We examined the influences of localized aortic valve damage on coronary artery blood flow and the prognosis in acute aortic regurgitation. Aortic regurgitation was produced in 18 open-chest dogs by extensively cutting one of the three aortic cusps with a nerve knife introduced via the cardiac apex. The dogs were separated into three groups of six dogs each. In each group the noncoronary cusp (NCC), the right coronary cusp (RCC), or the left coronary cusp (LCC) was cut. Aortic and left ventricular pressures; the phasic aortic, left anterior descending (LAD), and right coronary artery (RCA) blood flows; and electrocardiograms were simultaneously recorded before and after production of acute AR. All dogs in the NCC and RCC groups survived for at least 30 to 60 min, but all dogs in the LCC group died after 5 to 9 min of production of acute AR due to left ventricular failure. After 2 min of aortic regurgitation, the total, systolic, and diastolic LAD flows were 39 + 14, 19 9, and 20 8 ml/min (mean SD) inthe NCC group, 41 + 15, 31 ± 9, and 10 + 6 ml/min in the RCC group, and 9 + 5, 19 5, and -10 ± 2 ml/min in the LCC group, respectively. The
The purpose of this study was to evaluate the rupture and dissection of the vessel wall immediately after balloon dilatation by intravascular ultrasound (IVUS) imaging and to predict restenosis in patients who underwent subsequent coronary stent implantation. Stent implantation improves the long-term results of coronary angioplasty by reducing lesion elastic recoil and arterial remodeling. However, several studies have suggested that neointimal hyperplasia is the cause of instant restenosis. We recruited 60 patients in whom IVUS studies were performed immediately after successful balloon dilatation and just before stent implantation. We compared IVUS parameters with 6-month follow-up quantitative coronary angiography. This was performed in 51 lesions of 51 patients (85%). Qualitative analysis included assessment of plaque composition, plaque eccentricity, plaque fracture and the presence of dissection. In addition, minimal luminal diameter, percent diameter stenosis, percent area stenosis and plaque burden were quantitatively analyzed. Two morphological patterns after balloon dilatation were classified by IVUS. Type I was defined as absence or partial tear of the plaque without disclosure of the media to lumen (22 lesions). Type II was defined as a split in the plaque or dissection of the vessel wall with disclosure of the media to the lumen (29 lesions). At 6 months follow-up, angiographic restenosis occurred in 17 of the 51 lesions (33%). Restenosis was significantly (p < 0.05) more likely to occur in type II (13/29: 45% incidence) than in type I (4/22: 18% incidence). The assessment of plaque morphology immediately after balloon dilatation and before stent implantation provides important therapeutic and prognostic implications.
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