Biomedical subjects
Publications and source records attributed to S R Ramee.
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OBJECTIVES: 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. BACKGROUND: 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. METHODS: Percutaneous coronary angioscopy was performed in 17 patients (17 vessels) after angiographic confirmation of postangioplasty vessel occlusion. RESULTS: 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. CONCLUSIONS: 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.
The major cause of late death in cardiac transplant recipients is cardiac allograft vasculopathy, also referred to as cardiac transplant atherosclerosis, which occurs in as many as 45% of transplant recipients who survive longer than 1 year. It differs from typical atherosclerosis in that intimal hyperplasia is concentric and diffuse, the internal elastic lamina remains intact, calcification is rare, and the disease tends to develop rapidly. Intravascular ultrasound and coronary angioscopy are more sensitive diagnostic measures of cardiac allograft vasculopathy than is coronary angiography. Although retransplantation at present seems to be the only definitive therapy for cardiac allograft vasculopathy, it has shown only fair results. Recent studies have suggested that calcium entry blockers and angiotensin-converting enzyme inhibitors may play a beneficial role in delaying the progression of cardiac allograft vasculopathy.
Coronary angioscopy will not replace angiography as the gold standard for imaging atherosclerotic coronary arteries. However, there may well be a clinical niche for a technology that gives accurate information regarding a specific lesion, if that information can be used to improve the acute or chronic outcome of an interventional procedure. Our experience demonstrates that angioscopy indeed provides this information. Using angioscopy, we now have access to information regarding arterial wall disease that heretofore has been available only at necropsy. In addition, whereas angiography has provided only a 2-dimensional, gray-scale image of the coronary vessels, angioscopy offers a full-color, 3-dimensional perspective of the intracoronary surface morphology. These important lesion-specific details, not reliably available from angiography alone, may ultimately be used to improve patient outcome and to assess risk.
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)
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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.
BACKGROUND: Cardiac allograft vasculopathy remains the leading limitation to long-term survival after cardiac transplantation. While the influence of donor and recipient gender in the pathogenesis of cardiac vasculopathy is still poorly understood, studies have indicated that female allografts may be at higher risk for the development of cardiac allograft vasculopathy. The purpose of this study was to characterize the influence of donor and recipient gender on the early genesis of cardiac allograft vasculopathy by using intravascular ultrasound. METHODS AND RESULTS: Thirty-six consecutive cardiac transplant recipients were divided into three groups on the basis of donor and recipient gender as follows: group 1, female donor and male recipient (n = 8); group 2, male donor and female recipient (n = 7); and group 3, male donor and male recipient (n = 21). The three groups were similar with regard to donor and recipient age, weight, body surface area, serum lipids, left ventricular function, histocompatibility, cellular and vascular rejection, and cytomegalovirus infection. To precisely quantitate the extent of cardiac allograft vasculopathy, intravascular ultrasound was performed in all patients at the time of first annual angiography. Intimal thickening and intimal index were accurately quantitated by intravascular ultrasound. Intimal thickening was significantly greater in group 1 (0.55 +/- 0.15 mm) than in group 2 (0.18 +/- 0.04 mm) or group 3 (0.29 +/- 0.05 mm) (P < .05). In addition, the intimal index was greater in group 1 (0.20 +/- 0.04) than in group 2 (0.07 +/- 0.02) or group 3 (0.15 +/- 0.02) (P < .01, group 1 versus group 2). CONCLUSIONS: Male recipients of female allografts have a higher degree of vascular intimal hyperplasia detected by intravascular ultrasound at 1 year after heart transplantation. These findings indicate that donor and recipient gender influences the early genesis of cardiac allograft vasculopathy.
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.
Congenital defects of the pericardium are extremely rare and frequently difficult to diagnose. We present a diagnosis of partial congenital defect of the left pericardium based on a characteristic chest X-ray and left ventriculogram. Additionally, we report findings of a diastolic, migratory coronary stenosis on coronary arteriography which, to date, has not been reported. Confirmation of the diagnosis by mediastinoscopy was followed by thoracoscopic pericardiectomy.
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.
A strategy of using a single, conservatively sized percutaneous transluminal rotational ablation device with or without adjunctive balloon angioplasty was employed in 18 vessels in 17 patients selected because of unfavorable lesion morphology for balloon angioplasty alone. Fifteen patients had lower extremity occlusions and/or heavily calcified lesions and two patients had ostial renal artery stenoses. We were able to achieve a 94% (17/18 lesions) technical success rate, and a 94% (16/17 patients) clinical success rate. In the patients with lower extremity lesions, the baseline ankle-brachial blood pressure index increased from 0.55 +/- 0.15 to 0.90 +/- 0.19 (p < .001) 1 day after the procedure. Follow-up at 6.8 +/- 2.8 months revealed clinical evidence of restenosis in only one patient. We conclude that a cost-effective strategy of treating unfavorable lesions with a single Rotablator burr and adjunctive balloon angioplasty is safe and effective.
Mid-infrared lasers are attractive for coronary angioplasty based upon their excellent fiberoptic transmission and enhanced tissue absorption. Using a solid-state, mid-infrared holmium:YAG laser with prototype multifiber laser delivery catheters, we performed coronary laser angioplasty with or without adjunctive balloon angioplasty or directional atherectomy in 14 patients with 17 stenoses. Procedural laser success was obtained in 13/14 (93%) patients and 16/17 (94%) lesions; however clinical success was achieved in 9/14 (64%) patients and 12/17 (71%) stenoses. Angiographic restenosis at 4.6 +/- 1.6 months was found in 5/8 (63%) patients. We achieved an excellent procedural laser success rate in patients with generally unfavorable angioplasty anatomy. However, our clinical success rate was not different from that expected with conventional angioplasty alone. The holmium laser remains an attractive energy source for laser angioplasty; but as is the case for all coronary laser systems, its utility as a stand-alone therapy is limited by catheters which create small channels. In this small group, we could demonstrate no clinical benefit for laser-assisted angioplasty in complex coronary lesions. Our results suggest that a randomized trial comparing laser-assisted angioplasty and conventional angioplasty be performed to determine the clinical benefits of this more expensive therapy.
