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Biomedical subjects

R Virmani

Publications and source records attributed to R Virmani.

At least 19 recordsLinked to original sources
PubMed1992

Comparison of cardiac findings in patients with mitral valve prolapse who die suddenly to those who have congestive heart failure from mitral regurgitation and to those with fatal noncardiac conditions.

Sudden death occurs in a small but important subset of patients with mitral valve prolapse (MVP). Clinical criteria for identifying patients at risk for sudden death have been elusive. To determine if certain morphologic characteristics were present in hearts from patients with sudden cardiac death and MVP, autopsy hearts from persons with sudden death and isolated MVP who were previously asymptomatic or had a history of cardiac arrhythmias (n = 27) were compared with (1) hearts from patients with congestive heart failure (CHF) and mitral regurgitation (MR) secondary to MVP (n = 14), and (2) hearts from persons dying from non-cardiac causes in which MVP was an incidental finding (n = 19). Patients who died suddenly were younger than both patients with MR/CHF and incidental cases (37 +/- 10 vs 65 +/- 16 and 58 +/- 21 years, respectively, p less than 0.001). Mitral valve annular circumference, anterior and posterior mitral valve leaflet lengths, posterior mitral valve thickness, and presence and extent of endocardial plaque were greater in hearts from patients with sudden death than hearts from those with incidental MVP. Hearts from patients with MR/CHF weighed significantly more, had greater left and right atrial cavity sizes and left ventricular cavity diameter than hearts from both sudden death and incidental cases.

Age Factors↗
PubMed1992

Primary sarcomas of the heart.

Seventy-five primary sarcomas of the heart were classified by histologic appearance as angiosarcoma (26 cases), undifferentiated sarcoma (18 cases), osteosarcoma (9 cases), fibrosarcoma (6 cases), malignant fibrous histiocytoma (6 cases), leiomyosarcoma (4 cases), myxosarcoma (3 cases), synovial sarcoma (2 cases), and neurofibrosarcoma (1 case). The ages of the patients ranged from 1 to 75 years at the time of presentation (mean, 39 years). Angiosarcomas were predominantly right-sided and osteosarcomas left-sided. Forty patients treated surgically were examined, and survival correlated with clinical and histologic parameters. the survival rate was poor, with a mean of 11 months and median of 6 months. By univariate analysis, the survival rate was more favorable for patients with tumors located on the left side of the heart, without necrosis, with a low mitotic count, and without metastasis at diagnosis. Survival rates were better in patients receiving chemotherapy and radiation therapy. Age, gender, presence of differentiation, and histologic type did not affect prognosis. By multivariate analysis, a low level of mitotic activity and any therapy were the only significant factors affecting survival rate. Immunostaining with commercially available antisera was useful in the diagnosis of sarcoma but not in subclassification of 19 tumors so tested. Although the prognosis for patients with cardiac sarcomas is dismal, histologic grading is useful in predicting outcome, as has been shown for soft tissue sarcomas of other sites.

Adolescent↗
PubMed1992

Necrotizing arteritis in uncorrected tetralogy of Fallot with pulmonary artery.

A 10-year-old girl with uncorrected tetralogy of Fallot with pulmonary atresia presented with fevers of unknown origin and left lung infiltrates. At autopsy, necrotizing vascular changes resembling those of severe pulmonary hypertension (grade VI in the Health-Edwards classification) were confined to the left lung. Pulmonary blood flow and pressure were greater in the left lung and were provided by an enlarged collateral artery arising directly from the descending thoracic aorta. To our knowledge, this is the first report of necrotizing arteritis of the pulmonary arteries in uncorrected tetralogy of Fallot with pulmonary atresia.

Arteritis↗
PubMed1992

The effects of intravenous infusions of selective adenosine A1-receptor and A2-receptor agonists on myocardial reperfusion injury.

