. In spite of the abundance of epidemiological evidence that links cigarette smoking to vascular disease, the pathologic mechanisms for such interaction are not clear. The endothelium is a major target organ that undergoes activation when exposed to common vascular triggers, including hypertension, hypercholesterolemia, hyperglycaemia and smoking. Changes in endothelial function may lead to a dysfunctional vascular phenotype characterized by anomalous responses of the vascular tone, abnormal endothelial proliferation and prothrombotic activation. Several studies have demonstrated that smoking may alter endothelial function by a direct toxic effect and consequently trigger haemostatic activation and thrombosis. In this article we will review the evidence that loss of normal endothelial function may result in a loss of the balance of the haemostatic system and in changes of the platelet physiology that may be relevant for the pathogenic effect of smoking on the development of atherothrombosis.

Keywords: Cigarette smoking; endothelium; platelet; haemostasis; thrombosis

Document Type: Research article

DOI: http://dx.doi.org/10.2174/092986707781058832

Affiliations: 1: Dipartimento di Medicina Interna e Specialistica, Ascoli-Tomaselli Hospitals - University of Catania, Via Passo Gravina 187, 95125 Catania, Italy.

Publication date: 2007-07-01

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