The pH of setting cements. 3. In vivo.
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Copper↗
Biomedical subjects
R Virmani
Publications and source records attributed to R Virmani.
Displacement of cement bases by condensation of direct gold.
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Calcium Hydroxide↗
A comparison of the intraoral disintegration of three dental cements.
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Acetates↗
An analytical comparison of cobalt cardiomyopathy and idiopathic dilated cardiomyopathy.
Toxic cardiomyopathy (TC) has a rapid clinical course and morphologically resembles idiopathic dilated cardiomyopathy (IDC). To further characterize TC, we used light microscopy to compare lesions caused by cobalt (Co) to those of IDC. Cobalt levels were also measured as a chemical marker to differentiate TC from IDC. We reviewed cases with TC and IDC and excluded all cases with chemotherapy-induced myopathy and catecholamine toxicity as well as cases with possible infectious, ischemic, or hypersensitivity-induced myopathies. We compared the light microscopic findings of 12 TC cases of 12 cases of IDC, and measured trace Co levels on digested heart tissue samples. The TC cases had prominent myofibrillar loss and atrophy; no cases had neutrophil infiltration or frank myocyte necrosis. In contrast, IDC had minimal myofibril loss and atrophy. Cobalt levels in the range of 0.6 to 5.45 micrograms/g of dry tissue were obtained for the TC cases, while IDC demonstrated Co levels of 0.01-0.2 micrograms/g. Distinction between TC and IDC is predominantly a function of myocyte change, with TC showing myofibrillar loss and atrophy in the absence of inflammatory infiltrates and fibrosis; IDC is predominantly associated with myocyte hypertrophy, atrophy, and fibrosis.
Adult↗
Nonbiodegradable expanded polytetrafluoroethylene-covered stent implantation in porcine peripheral arteries: histologic evaluation of vascular wall response compared with uncoated stents.
PURPOSE: To test the vascular wall response to an expanded polytetrafluoroethylene-covered stent, compared with conventional stenting, up to 6 months after deployment in the vascular district of a swine model. METHODS: Fourteen minipigs underwent implantation of expanded polytetrafluoroethylene-covered stents (CS) and bare stents (BS) in five peripheral arteries. Animals were killed at different time points (from 1 to 180 days). Histopathologic assessment by morphologic and morphometric analysis and by scanning electron microscopy (SEM) were used to assess the incorporation characteristics and re-endothelialization extent of the two types of stents. RESULTS: A total of 70 stents (14 CS and 14 BS in the renal arteries; 28 CS in the iliac arteries, and 14 CS in the aorta) were implanted. Microscopic examination confirmed the absence of occlusive thrombi in both the CS and BS groups. Microthrombi were observed in 10 of 13 CS (77% of cases) and in four of four BS (100% of cases, p < 0.05). Inflammation was mild in 69% of segments in which a CS was implanted and in 74% of segments in which a BS was implanted (p = NS), while a severe inflammatory reaction was observed in 6% of CS segments and in 8% of BS segments (p = NS). No differences were detected at the long-term analysis between neointimal thickness in CS compared with BS segments (0.46 +/- 0.18 mm vs 0.42 +/- 0.26 mm at 90 days and 0.36 +/- 0.08 mm vs 0.35 +/- 0.04 mm at 180 days; p = NS, respectively). At SEM analysis, re-endothelization was evident 15 days after the implant in both CS and BS starting from the stent edges. CONCLUSION: CS implantation did not elicit a more severe thrombotic deposition compared with that of BS. A similar inflammatory reaction of the arterial wall was present in the two stent groups 3 and 6 months following the implant. In addition, CS implantation did not stimulate excessive neointimal formation when compared with BS.
Animals↗
Optical coherence tomography.
