EFFECT OF DILTIAZEM ON CORONARY FLOW RESERVE IN PATIENTS WITH MICROVASCULAR ANGINA

Microvascular angina is characterized by ischemia-like symptoms in pat ients with normal coronary arteries and reduced coronary flow reserve. Clinical observations suggested an improvement in clinical symptomato logy and exercise tolerance after treatment with calcium antagonists. The effect of diltiazem on coronary flow reserve was evaluated in cont rols and in patients with microvascular angina. Coronary flow reserve was measured in 16 normotensive patients (7 females, 9 males, mean age 51 +/- 10 years) with angiographically normal coronary arteries. Coro nary blood flow was determined at rest, after dipyridamole (0.5 mg/kg) and following intravenous administration of diltiazem (10 mg) using c oronary sinus thermodilution technique. Coronary flow reserve was calc ulated as coronary blood flow after dipyridamole divided by coronary b lood flow at rest. Patients with normal coronary flow reserve (coronar y flow reserve > 2.0) received either dipyridamole alone (group 1, con trols, n = 6) or dipyridamole and diltiazem (group 2, n = 5), whereas patients with reduced coronary flow reserve (coronary flow reserve < 2 .0) obtained dipyridamole and diltiazem (group 3, n = 5). Resting coro nary flow was identical in the three groups, but after maximal vasodil ation with dipyridamole, coronary flow increased significantly more in groups 1 and 2 than in group 3 (P < 0.05, analysis of variance (ANOVA )). Coronary flow reserve was 2.5 in group 1 and 2.3 in group 2, but w as significantly reduced in group 3 (1.3; P < 0.05, ANOVA). Intravenou s diltiazem failed to increase coronary blood flow in groups 2 and 3. Therefore, diltiazem does not improve reduced coronary flow reserve in patients with microvascular angina, but leaves coronary flow reserve unaffected. The failure to ameliorate impaired coronary flow reserve w ith diltiazem is in contrast to the reported clinical improvement afte r calcium channel blockade in these patients. Thus, other factors such as structural abnormalities in the microcirculation or functional abn ormality in smooth muscle relaxation not responsive to calcium channel blockade are probably responsible for the occurrence of myocardial is chemia in patients with microvascular angina.