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Publications (5)26.75 Total impact

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    ABSTRACT: This study used angioscopy to determine the specific cause of vessel occlusion after percutaneous transluminal coronary angioplasty and compared the angiographic and angioscopic lesion morphologies in this setting. Occlusion of a dilated coronary artery is the major cause of morbidity and mortality after coronary angioplasty. Attempts to reopen occluded vessels are either empirically guided or directed by angiography, which has inherent limitations. Angioscopy, the in vivo direct visualization of the endovascular surface, is potentially a more accurate means of identifying the cause of vessel occlusion after angioplasty. Percutaneous coronary angioscopy was performed in 17 patients (17 vessels) after angiographic confirmation of postangioplasty vessel occlusion. Angioscopy demonstrated the primary cause of the postangioplasty occlusion to be dissection in 14 patients (82%) and intracoronary thrombi in 3 (18%). Compared with angioscopy, angiography was significantly less accurate in identifying the specific cause of the occlusion and correctly identified the cause of vessel occlusion in only 5 (29%) of 17 patients (p < 0.001), including 4 (29%) of 14 deep dissections and 1 (33%) of 3 occlusive thrombi. Angioscopy specifically identified the cause of occlusion in every patient, with coronary dissection the predominant cause of abrupt occlusion after coronary angioplasty. However, angiography was unable to identify a specific cause for vessel occlusion in the majority of our patients. Angioscopy may therefore prove useful in selecting specific treatment strategies for patients with abrupt occlusion after angioplasty, such as stent placement, atherectomy, repeat dilation or thrombolysis.
    Journal of the American College of Cardiology 06/1995; 25(7):1681-4. · 15.34 Impact Factor
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    ABSTRACT: The genesis of cardiac allograft vasculopathy has been linked to nonimmunologic endothelial injury. Studies evaluating the role of nonimmunologic risk factors have thus far been limited to angiographic assessment. Intravascular ultrasound can detect cardiac allograft vasculopathy before it becomes angiographically evident. To assess the influence of nonimmunologic risk factors in the development of cardiac allograft vasculopathy, we studied 101 consecutive cardiac transplant recipients who underwent intracoronary ultrasound imaging during routine, annual coronary angiography. Based on the severity of intimal thickening, patients were divided into 2 groups: group 1 = minimal, mild, or moderate intimal thickness; and group 2 = severe intimal thickness. Cardiac transplant recipients with severe intimal thickness had higher levels of total cholesterol (267 +/- 70 vs 227 +/- 41 mg/dl, p = 0.0008), low-density lipoprotein cholesterol (187 +/- 47 vs 139 +/- 31 mg/dl, p = 0.0001), and triglycerides (237 +/- 75 vs 182 +/- 88 mg/dl, p = 0.0004), a higher percentage of weight gain (12 +/- 4% vs 8 +/- 5%, p = 0.0001), a larger body mass index (30 +/- 4 vs 25 +/- 3, p = 0.0001), and older donor age (27 +/- 5 vs 23 +/- 7 years, p = 0.005) than recipients with mild or moderate intimal thickness. Multiple regression analysis established that total cholesterol, low-density lipoprotein cholesterol, triglyceride levels, obesity indexes, donor age, and years following cardiac transplantation (p < 0.01) were independent predictors of the severity of intimal thickening, and thus the severity of cardiac allograft vasculopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
    The American Journal of Cardiology 11/1994; 74(10):1042-6. · 3.43 Impact Factor