BACKGROUND: Optical coherence tomography (OCT) is a light-based imaging modality that can be used in biological systems to study tissues in vivo with near-histologic, ultrahigh resolution. The rationale for intravascular application of OCT is its potential for in vivo visualisation of the coronary artery microstructure. METHODS AND RESULTS: The principle is analogous to pulse-echo ultrasound imaging; however, light is used rather than sound to create the image. Low-coherent near-infrared light is emitted by a superluminescent diode and reflected by the microstructures within biological tissues. The echo time delay of reflected light waves is converted into a two-dimensional spatial image. The intensity of the reflected light waves is translated into an intensity map. Experimental studies confirmed the ability of intravascular OCT for plaque characterisation and accurate assessment of vascular structures that are close to the luminal surface. Preliminary clinical experience proved in vivo feasibility of intravascular OCT. A variety of atherosclerotic plaque structures including thin cap fibroatheromas can be visualized in vivo. CONCLUSIONS: Intravascular OCT allows for accurate assessment of vessel structures close to the luminal side. Clinical application is feasible. To date, however, the clinical relevance of OCT findings in coronary arteries is unclear and further validation of OCT imaging is mandatory.
Coronary Artery Disease↗
Histopathologic appearance of arterial occlusions with hydrogel and polyvinyl alcohol embolic material in domestic swine.
PURPOSE: This study observes the histologic changes resulting from a hydrogel embolic agent (polyacrylonitrile [PAN]) compared with polyvinyl alcohol particles (PVA) of similar size. MATERIALS AND METHODS: Hepatic and renal embolizations were performed in 13 domestic swine by selecting small (1-mm) branches utilizing a coaxial 3-F microcatheter. The hydrogel embolic agent (tantalum-loaded and plain) and PVA were delivered through microcatheters. The longest follow-up period was 8 weeks. Postmortem examination of the embolized tissues included gross examination and histologic analysis. RESULTS: Tantalum-loaded PAN particles were radiopaque and seen in groups fluoroscopically and individually with specimen radiography. Histologic studies showed similar luminal and cellular response to PVA and the hydrogel embolic agents. The arterial lesion induced by the hydrogel embolic agents led to an absence of the arterial wall locally in the area of deployment. Hydrogel embolic particles became surrounded in fibrous connective tissue with no arterial wall. PVA and porous hydrogel capsules produced an inflammatory response, resulting in less wall reorganization, and surrounding fibrous connective tissue at 8 weeks than the solid PAN particles. CONCLUSION: These hydrogel embolic create a permanent arterial occlusion by transmural arterial damage. Mechanical effects and, to a lesser degree, inflammatory changes are responsible.
Acrylic Resins↗
Sudden cardiac death.
The rate of cardiac deaths that are sudden is approximately 50%, and decreases with age. The causes of sudden cardiac death are diverse, and are a function of age. In children and adolescents, coronary anomalies, hypertrophic cardiomyopathy and myocarditis are frequent substrates for lethal arrhythmias; in adults, coronary atherosclerosis and acquired forms of cardiomyopathy are the most common findings at autopsies of sudden cardiac death. This review focuses on coronary causes of sudden cardiac death, especially congenital coronary artery anomalies, which result in sudden death almost exclusively in adults younger than age 35, and coronary thrombosis. The most lethal coronary artery anomaly is the left coronary artery arising from the right sinus of Valsalva; this anomaly often results in fatal arrhythmias, often with exercise. The right coronary artery arising from the left sinus of Valsalva may also be lethal in adolescents and young adults, but, unlike the anomalous left, is more often an incidental finding at autopsy. Approximately 60% of sudden coronary death is caused by coronary thrombosis, the rest die with severe coronary disease in the absence of thrombosis. The two major substrates of coronary thrombosis are plaque rupture and plaque erosion, and are not only different pathologically, but are seen in patients with divergent risk factor profiles. Plaque rupture is the most common cause of fatal coronary thrombus, and is characterized by necrotic core with a thin fibrous cap, infiltrated by macrophages. The factors that result in plaque instability and rupture are largely unknown, and are under intense scrutiny; morphologic studies have identified serum lipid abnormalities as a key risk factor in the development of plaque rupture. Plaque erosion, in contrast to plaque rupture, is seen in younger men and women, is not associated with lipid abnormalities, and does not result from exposure of the lipid core to the lumen. The heterogeneity of the atherosclerotic plaque and the diverse mechanics of plaque progression and thrombosis have only been relatively recently explored, and are largely elucidated by autopsy studies of victims of sudden coronary death.
Coronary Artery Disease↗
The degree of neointimal formation after stent placement in atherosclerotic rabbit iliac arteries is dependent on the underlying plaque.
