Vessel, plaque, and lumen morphology after transluminal balloon angioplasty. Quantitative study in distended human arteries.

Abstract

We performed transluminal balloon angioplasty In 24 cadaver and nine amputated limb superficial femoral arteries under controlled experimental conditions. The cadaver arteries were excised, restored to in situ length, redistended, and maintained at 100 mm Hg Intraluminal pressure at 37° C throughout the anglographlc and dilation procedure and during fixation. The amputated limb arteries were dilated and pressure perfusion-flxed after dilation. Quantitative analysis of cadaver vessels revealed that arteries with prominent atherosclerotic lesions had the same internal elastic lamina (IEL) circumference (15.6 ± 1.0 mm) as those with little or no stenosis (16.8 ± 0.5 mm) but lumen area (8.8 ± 1 . 7 mm 2 ) was markedly reduced compared to nonstenotlc sites (20.0 ± 1.9 mm 2 , p < 0.01). Lesions occupied 49 ± 6% of the area circumscribed by the IEL In cadaver arteries with prominent plaques. After dilatation, lumen areas at stenotic sites were enlarged 43% on hlstologic sections (12.6 ± 1.8 mm 2 vs 8.8 ± 1 . 7 mm 2 , p < 0.

Intravascular ultrasound imaging following balloon angioplasty

“…The tear was frequently associated with a dissection plane between the plaque and the internal elastic membrane. These observations by intravascular ultrasound are similar to previously reported histologie in vitro studies or pathologic studies in patients who died following coronary balloon angioplasty [3]. In several instances, the ultrasound images also visualized the presence of an intimal flap (Fig.…”

Coronary artery vasoconstriction routinely occurs after percutaneous transluminal coronary angioplasty. A quantitative arteriographic analysis.

“…In an in vitro model of balloon angioplasty in rabbit aorta and pig carotid arteries, only severe degrees of arterial stretching (e.g., >60-70% beyond physiological relaxed diameter) produced significant impairment of arterial vasoconstrictor responsiveness. 13 In contrast to the findings of angioplasty-induced arterial paralysis cited above, there is evidence in both animal models" [1][2][3][4][5][6][7][8][9][10][11][12][13] that intravascular thrombus formation may occur despite full heparinization, it is unlikely that the loss of coronary artery diameter after PTCA was primarily the result of thrombus formation because no intraluminal filling defects were identified even in those cases in which orthogonal projections were analyzed. More importantly, nitroglycerin was very effective in both reversing and preventing the loss of diameter after PTCA, a finding that would not be expected if the luminal compromise were due primarily to thrombus.…”

A Numerical Model to Study the Interaction of Vascular Stents with Human Atherosclerotic Lesions

“…7 The initial cracks are placed at the edges of the plaque (the plaque shoulder) because experimental studies indicate these locations as the most prominent ones to plaque rupture. 27,29 The arterial slice described above is depicted in Fig. 1(II).…”

“…22,38 The proposed computational model also attempts to provide a deeper insight into the dominating effect of plaque fissuring and dissection during stenting. 5,27,29 This is performed by introducing two (small) initial cracks near the edges of the plaque.…”