Ballantyne C M, Masri B M, Clubb F J, Radovancević B, Smith C W, Hawkins H K, Frazier O H, Willerson J T
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
Tex Heart Inst J. 1996;23(4):293-5.
The development of accelerated coronary artery disease after heart transplantation remains the limiting factor for long-term survival. The most widely accepted hypothesis to explain the development of this vascular lesion is chronic immunologic injury to the vessel wall, which leads to recruitment of monocytes and lymphocytes into the intima and to subsequent neointimal proliferation. In this report, we describe a case of accelerated coronary artery disease that led to allograft failure and repeat heart transplantation 3 years after the initial procedure. Pathologic examination showed striking intimal proliferation with abundant expression of intercellular adhesion molecule-1 in both endothelial cells and cells deep within the intima. Cardiac myocytes also stained for intercellular adhesion molecule-1, with the most intense staining noted in intercalated disks, whereas staining for E-selectin was restricted to endothelial cells. These findings are similar to those we observed in a canine model of transplant arteriopathy and highlight the need for further studies to examine whether inhibitors of endothelial cell adhesion molecules or their leukocyte ligands can successfully ameliorate transplant vasculopathy.
心脏移植后加速性冠状动脉疾病的发展仍然是长期生存的限制因素。解释这种血管病变发展的最广泛接受的假说是血管壁的慢性免疫损伤，这会导致单核细胞和淋巴细胞募集到内膜，并随后导致内膜增生。在本报告中，我们描述了一例加速性冠状动脉疾病病例，该病例导致初次手术后3年移植心脏失败并再次进行心脏移植。病理检查显示内膜显著增生，内皮细胞和内膜深层细胞中细胞间黏附分子-1大量表达。心肌细胞也表达细胞间黏附分子-1，在闰盘中染色最强烈，而E-选择素的染色仅限于内皮细胞。这些发现与我们在移植性动脉病犬模型中观察到的结果相似，并突出了进一步研究的必要性，以检查内皮细胞黏附分子或其白细胞配体的抑制剂是否能成功改善移植血管病变。