The purpose of this study was to determine the effects of stent placement on the underlying arterial morphology and the relations of stent-vessel wall interactions with subsequent neointimal formation in an atherosclerotic artery. Seven New Zealand White rabbits with experimentally induced atherosclerosis underwent balloon angioplasty (n = 7) and stent placement after balloon angioplasty (n = 7) in the iliac arteries. Histologic analysis of the treated arteries was performed at 28 days to assess device interactions with the artery and the pattern of the neointimal response. The area within the external elastic lamina of the stented vessels was 66% greater than the arteries with balloon angioplasty alone (p = 0.001) which contributed to a significantly greater late lumen area (3.33 +/- 0.51 mm2 versus 1.33 +/- 0.20 mm2, p = 0.0028). Neointimal thickness was measured at 220 stent wire sites from 21 sections of stented arteries of which 139 (63%) had underlying plaque and 81 (37%) were adjacent to normal media. Rupture of the internal elastic lamina (IEL) occurred at only 9 (11%) of the 81 stent wire sites over normal media. The mean neointimal thickness was 0.16 +/- 0.01 mm lor all stent wire sites. The neointimal thickness was greater at the stent wire sites with underlying plaque (0.23 +/- 0.01 min) than at the stent wire sites adjacent to normal media (0.08 +/- 0.01 mm) or at sites with rupture of the internal elastic lamina (0.16 +/- 0.02 mm, p = 0.0001). The degree of neointimal formation within the stents strongly correlated with the area of the underlying atherosclerotic plaque (r = 0.76, p = 0.0007) and the extent of plaque or medial compression by the struts (r = 0.90, p = 0.006). The present study characterizes stent interactions in a model commonly employed to evaluate novel therapies for the prevention of restenosis. The neointimal response was influenced by the local arterial morphology and correlated with the extent of plaque or medial compression by the stent. These data may be useful for future studies in this model and understanding the mechanism of in-stent restenosis.
Angioplasty, Balloon, Coronary↗
Anaplastic large cell lymphoma (CD 30+), T-phenotype, in the heart of an HIV-positive man.
Non-Hodgkin's lymphomas described in patients with HIV-infection are most often high-grade B-cell lymphomas. Anaplastic large cell lymphoma (CD 30+) has been described in a minority of immunocompromised patients. Although sporadic reports of T-cell lymphomas associated with HIV infection are found in the literature, they have not been described to occur in the myocardium. We present a case of anaplastic large cell lymphoma (CD 30+), T-phenotype involving the heart in a 42-year-old HIV-positive patient.
Adult↗
Burden of myocardial damage in cardiac allograft rejection: scintigraphic evidence of myocardial injury and histologic evidence of myocyte necrosis and apoptosis.
BACKGROUND: Because myocardial damage determines morbidity and outcomes in heart transplant rejection, assessment of total burden of myocardial damage is highly desirable. In addition to myocyte necrosis, programmed cell death, or apoptosis, has recently been shown to contribute to cardiac allograft rejection. In the present study, we noninvasively determined myocardial damage by antimyosin scintigraphy and compared it with necrotic and apoptotic myocardial damage in endomyocardial biopsy (EMB) specimens. METHODS AND RESULTS: Forty scintigraphic and histologic studies were simultaneously performed. Of these, 19 patients had no EMB evidence of allograft rejection (group I, International Society of Heart and Lung Transplantation [ISHLT] grade 0/4), 12 had mild rejection (group II, ISHLT grades 1A and 1B), and 9 had evidence of moderate allograft rejection (group III, ISHLT grades 2, 3A, and 3B). None of the biopsies demonstrated severe allograft rejection (ISHLT grade 4/4). The severity of global myocyte damage in 40 patients was assessed by antimyosin scintigraphy. Endomyocardial biopsies were performed in these patients within 48 hours of imaging study; biopsy specimens were characterized for presence of myocyte necrosis and apoptosis. Evidence of myocyte necrosis was observed in 9 (23%) of 40 EMB specimens. Nineteen EMB specimens of group I had no inflammation and no myocyte necrosis, 12 of group II specimens showed interstitial mononuclear cell infiltration (only) but no myocyte necrosis, and all 9 of group III specimens had evidence of cellular infiltration and myocyte damage. Myocyte necrosis was assessed by hematoxylin-eosin and trichrome staining of EMB specimens. On the other hand, apoptosis of myocytes, as assessed by TUNEL staining of DNA fragments, was seen in 22 (55%) of the 40 biopsy specimens: 47%, 58%, and 67% in groups I, II and III, respectively. Abnormal antimyosin scan findings, indicating presence of myocardial damage, were observed in 9 of the 19 patients in group I and in all patients in groups II and III. Although positive antimyosin scan results in group III patients are concordant with the presence of histologic myocardial necrosis, myocardial uptake of antimyosin antibodies in groups I and II (no apparent myocyte damage at light microscopic examination) could reflect either sampling error of the biopsy or ongoing apoptotic myocyte damage. CONCLUSIONS: Apoptosis of myocytes is frequently observed during cardiac allograft rejection. The presence of apoptotic myocytes in the absence of histologic rejection activity in patients with antimyosin uptake suggests that apoptosis could be an additional mechanism of transplant-associated myocardial damage.
