现有大量证据证明,在人类,由脂肪充填的细胞构成的未成熟脂肪斑纹,并非引起动脉粥样硬化大纤维斑块的前驱病变。有人发现:早期平滑肌细胞灶性内膜增生并没有胆固醇沉积的证据。并且己报导过30—50%白色纤维斑块内胆固醇含量是低的。在几种动物体内,可自发地产生低脂性增生病变。且常发于特定部位。并且,在饲以胆固醇时,这些部位可优先沉积胆固醇。因此,血浆胆固醇和脂蛋白在动脉粥样硬化中的作用,可能只是继发的和加剧的因素。而关键的问题是平滑肌细胞的开始增生。1973年 Benditt 氏兄弟提出了大多数人类 There is ample evidence that immature fat plaques in fat-filled cells in humans do not contribute to the prodromal pathology of atherosclerotic macrofibrillar plaques. It was found: early smooth muscle cell focal intimal hyperplasia and no evidence of cholesterol deposition. And cholesterol levels in 30-50% of white fiber plaques have been reported to be low. In several animals, low fat hyperplasia can spontaneously develop. And often in specific parts. And, when cholesterol is fed, these sites preferentially deposit cholesterol. Therefore, the role of plasma cholesterol and lipoproteins in atherosclerosis may be secondary and aggravating. The key issue is the beginning of proliferation of smooth muscle cells. In 1973 Benditt Brothers proposed most humans