To determine the efficacy of very low doses of adenosine on myocardial reperfusion injury and whether its effect is receptor mediated, 78 rabbits underwent 30 minutes of left circumflex artery occlusion and 48 hours of reperfusion. Animals were randomly assigned to receive one of three doses of adenosine, cyclopentyladenosine (a selective A1-receptor agonist), or CGS 21680C (a selective A2-receptor agonist). The drugs were infused for 65 minutes beginning 5 minutes before reperfusion. A significant reduction in histologically determined infarct size was noted with all three doses of adenosine, intermediate and low doses of the A1-receptor agonist (cyclopentyladenosine), and high and intermediate doses of the A2-receptor agonist (CGS 21680C). Furthermore, all three adenosine receptor agonists afforded similar degrees of protection. Results of this study demonstrate that intravenous infusions of very low doses of adenosine significantly enhance myocardial salvage and this protection is receptor mediated. Furthermore, the administration of the A1-receptor agonist would be clinically appealing, since it would avoid the potential side effects associated with activation of A2 receptors.

Adenosine↗
PubMed1992

Cocaine: an independent risk factor for aortic sudanophilia. A preliminary report.

Several recent autopsy reports indicate an increased prevalence of coronary atherosclerosis in ischemic heart disease temporally associated with cocaine abuse. The objective of this study was to conduct a retrospective analysis of sudanophilic lesions in young asymptomatic individuals who abused cocaine. Twenty-six cases (15-34-year-old black males) were examined from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study. Sixteen subjects (mean age 25 +/- 1 years) had a positive toxicologic screen for cocaine and/or its major metabolites at autopsy and were confirmed habitual cocaine abusers. The remaining 10 cases (mean age 24 +/- 2 years) were subjects with a negative toxicologic screen at autopsy and no history of illicit drug abuse. Post-mortem blood was collected for lipoprotein analysis and determination of smoking status. The aorta and right coronary arteries were stained with Sudan IV and the degree and extent of sudanophilia was quantitated by image analysis. Multiple linear regression analysis of cocaine, age, smoking status, VLDL+LDL-C/HDL-C ratio and HDL-C as predictor variables of percentage intimal surface involvement, revealed an association between cocaine abuse and the extent of sudanophilia in both the thoracic and abdominal aorta (P = 0.002 and 0.049, respectively). Analysis of risk factors or of cocaine abuse as predictors of sudanophilia did not achieve statistical significance in the right coronary artery. These preliminary results suggest that habitual use of cocaine, through unknown mechanism(s), increases aortic sudanophilia independent of traditional risk factors.

Adolescent↗
PubMed1992

Sudden cardiac death associated with isolated congenital coronary artery anomalies.

OBJECTIVES AND BACKGROUND: Congenital coronary anomalies are associated with sudden death and exercise-related death. Clarification of the risk and mechanisms of sudden death in patients with coronary anomalies may aid in decisions on intervention. METHODS: The clinicopathologic records of 242 patients with isolated coronary artery anomalies were reviewed for information on mode of death and abnormalities of the initial segment (acute angle takeoff, valvelike ridges or aortic intramural segments) and course of the anomalous coronary artery. RESULTS: Cardiac death occurred in 142 patients (59%); 78 (32%) of these deaths occurred suddenly. Of sudden deaths, 45% occurred with exercise. Sudden death (28 of 49, 57%) and exercise-related death (18 of 28, 64%) were most common with origin of the left main coronary artery from the right coronary sinus. Anomalous origin of the right coronary artery from the left coronary sinus was also commonly associated with exercise-related sudden death (6 of 13 sudden deaths, 46%). High risk anatomy involved abnormalities of the initial coronary artery segment or coursing of the anomalous artery between the pulmonary artery and aorta. Younger patients (less than or equal to 30 years old) were significantly more likely than older patients (greater than or equal to 30 years old) to die suddenly (62% vs. 12%, p = 0.0001) or during exercise (40% vs. 2%, p = 0.00001) despite their low frequency of significant atherosclerotic coronary artery disease (1% vs. 40%, p = 0.00001). CONCLUSIONS: Younger patients (less than or equal to 30 years old) with an isolated coronary artery anomaly are at risk of dying suddenly and with exercise. Therefore, greater effort for early detection and surgical repair of these lesions is warranted.

