Pathophysiology of vascular endothelium and circulating platelets: implications for coronary revascularisation and treatment.

Constant vasodilatation, inhibition of platelet and leukocyte adhesion, and local thrombolysis are the mechanisms through which an intact endothelial layer exerts its protective action on coronary circulation. A loss in these features is not only the first step in the development of atherosclerosis, but also a potent trigger for complications after revascularisation procedures. Percutaneous coronary interventions, particularly in the course of stenting, induce endothelial injury that can last up to months after the procedure. On the other hand, the preservation of endothelial function appears the best feature of arterial versus venous grafts after coronary bypass surgery. An early diagnosis either by invasive or non-invasive techniques has important implications for prognosis, and endothelial dysfunction can be effectively counteracted by medical treatment (ACE inhibitors, statins). Activated circulating platelets are present in the course of coronary artery disease, increasing the risk of thrombotic occlusion and/or plaque regrowth, after both percutaneous and surgical revascularisation. New antiplatelet agents are under development to reduce endothelium-platelet interaction. On the basis of the latest studies, coronary revascularisation should be integrated in a more complete treatment, which would take into account the complex processes involving the underlying atherosclerotic plaque.