Restenosis after percutaneous transluminal coronary angioplasty--anatomic and pathophysiological mechanisms. Strategies for prevention.

Abstract

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) probably results from pathophysiological mechanisms that are initiated during PTCA. Platelet deposition or exposed subendothelial connective tissue initiates complex blood element and vessel wall interactions that are not completely understood and leads to a proliferative response at the site of injury. The incidence of restenosis is also related to clinical, anatomic, and procedural variables. An increased frequency of restenosis is seen in patients who have recent onset of angina, unstable angina, or vasospastic angina, and in those who have diabetes. Stenoses in the proximal left anterior descending coronary artery, the ostium of the right coronary artery, and the proximal portion of a bypass vein graft have higher rates of restenosis than lesions at other sites. Restenosis can be predicted by an incomplete PTCA, which is identified by a high residual pressure gradient across the stenosis. Mechanical and pharmacological methods of preventing restenosis are under investigation. Intravascular stenting with expandable metal sleeves and laser angioplasty have shown encouraging results. Longer balloon inflation time can help prevent early elastic recoil. Platelet inhibitors (e.g., aspirin, dipyridamole, and sulfinpyrazone) do not appear to have an effect on restenosis. Agents, however, that interfere with platelet deposition at the PTCA site and that modify the effect of platelet-derived growth factor and medial cell proliferation show promise for control of restenosis.