Adolescent↗
PubMed1992

Pharmacologic perturbation of neutrophils by Fluosol results in a sustained reduction in infarct size in the canine model of reperfusion.

Previous studies have demonstrated that intravenous administration of large doses of Fluosol, a perfluorochemical preparation, reduced infarct size 24 h after reperfusion, an effect that was associated with reduced neutrophil infiltration. The effect of a clinically tolerable dose of Fluosol on infarct size after a prolonged period of reperfusion and its mechanism of action on neutrophils remain unknown. Twenty-one anesthesized closed chest dogs were subjected to 90 min of proximal left anterior descending coronary artery occlusion and 72 h of reperfusion. An additional five dogs that did not undergo regional myocardial ischemia were utilized to explore the mechanism of action of Fluosol on neutrophil function. In the infarct study, animals were randomized to receive either intravenous Fluosol (n = 10) or an equivalent volume of Ringer's lactate solution (control; n = 11) at 15 ml/kg body weight during the last 30 min of occlusion and for the 1st 30 min of reperfusion. Fluosol significantly reduced infarct size when expressed as percent area at risk 72 h after reperfusion (13.7 +/- 2.7% vs. 38.3 +/- 4.5%, respectively, p less than 0.001). This reduction was associated with significant improvement in regional wall motion (18.4 +/- 2.3% vs. 5.5 +/- 2%, p less than 0.001). Endocardial blood flow in the ischemic bed was significantly higher 3 h after reperfusion in Fluosol-treated dogs (0.63 +/- 0.08 vs. 0.34 +/- 0.07 ml/min per g, p = 0.01). Reduced capillary plugging by neutrophils with relative preservation of endothelial cell structure was observed in Fluosol-treated animals. Infusion of Fluosol produced a marked transient decrease in peripheral neutrophil and platelet counts in both ischemic and nonischemic dogs and was associated with a significant reduction in total hemolytic complement levels. Studies of neutrophil function ex vivo revealed a reduction in chemotaxis and lysozyme degranulation after infusion of Fluosol. In vitro experiments showed that Fluosol produced a rapid and sustained activation of neutrophils determined by superoxide anion production. These data demonstrate that low dose intravenous Fluosol produces a sustained reduction in infarct size in the canine model. The beneficial effect may be in part due to the suppression of various neutrophil functions in the reperfused myocardium subsequent to peripheral activation by Fluosol. Such interventions may offer a novel therapy to enhance myocardial salvage by sequestration of circulating neutrophils during the critical early reperfusion period.

Animals↗
PubMed1992

Real-time assessment of experimental arterial angioplasty with transvenous intravascular ultrasound.

Optimal evaluation of experimental angioplasty procedures would allow real-time simultaneous assessment during the procedure without direct manipulation of treated arterial segments. To assess the feasibility and utility of transvenous real-time intravascular ultrasound imaging during experimental angioplasty, 11 consecutive atherosclerotic iliac artery segments in rabbits were imaged before, during and after thermal or conventional perfusion balloon angioplasty. A 20-MHz intravascular ultrasound catheter was positioned in the adjacent vein, and images were correlated with data from quantitative angiography and histologic studies. Images suitable for analysis were obtained at all 11 sites. Arterial distension and recoil were observed during balloon inflation and deflation. Measurements of lumen diameter and cross-sectional area by intravascular ultrasound and angiography were closely correlated (r2 = 0.90, SEE = 0.2 mm, and r2 = 0.90, SEE = 0.8 mm2, respectively). Intimal dissections were identified in six segments by intravascular ultrasound and all were concordant with histologic findings. Thus, real-time transvenous ultrasound avoids manipulation of the treated artery, and is a feasible modality for dynamic quantitative and qualitative assessment of arterial interventions.

