Differentiation of cardiac tumor from thrombus by combined MRI and F-18 FDG PET imaging.
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Adult↗
Biomedical subjects
J Weinberger
Publications and source records attributed to J Weinberger.
Stroke recurrence is more frequent in Blacks and Hispanics.
This study was designed to measure recurrent stroke rates and identify their determinants in a mixed ethnic population. A cohort of 299 patients (110 black, 57 Hispanic and 132 white) admitted to a large urban hospital with an acute stroke between November 1, 1991, and July 1, 1993, was followed for a mean of 17.8 months. Demographic and historical data and stroke subtype and severity were recorded at the time of the index stroke. The main outcome measure was stroke recurrence. The unadjusted relative risk of stroke recurrence for blacks, relative to white, was 2.0 (95% CI: 0.9-4.4) and for Hispanics, relative to whites, it was 2.6 (95% CI: 1.08-60). Ethnicity appeared to be associated with recurrence risk only among first-ever strokes: the risk for blacks, relative to whites, was 2.4 (95% CI: 1.02-5.5) and for Hispanics it was 2.9 (95% CI: 1.2-7.4). None of the other putative risk factors for stroke recurrence identified at the time of initial hospitalization were associated with risk of recurrence.
Black or African American↗
A new noninvasive technique for imaging atherosclerotic plaque in the aortic arch of stroke patients by transcutaneous real-time B-mode ultrasonography: an initial report.
BACKGROUND AND PURPOSE: Aortic arch atherosclerotic plaque is a probable source of atheroembolic stroke. Transesophageal echocardiography (TEE) has been used to image the aorta of patients with stroke to identify atherosclerotic plaque. TEE is moderately invasive and does not always visualize plaques present in the distal ascending aorta and proximal aortic arch. METHODS: In the current study, transcutaneous B-mode ultrasonography was performed to image the aortic arch through a lateral supraclavicular window, and the results were compared with those of TEE in 20 patients. The aorta was subdivided into the proximal ascending (PAsc), distal ascending (DAsc), proximal aortic arch (PAA), and distal aortic arch (DAA) to be certain the plaques identified by each technique were the same. Plaques were characterized as simple (<4 mm thick) or complex (>4 mm thick). RESULTS: In the PAsc, 8 simple plaques were identified with TEE but not with B-mode. In the DAsc, 1 complex plaque was identified with both techniques, and B-mode identified 1 additional complex and 1 simple plaque. In the PAA, 6 simple and 5 complex plaques were identified by both techniques, and TEE identified 1 additional complex plaque. In the DAA, TEE identified 2 simple and 2 complex plaques; B-mode identified 3 complex plaques. CONCLUSIONS: B-mode imaging compared favorably with TEE in identification of plaques in the aortic arch and distal ascending aorta, although it could not identify simple plaques in the proximal ascending. B-mode could visualize plaques not seen by TEE in the distal ascending aorta. B-mode ultrasonography is complementary to TEE in performance of a comprehensive assessment of plaque in the aortic arch and provides a noninvasive method for sequential studies of plaques that can be visualized.
Aorta, Thoracic↗
Basic fibroblast growth factor as a biochemical marker of exercise-induced ischemia.
BACKGROUND: Basic fibroblast growth factor (bFGF) is a mitogenic polypeptide that demonstrates enhanced expression and promotes angiogenesis in animal models of myocardial ischemia and infarction. Elevated levels of bFGF are present in the urine of humans with metastatic tumors, but its expression in human myocardial ischemia is unknown. Thus, we sought to determine whether urine levels of bFGF are altered by exercise-induced ischemia in humans. METHODS AND RESULTS: Eighty-six patients underwent exercise thallium studies for evaluation of anginal symptoms. Urine levels of bFGF (corrected for urine creatinine) were determined by ELISA immediately before and between 2 and 4 hours after exercise. The change in urine bFGF level was compared between 43 patients with and 43 patients without exercise-induced ischemia. Patients with ischemia had an increase in urine bFGF compared with nonischemic patients (1052 +/- 245 versus -278 +/- 130 pg/g creatinine, P < .0001). Exercise, demographic, and clinical variables were assessed and analyzed for possible effect on bFGF response to exercise. By univariate analysis, a history of hypertension was negatively associated with a change in bFGF level (P < .05). No other variables were associated. By multivariate analysis, only bFGF response (P < .001) and age (P < .05) were independently related to exercise-induced ischemia. CONCLUSIONS: Significantly increased levels of bFGF are detected in the urine within hours of exercise-induced ischemia. Further studies are warranted to determine whether bFGF might serve as a useful circulating marker of myocardial ischemia in humans.
