Boden W E
Department of Veterans Affairs Medical Center, Boston, Massachusetts 02130.
J Cardiovasc Pharmacol. 1991;18 Suppl 9:S1-6.
The management of unstable angina continues to undergo rapid evolution as new therapies and techniques become increasingly available to clinicians. It appears that the pathogenesis of unstable angina involves endothelial factors (plaque rupture of fissure resulting in a complex coronary stenotic lesion) together with dynamic factors (including platelet aggregation, thrombosis, and altered coronary vasomotor tone), and therefore it is clear why the approach to the patient with acute coronary syndromes has become multidimensional. This article summarizes the current views of the pathogenesis of unstable angina, and the role that the above factors may play in the clinical syndrome of acute coronary insufficiency. In addition, the newer therapeutic approaches to the pharmacologic management of unstable angina are discussed, including the use of nitrates, heparin, aspirin, and beta-blockers. Increasingly, calcium-channel blockers are being utilized in the early pharmacologic management of unstable angina, particularly because these agents have a salutary effect on reducing increased coronary vasomotor tone, reducing myocardial oxygen demand while at the same time augmenting coronary blood flow, and decreasing platelet aggregation. Numerous small clinical trials have examined the role of intravenous calcium-channel-blocker therapy for the acute management of unstable angina. In particular, intravenous diltiazem appears to be both safe and efficacious in this setting, and may offer some advantages to intravenous nitroglycerin, when used in the Coronary Care Unit setting. Because diltiazem is a heart rate-lowering vasoactive drug, it may attenuate myocardial ischemia without causing reflex tachycardia associated with other vasoactive pharmacologic therapies. Several of these studies utilizing intravenous diltiazem in unstable angina are reviewed and discussed.
随着新的治疗方法和技术越来越多地为临床医生所用，不稳定型心绞痛的治疗方法持续快速演变。不稳定型心绞痛的发病机制似乎涉及内皮因素（斑块破裂或裂隙导致复杂的冠状动脉狭窄病变）以及动态因素（包括血小板聚集、血栓形成和冠状动脉血管舒缩张力改变），因此，对于急性冠状动脉综合征患者的治疗方法为何已变得多元化也就显而易见了。本文总结了目前对不稳定型心绞痛发病机制的观点，以及上述因素在急性冠状动脉供血不足临床综合征中可能发挥的作用。此外，还讨论了不稳定型心绞痛药物治疗的更新方法，包括硝酸盐、肝素、阿司匹林和β受体阻滞剂的使用。越来越多的钙通道阻滞剂被用于不稳定型心绞痛的早期药物治疗，特别是因为这些药物对降低冠状动脉血管舒缩张力增加、降低心肌需氧量、同时增加冠状动脉血流量以及减少血小板聚集具有有益作用。众多小型临床试验研究了静脉注射钙通道阻滞剂治疗不稳定型心绞痛急性发作的作用。特别是，静脉注射地尔硫䓬在这种情况下似乎既安全又有效，在冠心病监护病房使用时，可能比静脉注射硝酸甘油具有一些优势。由于地尔硫䓬是一种降低心率的血管活性药物，它可能减轻心肌缺血，而不会引起与其他血管活性药物治疗相关的反射性心动过速。本文对其中几项在不稳定型心绞痛中使用静脉注射地尔硫䓬的研究进行了综述和讨论。
