Ijem J, Granlie C
S D J Med. 2000 Nov;53(11):489-91.
There have been many recent articles published that emphasize the fact that cholesterol deposits are only one of many mechanisms through which acute coronary artery disease develops. Recently, a meta-analysis shows that only 14% of acute coronary events occur in stenotic lesions in coronary arteries that are greater than 70% occluded. The majority of acute coronary events (68%) occur in coronary arteries that have less than 50% stenotic lesions. The acute coronary syndrome is a very complex and unpredictable disease. Recent information now points to the endothelium as a modulating factor in the pathogenesis of coronary artery disease through the production of nitric oxide and angiotensin-II which maintain the homeostatic environment influencing the progression of coronary artery disease. With dysfunctional endothelium there seems to be an imbalance in terms of angiotensin production with regards to the nitric oxide production. This imbalance tends to promote coronary artery disease in individuals who have multiple risk factors. Furthermore, it has been suggested that certain inflammatory compounds are produced in a very dysfunctional endothelium, thereby propagating or leading to acute coronary syndromes. Specifically, this includes C-reactive protein which promotes chronic inflammation at various sites. There are also other acute phase reactants, such as fibrinogen, which may play a role in atherogenesis. Certain statin drugs, as they are called, tend to ameliorate the levels of the above acute phase reactants, while other statins do not. This reduction of coronary events by statins is independent of the LDL lowering benefits from statin drugs. This article delineates some of the beneficial effects of the different statin agents and points out that all statins are not equal in terms of their known lipid beneficial effects. For the practicing physician, choosing a particular statin agent is important. Some have more drug/drug interaction potential as compared with the others because of their inability to be metabolized through the cytochrome P450 system. There are also some, because of their lipophilic and hydrophilic nature, that tend to enter cells more readily than other statin agents. The effects conferred by these subtle differences among the currently available statins tend to be beneficial in patients with low to moderate levels of LDL cholesterol.
最近发表了许多文章，强调胆固醇沉积只是急性冠状动脉疾病发生的众多机制之一。最近一项荟萃分析表明，只有14%的急性冠状动脉事件发生在冠状动脉狭窄病变处，这些病变的阻塞程度大于70%。大多数急性冠状动脉事件（68%）发生在狭窄病变小于50%的冠状动脉中。急性冠状动脉综合征是一种非常复杂且不可预测的疾病。现在最新信息指出，内皮细胞通过产生一氧化氮和血管紧张素-II在冠状动脉疾病的发病机制中作为调节因子，维持影响冠状动脉疾病进展的内环境稳定。内皮功能障碍时，血管紧张素生成与一氧化氮生成似乎失衡。这种失衡往往会在有多种危险因素的个体中促进冠状动脉疾病。此外，有人提出在功能失调的内皮细胞中会产生某些炎症化合物，从而引发或导致急性冠状动脉综合征。具体来说，这包括促进各个部位慢性炎症的C反应蛋白。还有其他急性期反应物，如纤维蛋白原，可能在动脉粥样硬化形成中起作用。某些所谓的他汀类药物往往会改善上述急性期反应物的水平，而其他他汀类药物则不会。他汀类药物减少冠状动脉事件与他汀类药物降低低密度脂蛋白的益处无关。本文阐述了不同他汀类药物的一些有益作用，并指出就其已知的脂质有益作用而言，并非所有他汀类药物都一样。对于执业医生来说，选择特定的他汀类药物很重要。与其他药物相比，有些药物因无法通过细胞色素P450系统代谢而具有更多药物相互作用的可能性。也有一些药物，由于其亲脂性和亲水性，比其他他汀类药物更容易进入细胞。目前可用的他汀类药物之间这些细微差异所带来的影响往往对低密度脂蛋白胆固醇水平低至中等的患者有益。