Analysis of Variance↗
Transesophageal echocardiography-guided transvenous biopsy of a cardiac sarcoma.
Transvenous endomyocardial biopsy is a well established procedure to diagnose rejection after heart transplantation as well as to assess for other cardiomyopathic processes. However, it is rarely used to obtain samples of unidentified cardiac masses. We report a case of a primary cardiac sarcoma in which the histologic diagnosis was provided by transesophageal echocardiography-guided transvenous biopsy. This procedure is accurate and can avoid the potential risk of a diagnostic thoracotomy.
Biopsy↗
Modulation of ischemic excitatory neurotransmitter and gamma-aminobutyric acid release during global temporary cerebral ischemia by selective neuronal nitric oxide synthase inhibition.
Nitric oxide release during cerebral ischemia is the result of both neuronal and endothelial subclasses of nitric oxide synthase (NOS). In this study, we examined the role of specific neuronal NOS inhibition (nNOSI) on excitatory neurotransmitter and gamma-aminobutyric acid (GABA) release during global cerebral ischemia. Microdialysis probes were placed into the striatum of 24 rats. After probe stabilization, rats were randomized to receive 7-nitroindazole (7-NI), a selective nNOSI, in doses of 0, 5, 10, or 20 mg/kg. Temporary global forebrain ischemia was induced for 15 min, followed by 60 min of reperfusion. nNOSI administration did not produce detectable changes in neurotransmitter recovery prior to ischemia. There were significant increases in aspartate (ASP), glutamate (GLU), glycine (GLY), and GABA recovery during ischemia in the absence of nNOSI. 7-NI resulted in an attenuation in GLU, GLY, and GABA recovery during ischemia and reperfusion. No differences in ASP recovery were detected with nNOSI. Differences between the present study and other studies that examine the role of nonspecific constitutive NOSI during cerebral ischemia demonstrate the contribution of neuronal NOS on the modulation of ischemic excitatory neurotransmitter and GABA release.
Animals↗
Modulation of ischemic excitatory neurotransmitter and gamma-aminobutyric acid release during global temporary cerebral ischemia by local nitric oxide synthase inhibition.
Systemic nitric oxide synthase inhibition (NOSI) decreases cerebral blood flow, which may worsen ischemic insults. To examine the local effects of NOSI without this confounding effect, we examined the role of a locally administered NOSI, NG-nitro-L-arginine-methyl-ester (L-NAME), on neurotransmitter recovery during cerebral ischemia. Rats were assigned to one of three groups: locally administered L-NAME via a striatal microdialysis probe (n = 11), systemic L-NAME (n = 5), or control (n = 11). Temporary global forebrain ischemia was induced for 15 min, followed by 60 min of reperfusion. L-NAME resulted in decreases of basal aspartate (ASP; 74% of basal) and glutamate (GLU; 60% of basal) recovery. While systemic L-NAME caused significant increases in ischemic ASP and GLU recovery (by 224% and 110%, respectively, compared with ischemic controls), local NOSI administration resulted in a significant attenuation of peak ASP, GLU, glycine, and gamma-aminobutyric acid recovery (43%, 38%, 53%, and 72%, respectively, compared with ischemic controls). We conclude that local NOSI attenuated ischemic neurotransmitter recovery during ischemia/reperfusion. Our results emphasize the importance of the systemic effects of NOSI and suggest both deleterious and beneficial effects of NOSI during ischemia/reperfusion.
Animals↗
The effects of subliminal symbiotic stimulation on free-response and self-report mood.
Research has shown that subliminal presentation of MOMMY AND I ARE ONE (MIO) can help improve adaptive functioning. Two experiments tried to determine whether changes in mood, especially free-response mood, could help explain these findings. In one experiment, 20 men were randomly assigned to receive either a subliminal MIO or control stimulus. Results showed predicted effects on a free-response and no effects on a self-report mood measure. In the other experiment, 54 male subjects randomly received one of three subliminal stimuli. They evidenced the same pattern of mood results. Sentential semantics were shown to be relevant to the obtained results. Ascending threshold and 150 forced-choice discrimination trials demonstrated that subjects could not report stimulus content. It was concluded that MIO effects were attributable to unconscious processing of the entire message and that free-response mood may partly mediate these effects. Suggestions for future research were offered.
