Ischemia: Reperfusion Injury and Restenosis after Coronary Angioplasty

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Abstract
Percutaneous transluminal coronary angioplasty (PTCA) is a very effective technology that allows, without surgery, successful mechanical revascularization of acutely or chronically obstructed coronary arteries. The success of PTCA in patients with acute myocardial infarction or unstable angina is questioned by early coronary reocclusion and by so-called reperfusion injury. In a biochemical context, reperfusion injury occurs as a very complex interaction between the different tissues that build heart muscle. Free radicals play a pivotal role and initiate a deleterious cascade of events after reperfusion. Protective mechanisms such as superoxide dismutase, glutathione peroxidase, and catalase are normally present in the cell to prevent damage by free radicals. Endothelial cells have a greater number of specific physiologic and metabolic functions and influence the microcirculatory flow. In the presence of exogenous glucose, coronary endothelial cells show a pronounced lactate production under well-oxygenated conditions. Low energy demand and high glycolytic activity may be the cause of why the coronary endothelium is less severely injured than the cardiomyocytes in the ischemic and anoxic heart. The success of PTCA in patients with chronically obstructed coronary arteries (stable angina) is questioned by vessel occlusion and restenosis. Restenosis is a very complex process involving clinical, morphological, procedural, regional flow-dependent, and biological determinants. Early platelet deposition, formation of mural thrombus, coronary vasospasm, and elastic recoil forces of stretched vessel wall may contribute to early restenosis in the first days after PTCA, but the peak incidence of restenosis occurs between two and three months after PTCA. Intimal hyperplasia or proliferation of smooth muscle cells is believed to be the fundamental process of restenosis. To solve the problem of restenosis, much effort has been expended, which includes several technical and pharmacological approaches. Pharmacological strategies, systemically or locally administered, aim at increased vasomotor tone, platelet function, smooth muscle cell proliferation/migration, and fibrocollagenous healing. Up to now none of the proposed drugs has been able to reduce the restenosis rate. There is experimental evidence for a claim that the antioxidant functions of vitamins (E, C, and beta-carotene) may prevent restenosis post-PTCA. Until recently, in most post-PTCA restenosis trials the angiographic analyses were not performed using computerized measurement methods. In order to assess the efficacy of acute or long-term interventions on the natural course or acute complications of coronary artery disease, quantitative measures have been introduced and validated that make use of digital coronary angiography and computerized image processing techniques.(ABSTRACT TRUNCATED AT 400 WORDS)