Adult↗
Strategic targeting of atherosclerotic lesions.
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Animals↗
Dose and dose rate effects of beta-particle emitting radioactive stents in a porcine model of restenosis.
BACKGROUND: Radioactive stents have been proposed as a means to prevent in-stent restenosis by inhibiting intimal proliferation with continuous low-dose irradiation. OBJECTIVES: The purpose of this study is to determine the effects of cumulative dose and dose-rate delivery on neointimal formation using 32P and 90Y beta-particle emitting radioactive stents in a porcine coronary model of restenosis. METHODS AND MATERIALS: We compared the late histologic results of 0.25 to 32.0 microCi 90Y (half-life 64 hours) (n = 64 stents) and 0.1 to 57.6 microCi 32P (half-life 14.3 days) (n = 55 stents) Beta-particle emitting radioactive stents with non-radioactive (n = 40) stents in a porcine coronary model of restenosis. A computer-based dosimetry modeling program was used to determine the 28 day cumulative dose and dose-rate delivery for the beta-particle emitting radioactive stents at a distance of 0.1 mm from the stent surface. RESULTS: Continuous low dose-rate (1 to 5 cGy/hr) radiation delivery for > 2 weeks via a 0.1 to 0.5 microCi 32P radioactive stent effectively reduced in-stent neointimal hyperplasia at 90 days. Cumulative doses of > 55 Gy induced severe adventitial fibrosis, microvascular damage and promoted the formation of a matrix-rich neointima. Delayed vascular repair was evident at focal regions within the body of radioactive stents that delivered cumulative doses of > or = 140 Gy at 28 days and cumulative doses of 1,100 Gy at 90 days. CONCLUSIONS: These data may be useful in predicting safe and effective dose and dose rate delivery for beta-particle emitting radioactive stents.
Animals↗
Local arterial responses to 32P beta-emitting stents.
PURPOSE: 32P beta-emitting stents reduce neointimal growth in rabbit iliac arteries for at least 12 months after deployment but are associated with incomplete healing. The aim of this study was to quantitate arterial cellularity, with emphasis on the inflammatory response following radioactive stenting. METHODS: 32P beta-emitting stents were placed in rabbit iliac arteries and analyzed at 3 months (6 and 24 microCi), and 6 and 12 months (6, 24, and 48 microCi). Arterial cellular proliferation and cell densities of smooth muscle cells (SMC), mononuclear cells (macrophages and lymphocytes), and neutrophils (PMN) were determined. RESULTS: Total intimal cell density was greatest in control stents at all three time points, composed mostly of SMCs. SMC density associated with radioactive stents increased from 3 to 12 months but was significantly less than control nonradioactive stents. There was a 4-fold increase in cellular proliferation in the 24 and 48 microCi group vs. control stents. In the media, SMC density of radioactive stent groups was significantly reduced vs. control stents at all three time points, for all three activities. At 3, 6 and 12 months, there was a dose-dependent increase in intimal inflammatory cell density, which consisted mostly of macrophages. For 6-microCi stents inflammation peaked at 3 months and decreased thereafter. Inflammation for 24-microCi stents peaked at 6 months and then decreased at 12 months. Inflammation associated with 48-microCi stents remained high at 6 and 12 months. Focal atherosclerotic change was seen in 11% of stents in the 24-microCi group, and 37% and 50% in the 48-microCi group at 6 and 12 months, respectively. CONCLUSION: Intimal SMC density remains suppressed out to 12 months after placement of 32P beta-emitting stents. However, inflammation and cell proliferation remain increased and may potentially result in greater neointimal formation over time.