Affect↗
The Minorities Risk Factors and Stroke Study (MRFASS). Design, methods and baseline characteristics.
African-Americans and probably Latinos are at increased risk of stroke compared with white, non-Latino Americans. This study seeks to determine if the known risk factors for stroke can account for this increased risk. In this case-control study controls (neighborhood volunteers) were group-matched to acute stroke cases by ethnicity in a ratio of approximately 2:1 for African-Americans and Latinos and 1:1 for whites. Extensive historical, clinical and laboratory data were collected on each subject. For each ethnic group cases were somewhat older and less well-educated than the volunteer controls. Patients in each ethnic group were similar with regard to time from stroke onset to hospital admission, stroke severity, length of stay, discharge disposition and mortality rate. With minor exceptions the distributions of stroke subtypes within each ethnic group appeared similar to those previously reported. Subject recruitment for this case-control study was completed in the manner and time frame planned. Analysis of risk factor information from this sample should provide valuable information regarding the relative risk associated with the major modifiable risk factors for stroke in the minority groups studied.
Adult↗
[Drug onset time of atracurium after pancuronium priming in elderly patients].
Synergism occurs between some combinations of non-depolarising muscle relaxants. To test the effect of pancuronium as a priming dose of atracurium, 45 adults were anaesthetised with 25 micrograms/kg alfentanil. 75 micrograms/kg midazolam, and 0.25 mg/kg edomidate, O2/N2O and enflurane, and were randomised to one of three groups. After induction, 15 patients received 0.5 mg/kg atracurium, 15 were primed with 0.075 mg/kg atracurium and another 15 with 0.0125 mg/kg pancuronium and three minutes later 0.45 mg/kg atracurium. Neuromuscular response was monitored by adductor pollicis electromyogram (EMG) by stimulating in a TOF pattern. Times for tI reduction of 75, 50, 25 and 0% and tI recovery to 10% were taken. There were no differences between the two groups that received only atracurium. The pancuronium priming group showed a significantly faster onset of neuromuscular blockade (tI = 0%: control group I: 76.3 +/- 15.4 sec vs. pancuronium group III: 64.3 +/- 11.3 sec) and a prolonged recovery. Pancuronium priming can shorten the onset time of atracurium while atracurium priming alone showed no shortening. This suggests a synergism for pancuronium priming in combination with atracurium.
Adult↗
Intracoronary irradiation for the prevention of restenosis.
Restenosis after coronary angioplasty is a major limitation of an otherwise highly effective and safe procedure for the treatment of atherosclerotic coronary artery disease. Although the advent of coronary stenting has reduced restenosis rates for selected patients, an overall restenosis rate of 20% to 25% remains. Despite numerous trials, no effective pharmacologic therapy has been found. Intracoronary irradiation is a new technique proposed to prevent restenosis after angioplasty. In animal models of restenosis after balloon injury, there is marked reduction of neointimal proliferation when the injured vessel is irradiated, using a variety of radiation sources and delivery systems. Early human trials have underscored the importance of careful source calibration and dosimetry. A small, randomized, double-blind, placebo-controlled study of intracoronary irradiation to prevent recurrent restenosis recently reported striking reductions in angiographic restenosis as well as clinical event rates. A number of important issues remain unresolved, such as defining which component of the arterial wall serves as the target tissue for radiation, the minimal effective dose, the maximum tolerable dose, and user-friendly radiation delivery systems. Further studies are needed to define the safety, efficacy and the ultimate usefulness of intracoronary irradiation as an adjunct to current procedures in interventional cardiology.
Angioplasty, Balloon, Coronary↗
Irradiation and stenting.
Intravascular irradiation by both gamma and beta sources has been shown to prevent neointimal proliferation after balloon injury in the overstretch pig coronary model. A number of clinical studies are underway that involve brachytherapy from gamma sources in vessels that have been stented. The purpose of this review is to analyse the physical nature of the interaction of various forms of radiation with stent materials and to summarize the available experimental information for relevant clinical correlates of these effects. The ultimate use of vascular radiation in the presence of metallic stents will require knowledge of the possible dose alterations, and where possible, techniques to compensate for these effects.
Animals↗
Intracoronary irradiation: dose response for the prevention of restenosis in swine.
