Symptomatic restenosis after carotid percutaneous transluminal angioplasty

Abstract

She elected to have carotid endarterectomy, which was performed in October, 1997. Pathologically, the plaque was composed of dense connective tissue with calcification. A few macrophages were present. Newer connective tissue with loosely arranged collagen was superimposed on the older plaque material. These areas of new connective tissue were rich in connective tissue proteoglycans and had a characteristic arrangement of smooth-muscle cells in a storiform pattern. The appearances were characteristic of accelerated smoothmuscle proliferation (figure). The finding of smooth-muscle proliferation rather than recurrent atherosclerosis after restenosis is consistent with the hypothesis that this patient’s recurrent symptoms after carotid PTA resulted from haemodynamic rather than embolic mechanisms. The precipitation of the transient ischaemic attack by a hot bath strongly suggests that vasodilatation and relative hypotension decreased cerebral perfusion. Haemodynamic symptoms are uncommon in the cerebral circulation because of the collateral supply provided by the circle of Willis. In our patient, however, this mechanism is likely to have been deficient because her restenosis was severe and her contralateral internal carotid artery was occluded. Such severe impairment of collateral supply is uncommon and, assuming that most restenoses after carotid PTA have a similar pathology to our patient, may explain why recurrent symptoms are much rarer after carotid PTA than after coronary PTA.