Pathogenesis and prevention of trauma-provoked atheromas

Arterial trauma in the presence of hyperlipidemia produces atheromas. We studied the pathogenesis of clamp injury in dogs with and without hyperlipidemia. Six dogs were operated on prior to induction of hyperlipidemia. Three clamps and loop occlusion were applied to both femoral arteries, both carotids, and the infrarenal abdominal aorta. Clamping was performed on normolipidemic control dog, and dissection without clamping was done on another hyperlipidemic control dog. These animals were put to death after 13 months. To determine the early effects of clamping, two additional normolipidemic controls were studied by perfusion fixation and scanning electron microscopy (SEM) l hour and 10 days respectively, after occlusion. The severity of the lesions in the animals was assessed by gross inspection and by light and scanning electron microscopy. No plaques occurred in the normolipidemic clamped control animals. Gross lesions were present in the femoral arteries of all hyperlipidemic animals at the sites of blade clamp application. No gross lesions were seen at the site of loop snare occlusion. Microscopically, the lesions were fibromuscular proliferative masses with lipid insudation and foam, cells. Early changes consisted of disruption of the internal elastic lamella and medial damage. Endothelial damage was noted on SEM 1 hour after clamping; by 10 days endothelial damage was more severe with adherence of platelets and fibrin. Loop snare occlusion and bulldog clamping produced minimal changes. Endothelial loss persisted after 13 months in clamped areas with scanty regrowth. The femoral arteries proved to be most sensitive to the development of progressive lesions. Trauma-provoked atheromas are caused by endothelial removal and disruption of the internal elastic lamella as well as medial damage. This results in smooth muscle proliferation. Loop snare occlusion produces negligible endothelial damage. Trauma-provoked atheromas can be minimized by measures which reduce arterial damage as well as by avoidance of subsequent hyperlipidemia.