OBJECTIVES: We compared the results of percutaneous angioscopy and angiography for detecting critical elements of surface lesion morphology in 21 patients undergoing balloon angioplasty of saphenous vein coronary bypass grafts. BACKGROUND: Angiography remains the standard for diagnosing and treating intravascular pathology associated with atherosclerotic coronary artery disease. It has been demonstrated that coronary angioscopy is more sensitive for identifying more complex atherosclerotic plaques and intracoronary thrombi in native coronary arteries. METHODS: Angioscopy and angiography were performed before and after angioplasty of "culprit lesions" in bypass grafts. All but one of the patients had unstable angina. The mean age of the saphenous vein coronary bypass grafts was 10.1 +/- 2.4 years (range 5 to 15). RESULTS: Restenosis at a prior angioplasty site was present in seven patients. Intravascular thrombi were seen by angioscopy in 15 (71%) of 21 versus 4 (19%) of 21 grafts by angiography (p < 0.001). Dissection was identified by angioscopy in 14 (66%) of 21 versus 2 (9.5%) of 21 grafts by angiography (p < 0.01). The presence of friable plaque lining the lumen surface of the vein graft was detected by angioscopy in 11 (52%) of 21 versus 4 (19%) of 21 grafts by angiography (p < 0.05). There was no correlation between age of the bypass graft and the finding of friable plaque. CONCLUSIONS: We conclude that angioscopy is superior to angiography for detecting complex lesion morphology in bypass grafts and that the presence of friable plaque does not preclude an uncomplicated angioplasty procedure.
To evaluate the efficacy of venous reconstruction versus percutaneous transluminal angioplasty for the treatment of obstruction of the superior vena cava and its major tributaries, we retrospectively reviewed the clinical course of 27 patients, of whom 13 underwent operative reconstruction and 15 had angioplasty (1 had both). Three patients had obstruction of the superior vena cava, 8 had occlusion of the innominate veins, and 16 had obstruction of the subclavian or axillary veins. In both treatment groups, mean age, indications, etiology, and location of the lesion were comparable. No major surgical complications occurred; one patient who underwent angioplasty experienced stent migration to the pulmonary artery without sequelae. Primary symptomatic relief at 1 year was achieved in 88% in the surgical group versus 36% in the angioplasty group (p < 0.05 by Fisher's exact test) and at 2 years in 71% versus 0%, respectively (p < 0.01). One- and 2-year success rates with repeated angioplasty, however, were 86% and 66% (p > 0.9), respectively. We conclude that the long-term success rate of operative reconstruction exceeds that of single percutaneous transluminal angioplasty. However, with repeated angioplasty, success rates approach those of operative reconstruction.
We performed percutaneous coronary angioscopy in 35 patients to study the surface morphology of coronary artery lesions. Twenty-five patients had angioscopy performed in conjunction with PTCA, including 20 patients with de novo lesions (16 patients with unstable angina, four patients with stable angina), and five patients with restenosis lesions. Ten cardiac transplant patients had angioscopy performed in conjunction with annual follow-up angiography in attempt to identify accelerated atherosclerotic lesions. There were no complications of angioscopy in any patient. There were no intracoronary thrombi seen either by angiography or angioscopy in the stable angina patients. In the unstable angina group, angiography identified thrombus in 2 out of 16 (12.5%) versus 15 out of 16 (94%) (P less than 0.001) with angioscopy. Following angioplasty, dissections were seen angiographically in 7 out of 16 (44%) of patients versus 16 of 16 (100%) of the patients by angioscopy (P less than 0.01). Restenosis lesions were characterized by a white, fibrous appearance instead of the usual yellow color of primary atherosclerotic lesions. In the ten cardiac transplant patients, angioscopy appeared to be more sensitive than angiography for the detection of atherosclerosis. Yellow (atherosclerotic) and white (fibrotic) plaques were seen in the transplant patients, which often were not detected by angiography. In summary, angioscopy is an excellent tool for visualizing the surface morphology of coronary artery lesions. The clinical indications for angioscopy remain undefined at present.(ABSTRACT TRUNCATED AT 250 WORDS)
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The angiographic patency and histologic characteristics of a new balloon-expandable tantalum stent were studied after implantation intervals ranging from 1 to 32 weeks in atherogenic miniature swine peripheral and coronary arteries. Stents were placed in 34 arteries (10 coronary and 24 iliac arteries) in a total of 13 swine. Two swine died within 24 h of stent implantation. Follow-up angiography was performed before death was induced in 11 swine (8 coronary and 19 iliac arteries) and revealed 100% patency without evidence of lumen stenosis, thrombosis or migration of the stents. The neointimal thickening was maximal at 4 weeks after stent implantation and was at its minimum at 32 weeks after implantation with reendothelialization of the stents generally complete at that time. An advantage of this balloon-expandable device is its inherent longitudinal flexibility. The coil configuration allowed the nondeployed stent to negotiate acute bends in coronary arteries to reach the site of implantation and also allowed the deployed stent to conform to the natural contour of tortuous coronary arteries. The tantalum device was remarkable for its radiographic visibility, which greatly aided its placement under fluoroscopic guidance. This study demonstrates this stent's ease of implantation, excellent patency rate and absence of restenosis due to neointimal proliferation for up to 8 months in this atherogenic swine model.