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Biomedical subjects

R Virmani

Publications and source records attributed to R Virmani.

At least 235 records · Page 13Linked to original sources
PubMed1989

Recently diagnosed idiopathic dilated cardiomyopathy: incidence of myocarditis and efficacy of prednisone therapy.

Fifty-two patients with recently diagnosed idiopathic dilated cardiomyopathy were studied to determine the incidence of myocarditis; patients were randomly assigned to receive either conventional therapy alone or conventional therapy plus prednisone to assess possible therapeutic efficacy with regard to survival. Inflammatory criteria were present in 23% of the population studied with 13% having overt myocarditis according to the Dallas criteria. The addition of prednisone to conventional therapy did not improve survival in a homogeneous population with new-onset dilated cardiomyopathy. Furthermore, the diagnosis of myocarditis by endomyocardial biopsy did not influence 2-year survival once dilated cardiomyopathy had developed. Biopsy-documented myocarditis resolved in all patients, according to results of 3-month follow-up endomyocardial biopsies, regardless of treatment group. There was a trend for patients with a left ventricular ejection fraction less than 20% to show reduced survival at 2 years compared to the group with a higher ejection fraction (p = 0.07). Right ventricular dysfunction determined at catheterization was present in 20 of 52 patients and was the most significant predictor of survival. Patients with preserved right ventricular function had a 95% 24-month survival rate compared to 47% for patients with right ventricular diastolic dysfunction (right ventricular end-diastolic pressure greater than or equal to 11 mm Hg) (p = 0.005).

Adult↗
PubMed1989

Eosinophilic products lead to myocardial damage.

Eosinophils have been associated with endomyocardial fibrosis. However, their effect on the myocardium and the reactions they elicit have not been emphasized. We describe four patients with extensive myocardial eosinophilic infiltration with and without endomyocardial fibrosis. Patients with a short duration of disease had eosinophilic infiltrates, myocardial eosinophilic abscesses containing granular eosinophilic material, and/or Charcot-Leyden crystals with and without profuse histiocytic and giant cell reaction with granuloma formation. In the early phase, the granular eosinophilic material can be visualized by the Luna stain and/or by electron microscopic examination. In patients with a long duration of symptoms, well-developed granulomas and profuse fibrosis are seen and eosinophilic material may not be visualized. Toxic eosinophil granular protein may be involved in the development of these lesions.

Adult↗
PubMed1989

Rheumatic heart disease in a patient with acquired immunodeficiency syndrome.

Acute rheumatic heart disease (RHD) with Aschoff nodules and biventricular dilation was diagnosed at autopsy in a patient with acquired immunodeficiency syndrome who died of pneumonia due to Pneumocystis carinii. The relationship of acute RHD and human immunodeficiency virus-associated immune deficiency is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Endothelial and myocardial injury during ischemia and reperfusion: pathogenesis and therapeutic implications.

Early reperfusion remains the most effective way of limiting myocardial necrosis and improving ventricular function in experimental models and human patients. However, the introduction of oxygen and cellular elements, especially the neutrophil, into the ischemic zone may initiate a deleterious cascade of events that limits myocardial salvage after reperfusion. Although the pathogenesis of reperfusion injury remains controversial, recent studies have suggested that the endothelium may play a critical role. Endothelial cells maintain flow in the microcirculation by secreting a number of vasodilatory compounds and substances that prevent plugging of capillaries by inhibiting neutrophil adherence and platelet aggregation. Reperfusion of ischemic myocardium accelerates structural and functional changes in endothelial cells, resulting in a progressive decrease in microcirculatory flow ("no reflow" phenomenon). Numerous studies suggest that activated neutrophils mediate vascular damage by releasing reactive oxygen species and potent proteolytic enzymes. The administration of therapeutic agents that limit endothelial disruption and neutrophil plugging has shown promising results in limiting myocardial reperfusion injury in experimental models.

Animals↗
PubMed1989

Congestive heart failure due to coronary artery disease without myocardial infarction: clinicopathologic description of an unusual cardiomyopathy.

Cardiomyopathies (CMs) can be classified as idiopathic dilated, hypertrophic, restrictive/obliterative, and so-called "ischemic cardiomyopathy." We have observed a subgroup of patients with congestive heart failure, dilated hearts, and severe coronary artery disease in the absence of myocardial infarction and therefore not fulfilling the criteria for ischemic CM. To better elucidate this group, which we called "coronary" CM, 54 consecutive necropsy patients who had congestive heart failure were retrospectively studied. Nineteen patients had idiopathic dilated CM, 26 had ischemic CM, and nine had coronary CM. The mean age of the patients with coronary CM and ischemic CM was significantly greater than that of the patients with idiopathic dilated CM (62 +/- 10 and 64 +/- 10 years versus 47 +/- 19 years, respectively). The duration of congestive heart failure was longest in the coronary CM group (4.1 +/- 3.4 years); half of these patients died suddenly or from arrhythmias. Hearts from patients with coronary CM had marked biventricular dilatation and severe coronary artery disease (mean number of coronary arteries with more than 75% narrowing, 2.2). No acute or healed infarcts were grossly visible, but interstitial and focal perivascular fibrosis were present in the myocardium of all coronary CM hearts. Although coronary CM may comprise a subset of so-called "ischemic cardiomyopathy," these cases may also represent idiopathic dilated CM with coincidental coronary artery disease.

