Clinical promise of calcium antagonists in the angioplasty patient.

Abstract

Depending upon the definition used, restenosis occurs in 10-60% of patients who undergo percutaneous transluminal coronary angioplasty. Restenosis appears to be the result of a combination of pathophysiological processes, including elastic recoil of arterial walls, platelet deposition and thrombus formation and resultant fibro-cellular neointimal hyperplasia. A range of pharmacological interventions has been used in an attempt to reduce the rate of restenosis following angioplasty, with little success. Furthermore, many patients who undergo angioplasty still suffer from ischaemia after the procedure. Calcium antagonists, such as the long-acting dihydropyridine amlodipine, have been demonstrated to be effective in the control of both symptomatic and asymptomatic ischaemia and are, therefore, likely to be of utility for this purpose in angioplasty patients. Calcium antagonists also exhibit characteristics that may lead to a reduction in restenosis, in that they inhibit platelet aggregation, reduce vasoplasm and inhibit the action of mitogens which stimulate proliferation and migration of smooth muscle cells. The results of five trials of calcium antagonists in angioplasty patients have been individually unconvincing in terms of prevention of restenosis, only one trial demonstrated a significant effect. However, a meta-analysis of these results has demonstrated an approximately 30% reduction in the chance of restenosis in those patients treated with calcium antagonists. The Coronary Angioplasty Amlodipine in Restenosis (CAPARES) trial has been initiated to assess the impact of amlodipine upon the rate of restenosis and angina/ischaemia after the procedure.