Animals↗
Intravascular radiation accelerates atherosclerotic lesion formation of hypercholesteremic rabbits.
OBJECTIVES: The purpose of the present study is to evaluate the effect of intravascular radiation (IR) on the arterial wall of uninjured vessels in the hypercholesteremic rabbit model. METHODS: Aortas of 24 New Zealand white rabbits were treated with either intravascular 192-Ir gamma-radiation (15 Gy at 2 mm from the center of the source) or were exposed to the source catheter without radiation (sham controls). Following the radiation treatment, the animals were fed a 2% cholesterol diet until euthanasia at 2 (n=8) or 6 (n=16) weeks. Arteries were analyzed using light and scanning electron microscopy (SEM); transforming growth factor beta (TGF-beta) 1, a promoter of connective tissue deposition, was also monitored. RESULTS: At 2 weeks, SEM analysis showed well-aligned endothelial cells in nonradiated segments, whereas irradiated arteries consistently contained adherent and subendothelial macrophages with focal areas of endothelial disruption. Further radiated segments at 2 weeks showed a 7-fold increase in active TGF beta-1 over nonradiated segments. At 6 weeks, there was a significant increase in plaque and vessel wall area relative to control arteries, however, no differences were noted in the density of actin-positive smooth muscle cells (SMCs) or macrophages. Similarly, no differences were noted in cell proliferation between groups as evidenced by the marker bromodeoxyuridine (BrdU). In contrast, nonirradiated segments frequently contained cellular areas with extracellular lipid. CONCLUSION: Exposure of previously uninjured vessels to IR and hypercholesterolemia is associated with increased plaque burden and leads to more advanced plaque types. Special care should be taken to minimize radiation exposure in normal vascular segments in hypercholesterolemic patients undergoing radiation therapy.
Animals↗
Pathology of radiation-induced coronary artery disease in human and pig.
PURPOSE: External beam mediastinal radiation-induced accelerated coronary atherosclerotic heart disease in humans has been recognized, especially when the condition occurs in young persons. The purpose of the present study was to compare external beam radiation-induced accelerated coronary atherosclerosis in humans with that seen in the pig coronary arteries following radioactive stent placement. METHODS: A literature review of radiation-induced coronary artery disease was performed. In addition, clinical records and coronary histology from the Armed Forces Institute of Pathology Registry were reviewed from patients who had received external beam radiation for mediastinal malignancies. Coronary arteries from pigs that had radioactive coronary stent placement were evaluated from our stent pathology laboratory and analyzed for comparison with the human disease. RESULTS: In humans, the characteristics of the intimal plaque in accelerated atherosclerosis postradiation therapy were similar to that seen in typical atherosclerotic coronary disease in the absence of radiation therapy. However, medial thinning and adventitial fibrosis were the distinguishing pathologic arterial changes secondary to radiation seen in humans. Radioactive stent placement in pig coronary arteries produced similar changes to that observed in humans post-external beam radiation, consisting of medial injury and adventitial thickening accompanied by intimal foam cell collections, calcification, and necrotic core formation containing cholesterol clefts resulting in severe luminal narrowing. CONCLUSIONS: Radiation, delivered via external beam or radioactive stent, induces changes of intimal atherosclerosis with medial thinning and adventitial scarring in human and pig. Therefore, pending completion of long-term clinical studies, caution should be exercised before the widespread use of brachytherapy is advocated for the treatment and prevention of coronary restenosis.
Animals↗
Assessing the advantages and disadvantages of novel radiation therapy for vascular restenosis: injury score, artery size, and short lengths.
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Angioplasty, Balloon↗