Angiography, Digital Subtraction↗
PubMed1992

Genetically engineered endothelial cells remain adherent and viable after stent deployment and exposure to flow in vitro.

Intravascular stents, currently in experimental human use for recurrent arterial stenosis, are plagued by subacute thrombosis. As a therapeutic approach to stent-related thrombosis, we and others have suggested coating stents with endothelial cells before implantation. In a previous study we demonstrated the feasibility of coating stents with endothelial cells that were genetically modified to secrete large amounts of human tissue plasminogen activator. In the present study we attempted both to develop a clinically applicable protocol for stent seeding and to test whether seeded cells would remain adherent to stents after exposure to pulsatile flow. Endothelial cells were harvested from the saphenous veins of sheep with survival of the donor animals. Harvested cells were transduced with a retroviral vector containing a marker gene and seeded onto catheter-mounted stents under sterile conditions. Scanning electron microscopy revealed complete coverage of the stent surfaces by seeded cells. Stents were expanded and exposed to pulsatile flow in vitro. Substantial cell retention was observed on the lateral stent surfaces by light microscopy and scanning electron microscopy; fewer cells were seen on the luminal and abluminal surfaces. Removal of seeded cells from flow-exposed stents by trypsin digestion resulted in the recovery of approximately 70% of the seeded cells. These cells were viable and healthy as judged by their ability to proliferate to confluence with the same kinetics as control (non-flow-exposed) cells. Autologous genetically modified endothelial cells can be seeded onto catheter-mounted stents in a sterile manner, and stent deployment under flow conditions results in substantial retention of viable cells.

Animals↗
PubMed1992

Cocaine produces coronary artery vasoconstriction independent of an intact endothelium.

Studies have demonstrated that cocaine causes coronary vasoconstriction, but this has been unassociated with myocardial ischemia. Therefore, cocaine seems unlikely to precipitate myocardial infarction in the absence of potentiating factors. We hypothesized that injury to coronary endothelium could potentiate cocaine-induced coronary vasoconstriction by decreasing EDRF. The effect of cocaine on LAD diameter was measured in dogs subjected to coronary endothelial denudation and compared with that in a non-denuded control group. Endothelial denudation was accomplished by abrasion with an inflated angioplasty balloon and confirmed in vivo by demonstrating a vasoconstrictive response to infused acetylcholine and by postmortem scanning electron microscopy. Cocaine produced a similar maximal reduction in LAD diameter in both groups. Thus, cocaine induces endothelium-independent coronary artery vasoconstriction. Failure of endothelial injury to potentiate the coronary vasoconstrictive effect by cocaine suggests that factors other than endothelial dysfunction may be important in pathogenesis of cocaine-associated myocardial infarction.

Acetylcholine↗
PubMed1992

Causes of sudden death in athletes.

The incidence of sudden death in athletes is low. Some pathologic conditions, such as hypertrophic cardiomyopathy, coronary artery anomalies, and right ventricular dysplasia may predispose to sudden death during exercise in young athletes. In older individuals, exercise may trigger terminal arrhythmias in patients with atherosclerosis. Screening programs for young individuals undertaking athletic regimens are currently recommended only for those with a suggestive clinical or family history. For older individuals, caution should be advised for patients with known or suspected atherosclerotic disease.

Cardiomegaly↗
PubMed1992

Anatomy and pathology of the right ventricle (including acquired tricuspid and pulmonic valve disease).

With the increased availability of various imaging techniques to assess right ventricular structure and function, there has been a greater appreciation of the importance of right ventricular performance in the setting of left ventricular dysfunction as well as intrinsic ventricular diseases. This article discusses the pathology of the right ventricle, tricuspid valve, and pulmonic valve and concentrates on the major acquired and congenital conditions that manifest in an adult population.

Adult↗
PubMed1991

Flow support catheter for prolonged maintenance of coronary blood flow.