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    ABSTRACT: Despite advances in catheter-based interventional techniques, restenosis remains a major complication of angioplasty. Recently, intravascular ultrasound imaging (IVUS) has provided new insight into plaque composition and geometric distribution inside the vessel. To investigate if IVUS-defined parameters can predict restenosis in patients after coronary angioplasty, we performed IVUS in 33 patients (33 lesions) after balloon angioplasty (n = 25) or directional atherectomy (n = 8). Qualitative analysis included assessment of plaque composition, plaque eccentricity, plaque fracture, and presence of dissection. In addition, minimal luminal diameter, percent diameter stenosis, percent area stenosis, plaque burden, and elastic recoil were quantitatively analyzed. Follow-up data were obtained 1, 2, and 6 months after angioplasty and were available for 30 patients. Angiographic restenosis occurred in 11 patients (group 1), and no restenosis occurred in 19 patients (group 2) by clinical (n = 10) or angiographic (n = 9) assessment. Plaque fracture was noted in 30% of group 1 patients and 74% of group 2 patients (p = 0.04). Major dissections were more frequent in group I than in group II (78% vs 10%, p = 0.009). Of the quantitative parameters analyzed, plaque burden was significantly higher in group 1 than in group 2 (0.50 +/- 0.05 vs 0.34 +/- 0.05, p = 0.0001). In 78% of the patients with plaque burden of > 0.40, restenosis developed. Thus, of the various parameters analyzed, the absence of plaque fracture, the existence of a major dissection, and greater plaque burden were associated with increased incidence of restenosis. Our results indicate that IVUS can identify a subset of patients in whom restenosis is likely to develop. Information about the morphologic features of the atheroma and its composition may be used to modify the interventional strategy and thus optimize lumen size and possibly reduce the chance of restenosis.
    American Heart Journal 10/1994; 128(4):664-73. · 4.56 Impact Factor
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    ABSTRACT: Angioplasty of coronary saphenous vein grafts has been associated with less favorable results than in native coronary arteries owing to a higher acute complication rate and an increased incidence of restenosis. We placed 16 nonarticulated balloon expandable stainless steel "biliary" stents at the sites of 13 stenotic or occluded aortocoronary saphenous vein graft lesions in 11 patients. All of the lesions were stented successfully. There were no instances of stent thrombosis or stent embolism. The percent diameter stenosis was reduced from 85.5 +/- 14.1% to 3.5 +/- 4.4% (p < .001), and the minimal lumen diameter of the lesion increased from 0.7 +/- 0.7 mm at baseline to 3.7 +/- 0.2 mm (p < .001) after stent placement. We conclude that this noncoronary stent appears to be safe and effective for treating saphenous vein coronary bypass grafts. The high procedural success rate and excellent angiographic results are very encouraging, while the restenosis rates remain to be determined.
    Catheterization and Cardiovascular Diagnosis 10/1993; 30(2):91-5.
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    ABSTRACT: Percutaneous coronary angioscopy and intravascular ultrasound are sensitive intravascular imaging methods for detecting early changes in coronary morphology in cardiac transplant recipients. To compare the 2 imaging modalities, 29 consecutive cardiac transplant recipients underwent percutaneous coronary angioscopy and intravascular ultrasound during annual coronary angiography. Surface morphology, presence of plaque, and percent area stenosis were determined with each procedure. Percutaneous coronary angioscopy was more sensitive in detecting the presence of plaque and stenosis than was coronary angiography (plaque: 79 vs 10% [p < 0.001]; and stenosis: 24 vs 3% [p < 0.01]). Intravascular ultrasound was also more sensitive in detecting plaque (76 vs 10%; p < 0.001) and stenosis (45 vs 3%; p < 0.001) than was coronary angiography. Although both angioscopy and ultrasound identified atherosclerotic plaque, only percutaneous coronary angioscopy could show luminal surface morphology and pigmentation of the plaque. Conversely, ultrasound could detect calcification and presence of intimal thickening, and was more accurate in assessing the severity of stenosis (45 vs 24%; p < 0.01). In conclusion, percutaneous coronary angioscopy and intravascular ultrasound, in conjunction, provide information not only regarding the appearance of the luminal surface, but also quantitative information regarding the structure and extent of the disease in the coronary artery wall.
    The American Journal of Cardiology 10/1993; 72(11):805-9. · 3.43 Impact Factor