A physical measurement of the mechanisms of transluminal angioplasty.
We report a quantitative determination of the relative contribution of various factors leading to arterial lumen enlargement during transluminal angioplasty. Mechanical tests were conducted on both normal and atherosclerotic artery necropsy specimens. In the range of dilating pressures tested (0 to 3.4 atm or 0 to 50 lb/in2), content extrusion of fluid from the plaque accounted for 6% to 12% of the overall lumen area increase, while compaction of the plaque accounted for only 1% to 1.5%. Most of the increase (86.8% to 93%) was due to plaque and arterial wall disruption. The mechanism of disruption involved shearing of the plaque from the underlying artery at relatively low dilating pressures, followed by longitudinal tearing in the arterial wall at higher pressures. Diseased arteries were observed to dilate significantly more than nondiseased arteries at dilating pressures greater than or equal to 1.36 atm or 20 lb/in2 (P less than 0.05). In the range of stenoses tested (10% to 50% based on diameter reduction), the mean dilating pressure required to increase the lumen cross-sectional area by 50% was approximately 1.5 atm or 22 lb/in2. Based on these studies, we conclude that balloon dilatation results arise mainly from plaque and arterial wall disruption.
D000800:Angioplasty, Balloon; D001158:Arteries / Q000503:physiopathology; D001161:Arteriosclerosis / Q000503:physiopathology; D001794:Blood Pressure; D004108:Dilatation, Pathologic; D006801:Humans; D008955:Models, Cardiovascular