The mechanism of transluminal angioplasty: evidence for formation of aneurysms in experimental atherosclerosis.

Abstract

Quantitative histologic examination (morphometric analysis) of pressure-perfused rabbit atherosclerotic arteries was used to determine whether compression of atheromatous material occurs with transluminal angioplasty. Experimental atherosclerosis was developed in both iliac arteries, with transluminal angioplasty performed on the left iliac while the right iliac served as a nondilated control. Angiography showed equal degrees of luminal narrowing before angioplasty (p = NS). Angioplasty reduced the left iliac narrowing in all animals studied. Morphometric analysis of histologic sections of the left and right iliac arteries disclosed significant differences in luminal and total vessel areas (p < .05), whereas arterial wall (intima and media) areas were similar (p = NS). Dilated areas often demonstrated marked intimal splitting with dissection into the media. At higher magnification, loss of nuclear staining and dense layers of extracellular matrix consistent with stretching were frequently seen. It is concluded that the major mechanism of successful transluminal angioplasty is stretching of the vessel, resulting in localized aneurysm formation. Intimal splitting implies inelasticity of the neointima. No evidence of compression and remodeling of atheromatous material was disclosed in this study. Circulation 68, No. 5, 1136No. 5, -1140No. 5, , 1983 THE MECHANISM by which transluminal angioplasty dilates obstructive atherosclerotic lesions is not completely understood. Originally, it was proposed that the procedure remodeled the atheromatous material in the arterial wall by compressing it into a smaller volume,' with release of its fluid constituents.4 More recently, human postmortem57 and in vivo animal studies7'-0 investigating the histopathologic effects of transluminal angioplasty suggest an alternative mechanism of intimal splitting, dissection, and stretching rather than compression. In the present study, quantitative analysis of morphologic sections of pressureperfused dilated and control segments of rabbit iliac atherosclerotic lesions are compared to determine whether compression of the lesion or formation of aneurysm represents the mechanism of successful angioplasty.

Restenosis following transluminal angioplasty in experimental atherosclerosis.

“…Morphometric analyses of dilated vessels have verified that angioplasty works primarily through stretching of the vessel with localized aneurysm formation. 8 No evidence for compression of the atheroma could be demonstrated in these studies. In addition, we have shown 9 that acute embolization of lipid or debris does not occur in this model.…”

“…10 " 11 We and others 6 " 8 have previously shown that the rabbit is a suitable model for the study of transluminal angioplasty; the results of the immediate effects show a variety of histopathological findings including dramatic intimal splitting as well as dissection or stretching of the vessel wall. In addition, we have shown that the primary mechanism in angioplasty is stretching of the vessel wall and localized aneurysm formation.…”

“…In addition, we have shown that the primary mechanism in angioplasty is stretching of the vessel wall and localized aneurysm formation. 8 To examine the mechanism by which angioplasty may induce restenosis, we undertook this experimental animal study.…”

Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty.

“…The balloon size, ratio of inflated balloon diameter to diameter of adjacent normal artery, total number of balloon inflations, total duration of inflations and post-PTCA incidence of angiographic intimal dissection were not significantly different for the three lesion severity subgroups. A number of studies have demonstrated that the severity of arterial trauma after balloon angioplasty, as judged by the incidence of intimal dissection and acute closure after PTCA (15)(16)(17) or determined histologically after in situ angioplasty (18) or after angioplasty in the cholesterol fed rabbit model (19) is not necessarily related to the severity ofthe lesion being dilated. Severe vessel injury, for example, is often observed after balloon dilatation of moderate lesions (19).…”

“…A number of studies have demonstrated that the severity of arterial trauma after balloon angioplasty, as judged by the incidence of intimal dissection and acute closure after PTCA (15)(16)(17) or determined histologically after in situ angioplasty (18) or after angioplasty in the cholesterol fed rabbit model (19) is not necessarily related to the severity ofthe lesion being dilated. Severe vessel injury, for example, is often observed after balloon dilatation of moderate lesions (19). If, despite the above considerations, one assumes that there was substantially greater injury and platelet deposition in the more severely narrowed segments, one would expect to see an association between lesion severity and (platelet-mediated) vasoconstriction in the dilated segment paralleling the changes seen in the distal segment.…”