Sütsch G, Oechslin E, Mayer I, Hess O M
Department of Internal Medicine, University Hospital, Zürich, Switzerland.
Int J Cardiol. 1995 Nov 24;52(2):135-43. doi: 10.1016/0167-5273(95)02458-9.
Microvascular angina is characterized by ischemia-like symptoms in patients with normal coronary arteries and reduced coronary flow reserve. Clinical observations suggested an improvement in clinical symptomatology and exercise tolerance after treatment with calcium antagonists. The effect of diltiazem on coronary flow reserve was evaluated in controls 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. Coronary blood flow was determined at rest, after dipyridamole (0.5 mg/kg) and following intravenous administration of diltiazem (10 mg) using coronary sinus thermodilution technique. Coronary flow reserve was calculated as coronary blood flow after dipyridamole divided by coronary blood flow at rest. Patients with normal coronary flow reserve (coronary flow reserve > 2.0) received either dipyridamole alone (group 1, controls, 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 coronary flow was identical in the three groups, but after maximal vasodilation 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 was significantly reduced in group 3 (1.3; P < 0.05, ANOVA). Intravenous 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 with diltiazem is in contrast to the reported clinical improvement after calcium channel blockade in these patients. Thus, other factors such as structural abnormalities in the microcirculation or functional abnormality in smooth muscle relaxation not responsive to calcium channel blockade are probably responsible for the occurrence of myocardial ischemia in patients with microvascular angina.
微血管性心绞痛的特征是冠状动脉正常但冠状动脉血流储备降低的患者出现类似缺血的症状。临床观察表明，使用钙拮抗剂治疗后临床症状和运动耐量有所改善。在对照组和微血管性心绞痛患者中评估了地尔硫䓬对冠状动脉血流储备的影响。对16例冠状动脉造影正常的血压正常患者（7名女性，9名男性，平均年龄51±10岁）测量冠状动脉血流储备。使用冠状窦热稀释技术，在静息状态下、静脉注射双嘧达莫（0.5mg/kg）后以及静脉注射地尔硫䓬（10mg）后测定冠状动脉血流量。冠状动脉血流储备计算为双嘧达莫后冠状动脉血流量除以静息状态下冠状动脉血流量。冠状动脉血流储备正常（冠状动脉血流储备>2.0）的患者单独接受双嘧达莫（第1组，对照组，n=6）或双嘧达莫和地尔硫䓬（第2组，n=5），而冠状动脉血流储备降低（冠状动脉血流储备<2.0）的患者接受双嘧达莫和地尔硫䓬（第3组，n=5）。三组的静息冠状动脉血流量相同，但在用双嘧达莫进行最大程度血管扩张后，第1组和第2组的冠状动脉血流量增加明显多于第3组（P<0.05，方差分析）。第1组冠状动脉血流储备为2.5，第2组为2.3，但第3组显著降低（1.3；P<0.05，方差分析）。静脉注射地尔硫䓬未能增加第2组和第3组的冠状动脉血流量。因此，地尔硫䓬不能改善微血管性心绞痛患者降低的冠状动脉血流储备，但对冠状动脉血流储备无影响。地尔硫䓬未能改善受损的冠状动脉血流储备与这些患者在钙通道阻滞剂治疗后报告的临床改善情况相反。因此，其他因素，如微循环结构异常或对钙通道阻滞剂无反应的平滑肌舒张功能异常，可能是微血管性心绞痛患者发生心肌缺血的原因。
