Ross R
Department of Pathology, University of Washington School of Medicine, Seattle.
Transplant Proc. 1993 Apr;25(2):2041-3.
The lesions of atherosclerosis represent a protective, inflammatory-fibroproliferative response against the different agents that can cause the disease. If the injury continues chronically over a sufficiently long period of time, and if opportunity is not given for restitution of normal architecture in the artery wall, lesions may progress to a point at which clinical sequelae develop. On the other hand, as demonstrated by Brown et al, Kane et al, and Blankenhorn et al, the advanced lesions of atherosclerosis can be shown to regress. A quantitative, statistical analysis of angiograms in patients who are aggressively treated with lipid-lowering agents, such as HMGCoA reductase inhibitors has clearly shown this to be the case. Thus, it is entirely conceivable that this chronic, excessive, inflammatory, and fibroproliferative response can be reversed, given sufficient opportunity for the factors that have led to the endothelial and arterial wall injury causing these events to be taken into hand and modified.
动脉粥样硬化病变代表了针对可引发该疾病的不同因素的一种保护性、炎症性纤维增生反应。如果损伤在足够长的时间内持续存在，并且不给动脉壁恢复正常结构的机会，病变可能会发展到出现临床后遗症的程度。另一方面，正如布朗等人、凯恩等人以及布兰肯霍恩等人所证明的，动脉粥样硬化的晚期病变可以显示出会消退。对积极使用降脂药物（如HMGCoA还原酶抑制剂）治疗的患者的血管造影进行定量统计分析，已清楚地表明情况确实如此。因此，完全可以想象，只要有足够的机会处理并改变导致这些事件的内皮和动脉壁损伤的因素，这种慢性、过度、炎症性和纤维增生性反应是可以逆转的。
