Salutary effect of nifedipine in pacing-induced angina: relation to afterload reduction.
Salutary effect of nifedipine in pacing-induced angina: relation to afterload reduction.
复制标题
硝苯地平对起搏引起的心绞痛的有益作用：与后负荷减少的关系。
DOI：
10.1002/ccd.1810090608
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Ludbrook,PA
中科院分区：
文献类型：
--
作者：
Tiefenbrunn,AJ;Sobel,BE;Ludbrook,PA
为了确定硝苯地平对起搏诱发的心绞痛有益作用的机制，对20例接受诊断性心导管插入术的患者进行了研究。左心室造影和冠状动脉造影后，右心房起搏前和舌下含服硝苯地平20 mg后30 min进行。心率每90秒增加10次/分钟（bpm），直至发生心绞痛。连续监测心电图、中心主动脉压和肺动脉闭塞压。心绞痛发作时的平均起搏心率从107 ± 12.6次/分增加到140.6 ± 19.9次/分（P <0.001）。心绞痛时的收缩压从143 ± 20 mm Hg降至112 ± 23 mm Hg（P <0.001）。因此，在胸痛发作时，双乘积心率×收缩压没有显著变化（149 ± 28 mm Hg × 10 − 2vs. 142 ± 28 mm Hg × 10 − 2）。肺动脉闭塞压也没有显著变化（10.4 ± 4.4 vs. 10.5 ± 5.9 mm Hg）。因此，硝苯地平通过减少左心室后负荷而降低给定心率下的心肌需氧量，但不增加缺血性疼痛的心率-压力乘积阈值。这些结果表明，硝苯地平的外周动脉血管扩张作用，从而降低心肌氧需求，占其抗心绞痛作用，在这种情况下，在固定的阻塞性冠状动脉疾病患者。
To determine the mechanisms responsible for beneficial effects of nifedipine in pacing‐induced angina pectoris, 20 patients undergoing diagnostic cardiac catheterization were studied. Following left ventriculography and coronary arteriography, right atrial pacing was performed before and 30 min after administration of 20 mg of nifedipine sublingually. Heart rate was increased by 10‐beat‐per‐minute (bpm) increments every 90 sec until angina occurred. Electrocardiogram, central aortic pressure, and pulmonary arterial occlusive pressure were monitored continuously. Mean paced heart rate at the onset of angina was increased from 107 ± 12.6 bpm to 140.6 ± 19.9 (P <.001) after nifedipine. Systolic arterial pressure at the time of angina declined from 143 ± 20 mm Hg to 112 ± 23 mm Hg (P <.001). Consequently, the double product heart rate × systolic blood pressure was not changed significantly at the onset of chest pain (149 ± 28 mm Hg × 10−2vs. 142 ± 28 mm Hg × 10−2). Pulmonary arterial occlusive pressure also did not change significantly (10.4 ± 4.4 vs. 10.5 ± 5.9 mm Hg). Thus, nifedipine decreased myocardial oxygen demand at a given heart rate by reducing left ventricular afterload, but did not increase the rate pressure product threshold for ischemic pain. These results indicate that peripheral arterial vasodilator effects of nifedipine, with a resultant decrease in myocardial oxygen requirements, account for its antianginal effect in this setting in patients with fixed obstructive coronary artery disease.