A newly designed flow support catheter with a supporting wire mesh cage which can be expanded into a tubular configuration and then readily reduced was evaluated in mongrel dogs. Regional myocardial blood flow (RMBF) was measured using the radioactive microsphere technique in the area of both balloon-denuded instrumented and control non-instrumented coronary arteries following placement of either a fixed-wire or a higher profile rapid exchange flow support catheter. At 5, 20, and 180 min following delivery and expansion of either device, RMBF was not significantly different in left ventricular subepicardium and subendocardium perfused by the instrumented vs. the control coronary arteries. Angiography demonstrated widely patent instrumented arteries in 15/18 dogs; in no dog was side branch occlusion observed. Significant cage thrombus deposition was seen angiographically in 3 animals causing temporary total coronary occlusion in 1. Following reduction and removal of the flow support catheter, vessel patency was present in all dogs. The flow support catheter is an effective endovascular stenting device capable of providing structural arterial support, while simultaneously maintaining distal coronary blood flow. It is envisioned that the primary application of this catheter will be to enable primary salvage of vessels acutely injured during coronary angioplasty, by "tacking up" intimal flaps for an extended period. It may also provide a bridge to emergency surgical revascularization.

Angioplasty, Balloon, Coronary↗
PubMed1991

Myocardial reperfusion injury in the canine model after 40 minutes of ischemia: effect of intracoronary adenosine.

To explore the contribution of reperfusion injury to final infarct size after a short duration of ischemia, closed-chest dogs underwent 40 minutes of proximal left anterior descending artery occlusion followed by 3 days of reperfusion. Animals randomly received intracoronary adenosine (n = 8) at 3.75 mg/min during the first hour of reperfusion or no therapy (control, n = 9). Infarct size was measured histologically. Regional ventricular function was determined with contrast ventriculography. The risk region was similar and collateral blood flow in the inner two thirds of the ischemic zone was markedly reduced in both groups (adenosine: 0.05 +/- 0.07 ml/min/gm; control: 0.02 +/- 0.07 ml/min/gm; p = NS). Infarct size as a percent of the area at risk was significantly reduced in the adenosine group (5.0 +/- 1.3% versus 13.5 +/- 3.2%; p = 0.03), associated with a trend for improved recovery of regional ventricular function. Relative endothelial preservation was seen in the adenosine group. These results suggest that reperfusion injury contributes to final myocardial cell necrosis in the closed-chest canine model subjected to 40 minutes of regional ischemia.

Adenosine↗
PubMed1991

Effect of intravenous adenosine on myocardial reperfusion injury in a model with low myocardial collateral blood flow.

The purpose of this study was to investigate the effects of various doses of adenosine administered intravenously on myocardial reperfusion injury in a model with poor collateral blood flow. New Zealand White rabbits were subjected to 30 minutes of occlusion of the obtuse marginal branch of the left circumflex artery and to 48 hours of reperfusion. Animals were randomized to receive intravenous adenosine in doses of 0.1 mg/min (low), 0.3 mg/min (intermediate), or 0.55 mg/min (high), or an equivalent volume of saline (control) commencing 5 minutes prior to reperfusion and continuing through the first 60 minutes of reperfusion. The area at risk was determined in vivo with Monastral blue dye and the area of necrosis was histologically examined with Masson's trichrome stain. Both the intermediate and high doses of adenosine, but not the low dose, significantly (p less than 0.05) decreased mean blood pressure. However, all three doses of adenosine produced a significant (p less than 0.05) and comparable decrease in infarct size expressed as a percent of area at risk (control, 52.0 +/- 4.6%; low, 35.3 +/- 4.1%; intermediate, 31.7 +/- 4.6%; high, 31.3 +/- 4.6%). Regional myocardial blood flow was significantly increased and coronary vascular resistance decreased by all three doses of adenosine in a subset of animals that did not undergo coronary occlusion (p less than 0.05). This study demonstrates that intravenous administration of nonhypotensive doses of adenosine given during the early reperfusion period attenuates reperfusion injury in a model with poor collateral blood flow.

Adenosine↗