PURPOSE: Restenosis after percutaneous transluminal coronary angioplasty represents, in part, a proliferative response of vascular smooth muscle at the site of injury. We have previously shown that high-dose radiation (20 Gy), delivered via an intracoronary 192Ir source, causes focal medial fibrosis and markedly impairs the restenosis process after balloon angioplasty in swine. This study sought to delineate the dose-response characteristics of this effect. METHODS AND MATERIALS: Forty juvenile swine underwent coronary angiography; a segment of the left coronary artery was chosen as a target for balloon injury. In 30 swine, a 2 cm ribbon of 192Ir was positioned at the target segment and 20, 15, or 10 Gy were delivered to the vessel wall (10 animals/dose). Subsequently, overdilatation balloon angioplasty was performed at the irradiated segment. In 10 control swine, overdilatation balloon angioplasty was performed without previous irradiation. Thirty-eight animals survived until sacrifice at 30 +/- 3 days. Histopathological analysis was performed by a pathologist in a blinded manner. The area of maximal luminal compromise within the target segment was analyzed via computer-assisted planimetry. RESULTS: Neointimal area was decreased by 71.4% at 20 Gy and by 58.3% at 15 Gy compared with control animals (p < 0.05 for both). A stimulatory effect on smooth muscle cell proliferation was noted at 10 Gy, with a 123% increase in neointimal area compared with controls (p < 0.05). Mean percent area stenosis was also reduced by 63% at 20 Gy and by 74.8% at 15 Gy compared with controls (p < 0.05 for both). CONCLUSIONS: Intracoronary irradiation prior to overstretch balloon angioplasty markedly reduces neointima formation; this effect is dose dependent, with evidence of a significant stimulatory effect at 10 Gy. The effective therapeutic dose range for the prevention of restenosis in this model begins at approximately 15 Gy delivered to the vessel wall.
Angioplasty, Balloon, Coronary↗
Dosimetric considerations for catheter-based beta and gamma emitters in the therapy of neointimal hyperplasia in human coronary arteries.
PURPOSE: Recent data indicate that intraluminal irradiation of coronary arteries following balloon angioplasty reduces proliferation of smooth muscle cells, neointima formation, and restenosis. We present calculations for various isotopes and geometries in an attempt to identify suitable source designs for such treatments. METHODS AND MATERIALS: Analytical calculations of dose distributions and dose rates are presented for 192Ir, 125I, 103Pd, 32P, and 90Sr for use in intracoronary irradiation. The effects of source geometry and positioning accuracy are studied. RESULTS: Accurate source centering, high dose rate, well-defined treatment volume, and radiation safety are all of concern; 15-20 Gy are required to a length of 2-3 cm of vessel wall (2-4 mm diameter). Dose must be confined to the region of the angioplasty, with reduced doses to normal tissues. Beta emitters have radiation safety advantages, but may not have suitable ranges for treating large diameter vessels. Gamma emitters deliver larger doses to normal tissues and to staff. Low energy x-ray emitters such as 125I and 103Pd reduce these risks but are not available at high enough activities. The feasibility of injecting a radioactive liquid directly into the angioplasty balloon is also explored. CONCLUSIONS: Accurate source centering is found to be of great importance. If this can be accomplished, then high energy beta emitters such as 90Sr would be ideal sources. Otherwise, gamma emitters such as 192Ir may be optimal. A liquid beta source would have optimal geometry and dose distribution, but available sources, such as 32P are unsafe for use with available balloon catheters.
Brachytherapy↗
Monitoring of soluble HLA alloantigens and anti-HLA antibodies identifies heart allograft recipients at risk of transplant-associated coronary artery disease.
The development of accelerated transplant-related coronary artery disease (T-CAD) is the major obstacle to long-term survival of cardiac allografts. We have investigated the role of various demographic and immunologic parameters as prognostic indicators of T-CAD in a population of 274 heart allograft recipients. Our data demonstrate that patients who experience more than 1 episode of acute rejection per year and/or develop antidonor HLA antibodies are at increased risk of developing T-CAD. Using HLA-A2 as a marker for the release of soluble HLA antigens from the donor, we established that recipients displaying circulating donor alloantigens for more than 26 weeks following transplantation are at increased risk of developing T-CAD (P=0.008). This association suggests that the release of alloantigens from the allograft is indicative of chronic injury and/or that it stimulates chronic rejection via the indirect allorecognition pathway. Our findings indicate that patients at risk of developing T-CAD can be identified by monitoring the release of donor alloantigens and production of antidonor HLA antibodies following transplantation.
Adolescent↗
Dosimetry of a radioactive coronary balloon dilatation catheter for treatment of neointimal hyperplasia.
