Transluminal angioplasty: a mechanical-pathophysiological correlation of its physical mechanisms.

Abstract

We quantitatively determined 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 our range of dilating pressures (0-3.4 atm or 0-50 lb/in2), content extrusion of fluid from the plaque accounted for 6-12% of the overall lumen area increase, while compaction of the plaque accounted for only 1-1.5%. The majority of the increase, 86.8-93%, was due to plaque and arterial wall disruption. The mechanism of disruption began with shearing of the plaque from the underlying artery at relatively low dilating pressures and continued with longitudinal tearing and stretching of the arterial wall at higher pressures. Diseased arteries dilated significantly more than nondiseased arteries at dilating pressures greater than or equal to 1.36 atm or 20 lb/in2 (P less than .05). In the range of stenoses that were tested (10-50%), the mean dilating pressure required to increase the lumen cross-sectional area by 50% was approximately 1.5 atm or 22 lb/in2.