De Cesare N, Bartorelli A, Fabbiocchi F, Loaldi A, Montorsi P, Polese A, Guazzi M D
Istituto di Cardiologia, University of Milan, Italy.
Chest. 1988 Mar;93(3):485-92. doi: 10.1378/chest.93.3.485.
Changes induced by nifedipine (10 mg sublingually) in the residual luminal diameter of significant (greater than 50 percent) coronary lesions were assessed angiographically in 69 patients with effort-induced angina (group 1), in 22 patients with mixed angina (group 2), and in 14 patients with Prinzmetal's angina (group 3). These changes were related to the clinical response to treatment with the same drug, as evaluated through diary records and Holter monitoring in the mixed (spontaneous component) and Prinzmetal forms and through exercise testing in effort-induced and mixed (effort-associated component) angina. In groups 1 and 2, segments of stenotic vessels showed either an increase or decrease or no change in diameter with the calcium antagonist; in group 3, the majority of the lesions had compliant portions which invariably responded with dilatation. Nifedipine failed to improve cases with exertional (20 percent [14/69] unchanged; 19 percent [13/69] worsened) and mixed (41 percent [9/22] exacerbated) forms; 100 percent of the 14 patients with the Prinzmetal form had relief of the anginal episodes. In group 1, the response to exercise tests was dissociated from the short-term vasomotor pattern, and the pressure-rate product failed to explain the clinical results. Forty-five percent (ten) of the patients in group 2 showed significant short-term widening of critical stenoses, as well as obvious improvement; patients who did worse with treatment in this group had reacted to nifedipine with narrowing of critical stenoses. These data suggest that the response to nifedipine of classic effort-induced angina is probably the net result of an interaction of changes in myocardial oxygen consumption and supply; coronary vasomotion has a role in mixed angina, and influences of nifedipine may be either favorable or unfavorable; stenotic lesions in the Prinzmetal form are quite sensitive to the relaxant action of calcium blockade, and this probably represents a background to the highly positive clinical response to treatment.
在69例劳力性心绞痛患者（第1组）、22例混合性心绞痛患者（第2组）和14例变异型心绞痛患者（第3组）中，通过血管造影评估了硝苯地平（10毫克舌下含服）对严重（大于50%）冠状动脉病变残余管腔直径的影响。这些变化与使用同一药物治疗的临床反应相关，在混合性（自发性成分）和变异型心绞痛中通过日记记录和动态心电图监测评估，在劳力性和混合性（劳力相关成分）心绞痛中通过运动试验评估。在第1组和第2组中，狭窄血管段在使用钙拮抗剂后直径可增加、减少或无变化；在第3组中，大多数病变有顺应性部分，总是对扩张有反应。硝苯地平未能改善劳力性（20%[14/69]无变化；19%[13/69]恶化）和混合性（41%[9/22]加重）心绞痛病例；14例变异型心绞痛患者中有100%的心绞痛发作得到缓解。在第1组中，运动试验的反应与短期血管运动模式无关，压力-心率乘积无法解释临床结果。第2组中45%（10例）的患者显示关键狭窄有明显的短期增宽，以及明显改善；该组中治疗效果较差的患者对硝苯地平的反应是关键狭窄变窄。这些数据表明，经典劳力性心绞痛对硝苯地平的反应可能是心肌氧消耗和供应变化相互作用的净结果；冠状动脉血管运动在混合性心绞痛中起作用，硝苯地平的影响可能是有利的或不利的；变异型心绞痛中的狭窄病变对钙通道阻滞的舒张作用相当敏感，这可能是对治疗有高度阳性临床反应的背景。
