Keogh A M, Schroeder J S
Division of Cardiology, Stanford University School of Medicine, California 94305-5246.
J Cardiovasc Pharmacol. 1990;16 Suppl 6:S28-35.
Many detailed studies have demonstrated that calcium antagonists can suppress development of diet-induced atherosclerosis in the thoracic aorta of animals. A number of possible mechanisms have been proposed based on in vitro work, but the exact mechanism remains unclear. Alteration of serum lipid levels and blood pressure does not appear to be the common pathway. Differing effects between calcium antagonists of different classes indicate that the voltage-dependent calcium channel-blocking action common to all calcium antagonists is not the sole mechanism. Preliminary results of several major quantitative angiographic studies in human coronary artery disease have recently become available and indicate that calcium antagonists are able to retard the progression of existing lesions in humans also. There is also evidence that calcium antagonists may prevent the development of new lesions and, in some cases, induce lesion regression. Longer follow-up and further trials are required to assess the appropriateness of widespread clinical application of these agents in coronary artery disease, to determine the optimal timing for their introduction, and to define their mechanism of action in influencing the natural history of atherosclerosis.
许多详细研究表明,钙拮抗剂可抑制动物胸主动脉中饮食诱导的动脉粥样硬化的发展。基于体外研究工作,已提出多种可能的机制,但确切机制仍不清楚。血清脂质水平和血压的改变似乎并非共同途径。不同类别钙拮抗剂之间的不同作用表明,所有钙拮抗剂共有的电压依赖性钙通道阻滞作用并非唯一机制。几项关于人类冠状动脉疾病的主要定量血管造影研究的初步结果最近已经可得,表明钙拮抗剂也能够延缓人类现有病变的进展。也有证据表明,钙拮抗剂可能预防新病变的发生,并且在某些情况下,促使病变消退。需要更长时间的随访和进一步试验,以评估这些药物在冠状动脉疾病中广泛临床应用的适宜性,确定引入它们的最佳时机,并明确它们影响动脉粥样硬化自然病程的作用机制。