Hypertension and hyperlipidaemia are major risk factors for the development of atherosclerosis. Calcium channel blockers (CCBs) have been used for decades and have established antihypertensive effects. Statins have been extensively used because of their potent lipid lowering properties. Amongst other factors, inflammation and oxidation are involved in enhanced progression of atherosclerosis and new lesion development. Therefore, research has been initiated focusing on the antioxidant and anti-inflammatory properties of CCBs and statins, beyond their primary effect, in order to evaluate the possible additive effects of combined treatment of CCBs with statins as antiatherosclerotic therapy. Clinical studies (e.g., the International Nifedipine Trial on Antiatherosclerotic Therapy [INTACT]) have demonstrated that the antiatherosclerotic action of CCBs is limited to the attenuation of the first stage of atherosclerogenesis (fatty streak formation or new lesion growth). The lesions that pre-existed at the start of CCB therapy did not demonstrate progression or regression on angiography. However, because the mechanisms of action of lipid-lowering drugs and CCBs, and their role in preventing the progression of atherosclerosis differ, it is conceivable to conclude that these two classes may have an additive or synergic effect, not only on new lesion formation but also on inhibiting the progression of established coronary atherosclerosis. Indeed, this combined effect of lipid-lowering therapy and CCBs on human coronary atherosclerosis has been reported in the Regression Growth Evaluation Statin Study (REGRESS) trial. This beneficial effect of combining CCBs with statins has now been replicated in transgenic atherosclerotic mice, where the combination of amlodipine and atorvastatin produced an additional 60% reduction of atherosclerosis compared with that observed with the statin alone. Serum markers of atherosclerosis and vascular integrity also improved most in the combination group. Synergistic effects of the combination of atorvastatin and amlodipine on acute nitric oxide release/endothelial function, and additive effects of the combination of amlodipine and atorvastatin in the improvement of arterial compliance in hypertensive hyperlipidaemic patients has been demonstrated. Collectively, these studies support the clinical antiatherosclerotic advantages of combination of CCBs and statins and in particular, of atorvastatin with amlodipine beyond their established antihyperlipidaemic and antihypertensive modes of action.

译文

高血压和高脂血症是动脉粥样硬化发展的主要危险因素。钙通道阻滞剂 (ccb) 已经使用了数十年,并已建立了抗高血压作用。他汀类药物因其有效的降脂特性而被广泛使用。除其他因素外,炎症和氧化参与动脉粥样硬化的进展和新的病变发展。因此,已经开始研究CCBs和他汀类药物的抗氧化和抗炎特性,超越其主要作用,以评估CCBs与他汀类药物联合治疗作为抗动脉粥样硬化疗法的可能的累加作用。临床研究 (例如,国际硝苯地平抗动脉粥样硬化治疗试验 [完整]) 表明,CCBs的抗动脉粥样硬化作用仅限于动脉粥样硬化发生的第一阶段 (脂肪条纹形成或新病变生长) 的衰减。CCB治疗开始时预先存在的病变在血管造影上没有显示出进展或消退。但是,由于降脂药物和ccb的作用机制以及它们在预防动脉粥样硬化进展中的作用不同,因此可以得出结论,这两类药物不仅对新的病变形成具有累加或协同作用,而且对抑制已建立的冠状动脉粥样硬化的进展。实际上,降脂治疗和CCBs对人冠状动脉粥样硬化的联合作用已在回归生长评估他汀研究 (REGRESS) 试验中报道。现在已经在转基因动脉粥样硬化小鼠中复制了将CCBs与他汀类药物组合的这种有益作用,其中与单独使用他汀类药物观察到的相比,氨氯地平和阿托伐他汀的组合产生了额外的动脉粥样硬化60% 降低。在联合组中,动脉粥样硬化和血管完整性的血清标志物也得到了最大的改善。已证明阿托伐他汀和氨氯地平联合使用对急性一氧化氮释放/内皮功能的协同作用,以及氨氯地平和阿托伐他汀联合使用对改善高血压高脂血症患者动脉顺应性的累加作用。总的来说,这些研究支持CCBs和他汀类药物,尤其是阿托伐他汀和氨氯地平的临床抗动脉粥样硬化优势,超出了其既定的抗高脂血症和抗高血压作用方式。

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