Tiefenbrunn A J, Sobel B E, Ludbrook P A
Cathet Cardiovasc Diagn. 1983;9(6):583-9. doi: 10.1002/ccd.1810090608.
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 less than .001) after nifedipine. Systolic arterial pressure at the time of angina declined from 143 +/- 20 mm Hg to 112 +/- 23 mm Hg (P less than .001). Consequently, the double product heart rate X systolic blood pressure was not changed significantly at the onset of chest pain (149 +/- 28 mm Hg X 10(-2) vs. 142 +/- 28 mm Hg X 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.
为了确定硝苯地平对起搏诱导型心绞痛有益作用的机制，对20例接受诊断性心导管检查的患者进行了研究。在左心室造影和冠状动脉造影后，在舌下含服20 mg硝苯地平之前和之后30分钟进行右心房起搏。每90秒将心率以每分钟增加10次搏动（bpm）的幅度递增，直至出现心绞痛。持续监测心电图、中心主动脉压和肺动脉闭塞压。硝苯地平治疗后，心绞痛发作时的平均起搏心率从107±12.6 bpm增加到140.6±19.9（P＜0.001）。心绞痛发作时的收缩压从143±20 mmHg降至112±23 mmHg（P＜0.001）。因此，胸痛发作时心率×收缩压的双乘积无显著变化（149±28 mmHg×10⁻² 与142±28 mmHg×10⁻²）。肺动脉闭塞压也无显著变化（10.4±4.4与10.5±5.9 mmHg）。因此，硝苯地平通过降低左心室后负荷，在给定心率下降低心肌需氧量，但并未提高缺血性疼痛的心率血压乘积阈值。这些结果表明，硝苯地平的外周动脉血管舒张作用导致心肌需氧量降低，这解释了其在固定性阻塞性冠状动脉疾病患者的这种情况下的抗心绞痛作用。
