The effect of diltiazem on coronary flow reserve in humans.
The effect of diltiazem on coronary flow reserve in humans.
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地尔硫卓对人体冠状动脉血流储备的影响。
DOI：
10.1161/01.cir.80.5.1240
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发表时间：
1989
期刊：
影响因子：
37.8
通讯作者：
Winniford,MD
中科院分区：
文献类型：
--
作者：
Rossen,JD;Simonetti,I;Marcus,ML;Braun,P;Winniford,MD
钙通道拮抗剂已被证明在短暂的冠状动脉闭塞后和在药物冠状动脉扩张期间的动物中钝最大冠状动脉流量。这种性质，如果存在于人体中，将导致冠状动脉血流储备减少，而冠状动脉循环没有内在异常。钙通道拮抗剂降低最大血管舒张能力也可能构成这些药物的重要抗缺血作用机制。为了评价钙通道拮抗剂对清醒人体冠状动脉血流储备的影响，我们使用冠状动脉多普勒导管和冠状动脉内罂粟碱测量了基线和静脉（125或250微克/千克推注，5微克/千克/分钟输注，n = 8）或冠状动脉内（150-600微克推注，n = 10）途径给予地尔硫卓后的冠状动脉血流储备。静脉注射地尔硫卓使心率从77 +/- 18降至72 +/- 17次/分（平均值+/- SD，p <0.005），平均动脉压从96 +/- 11降至86 +/- 15 mm Hg（p <0.005）。静脉注射地尔硫卓导致冠状动脉血流储备（峰值与静息流速比）从3.9 +/- 1.2降至3.6 +/- 1.1（p <0.01）。冠状动脉内给予地尔硫卓后，平均动脉压无变化（对照组99 +/- 12 mm Hg，地尔硫卓97 +/- 13 mm Hg），通过心房起搏维持心率恒定。冠状动脉血流储备在基线和冠状动脉内地尔硫卓后均为3.8 ± 0.9。因此，地尔硫卓治疗不会使用于诊断目的的冠状动脉血流储备测量无效。此外，这些结果表明，地尔硫卓对冠状动脉最大扩张的衰减不是其抗心绞痛作用的机制。
Calcium channel antagonists have been shown to blunt maximal coronary flow after brief coronary occlusion and during pharmacologic coronary dilation in animals. This property, if present in humans, would result in a reduction in coronary flow reserve in the absence of intrinsic abnormalities of the coronary circulation. A reduction of maximal vasodilator capacity by calcium channel antagonists could also constitute an important anti-ischemic mechanism of action of these agents. To evaluate the effect of calcium channel antagonists on coronary flow reserve in awake humans, we measured coronary flow reserve using the coronary Doppler catheter and intracoronary papaverine at baseline and after diltiazem administered by intravenous (125 or 250 micrograms/kg bolus, 5 micrograms/kg/min infusion, n = 8) or intracoronary (150-600 micrograms bolus, n = 10) routes. Intravenous diltiazem reduced heart rate from 77 +/- 18 to 72 +/- 17 beats/min (mean +/- SD, p less than 0.005) and reduced mean arterial pressure from 96 +/- 11 to 86 +/- 15 mm Hg (p less than 0.005). Intravenous diltiazem resulted in a small decrease in coronary flow reserve (peak-to-resting flow velocity ratio) from 3.9 +/- 1.2 to 3.6 +/- 1.1 (p less than 0.01). After intracoronary diltiazem, mean arterial pressure was unchanged (control 99 +/- 12 mm Hg, diltiazem 97 +/- 13 mm Hg), and heart rate was maintained constant by atrial pacing. Coronary flow reserve was unchanged at 3.8 +/- 0.9 at baseline and after intracoronary diltiazem. Thus, treatment with diltiazem does not invalidate the measurement of coronary flow reserve for diagnostic purposes. Furthermore, these results suggest that attenuation of maximal coronary dilation by diltiazem is not a mechanism responsible for its antianginal effects.