Recent reports suggest that intraluminal irradiation of coronary arteries in conjunction with balloon angioplasty reduces proliferation of smooth muscle cells and neointima formation, thereby inhibiting restenosis. One possible irradiation technique is to inflate the balloon dilitation catheter with a radioactive solution. This has advantages over other proposed irradiation procedures, in that accurate source positioning and uniform dose to the vessel wall are assured. Several high-energy beta-minus emitters may be suitable for this application. We present experimental measurements and analytical calculations of the dose distribution around a 3-mm-diam by 20-mm-long balloon filled with 90Y-chloride solution. The dose rate at the surface of the balloon is approximately 0.14 cGy/s per mCi/ml (3.78 x 10(-11) Gy/s per Bq/ml), with the dose decreasing to 53% at 0.5 mm, and < 5% at 3.5-mm radial distance. 90Y and other possible isotopes are currently available at specific concentrations > or = 50 mCi/ml (1.85 x 10(9) Bq/ml), which enables the delivery of 20 Gy in less than 5 min. The dosimetric and radiation safety advantages of this system warrant further feasibility studies. Issues of concern include incorporating the beta-emitter into a suitable chemical form, and assessing organ and whole body doses in the (< 1 in 10(3)) event of balloon failure.
Angioplasty, Balloon, Coronary↗
Intracoronary irradiation markedly reduces neointimal proliferation after balloon angioplasty in swine: persistent benefit at 6-month follow-up.
OBJECTIVES: This study examined the long-term efficacy of intracoronary irradiation for limiting neointimal proliferation after overstretch balloon angioplasty in a porcine model of restenosis. In addition, this study sought to identify any adverse late sequelae of this novel therapy for restenosis. BACKGROUND: Restenosis after coronary angioplasty represents in part a proliferative response of vascular smooth muscle at the site of injury. We have shown previously that high dose intracoronary radiation induces focal medial fibrosis and markedly reduces neointimal proliferation early after balloon angioplasty in swine. METHODS: Twenty-two juvenile swine underwent intervention at a target segment of the left coronary artery. In 11 swine, a 2-cm ribbon of iridium-192 was positioned at the target segment and 2,000 cGy was delivered to the vessel wall. Subsequently, overdilation balloon angioplasty was performed at the irradiated segment. In 11 control swine, overdilation balloon angioplasty was performed without previous irradiation. Twenty animals survived and underwent histopathologic analysis at 180 +/- 8 days. RESULTS: Mean (+/- SD) neointimal area was 1.59 +/- 0.78 and 0.46 +/- 0.35 mm2 (p < 0.001) in control and irradiated animals, respectively. Mean percent area stenosis was 37.9 +/- 12.4% and 14.2 +/- 9.0% (p < 0.001) in the control and irradiated animals, respectively. Thus, by 6-month follow-up, intracoronary irradiation before balloon angioplasty had reduced the bulk of the neointimal lesion by 71.1% and reduced percent area stenosis by 62.5% compared with that in control animals. There was no evidence of radiation vasculopathy or myocardial damage at 6 months. CONCLUSIONS: Intracoronary irradiation (2,000 cGy) produces persistent impairment of neointimal proliferation 6 months after balloon injury, with no evidence of late radiation sequelae.
Angioplasty, Balloon↗
Nitric oxide modulates dopamine release during global temporary cerebral ischemia.
Dopamine (DA) is released in large quantities from the striatum during cerebral ischemia. Along with excitatory neurotransmitters, DA plays a role in cellular neuronal ischemic injury. In this study we examined the role of nitric oxide (NO) in the ischemia-induced release of DA. A microdialysis probe was stereotactically placed into the corpus striatum of 16 Sprague-Dawley rats for DA, 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) level determinations. After probe stabilization, the animals received either NG-nitro-L-arginine-methyl ester (L-NAME), a NO synthase inhibitor, or vehicle through the microdialysis probe. Temporary global forebrain ischemia was induced using bilateral carotid artery ligature tightening and controlled hemorrhagic hypotension for 15 min. L-NAME administration caused a reduction in ischemic estimated extraneuronal DA concentration by 60% (P < 0.005) compared with control. There was an increase in both DOPAC and HVA concentrations during the recovery period compared to baseline values in the control group (P < 0.05). L-NAME also caused a reduction in HVA concentration compared to vehicle administration during the latter part of recovery (P < 0.05). These data support the concept that ischemic dopamine release may be mediated by NO. This NO-modulated DA release may contribute to the previously reported deleterious neurotoxic effects of NO during ischemia.
3,4-Dihydroxyphenylacetic Acid↗