Editorial Comment Medical Therapy of Chronic Stable Angina Pectoris

O ur understanding of chronic stable angina is gradually expanding, and two theories have developed in recent years. First, in patients with chronic stable angina, residual coronary flow reserve can be modulated to an important extent by dynamic changes in the caliber of pliable coronary artery stenoses with preserved muscular media.' This theory, coupled with the evidence of the remarkable efficacy of calcium antagonists in variant angina, suggested that these compounds could be very effective in the treatment of chronic stable angina. Second, asymptomatic episodes of ischemia are frequently detected by ambulatory electrocardiographic monitoring, and their causes are likely to be the same as those causing painful attacks. The results of a careful multicenter, double-blind, crossover study by Stone et a12 reported in this issue of Circulation, show that nifedipine has no significant anti-ischemic effect and that propranolol is much more effective than diltiazem in preventing asymptomatic ischemia but equally effective in preventing angina. Taken at face value, these observations seem inconsistent with the idea that coronary vasoconstriction contributes to the occurrence of ischemic episodes and that the causes of painful and painless episodes are the same. These apparent discrepancies remind us that we are attempting to prevent ischemic episodes by interfering with varying mechanisms of ischemia that are still incompletely understood. To interpret the intriguing results of the study by Stone et al, it is useful to briefly review the pathogenetic