Aged↗
PubMed1989

Limitation of myocardial reperfusion injury by intravenous perfluorochemicals. Role of neutrophil activation.

Neutrophil activation and infiltration into the ischemic myocardium after reperfusion may limit the amount of salvageable myocardium (reperfusion injury). The effects of intravenous perfluorochemicals (Fluosol-DA) on infarct size, ventricular contractility, and neutrophil function were assessed in an occlusion-reperfusion canine model. Closed-chest dogs were subjected to 90 minutes of left anterior descending artery occlusion followed by 24 hours of reperfusion. Animals were randomized to receive either Fluosol-DA (FDA, n = 8) or Ringer's lactate (CONT, n = 10) intravenously over 30 minutes just before left anterior descending artery reperfusion. Neutrophil demargination and infiltration into the myocardium were assessed in vivo with In111. Neutrophil chemotaxis, superoxide radical production, and lysozyme degranulation were evaluated ex vivo at baseline, 1 hour after occlusion, and 1 hour after reperfusion. Perfluorochemicals significantly reduced infarct size expressed as percent of area at risk (FDA, 7 +/- 4%; CONT, 24 +/- 6%; p less than 0.01). This was associated with positive wall motion in the jeopardized zone of Fluosol-DA animals compared with dyskinesis in control animals (FDA, +4.4 +/- 2.1%; CONT, -1.1 +/- 1.5%; p less than 0.05). Electron microscopy showed reduced neutrophil and erythrocyte plugging of capillaries with relative preservation of endothelial cells in the Fluosol-DA animals. Myocardial blood flow was greater in the ischemic endocardium of Fluosol-DA animals 1 hour after reperfusion (FDA, 1.23 +/- 0.21; CONT, 0.62 +/- 0.08 ml/g/min; p less than 0.01). Neutrophil demargination and infiltration into the ischemic myocardium was reduced in the animals treated with Fluosol-DA. (FDA, 2.5 +/- 0.7 x 10(3); CONT, 14.1 +/- 2.7 x 10(3) neutrophils/g; p less than 0.01). Neutrophil chemotaxis and lysozyme release were also markedly suppressed in the Fluosol-DA groups ex vivo. These results show that intravenous Fluosol-DA significantly reduces reperfusion injury with greater salvage of myocardium and improved left ventricular function. The chief mechanism of action of Fluosol-DA appears to be the suppression of neutrophil function.

Animals↗
PubMed1989

Intracoronary adenosine administered after reperfusion limits vascular injury after prolonged ischemia in the canine model.

Myocardial salvage after reperfusion may be limited by deleterious vascular changes in the previously ischemic microcirculatory bed. This could result in a progressive decrease in blood flow in the capillary bed to potentially viable myocytes (no-reflow phenomenon). The effect of intracoronary adenosine on these changes was assessed in 15 closed-chest dogs subjected to 2 hours of proximal left anterior descending artery (LAD) occlusion followed by 3 hours of reperfusion. Animals randomly received adenosine (n = 8) 3.75 mg/min into the proximal LAD or an equivalent volume of saline (control) (n = 7) for 1 hour after reperfusion. Endothelial-dependent and independent coronary vasodilator reserve was determined using a chronically implanted volume-flowmeter on the mid-LAD at baseline and 1 and 3 hours after reperfusion with acetylcholine and papaverine infusions, respectively, into the proximal vessel. Regional myocardial blood flow was measured serially with radioactive microspheres and regional contractile function with contrast ventriculography. Both agonists produced a significant increase in LAD flow before occlusion. Endothelial-dependent and independent vasodilatory reserve was significantly reduced (p less than 0.05) at 1 and 3 hours after reperfusion in control animals compared with adenosine treatment. A progressive decrease in mid-LAD flow and increase in coronary vascular resistance after reperfusion was observed in control animals (p less than 0.05). The treated group manifested improved regional myocardial blood flow in endocardial regions from the central (0.73 +/- 0.15 versus 0.24 +/- 0.11 ml/g/min; p less than 0.02) and lateral ischemic zones (0.80 +/- 0.15 versus 0.34 +/- 0.12 ml/g/min; p less than 0.05) 3 hours after reperfusion. A significant reduction (p less than 0.05) in endocardial and midmyocardial flow compared with baseline was seen in control animals at 3 hours. Intravascular and interstitial neutrophil infiltration was reduced in adenosine animals and this was associated with relative ultrastructural preservation of endothelial cells. Regional ventricular function in the ischemic zone was improved in the adenosine group 3 hours after reperfusion (13.4 +/- 3.9% versus -5.3 +/- 1.6%; p less than 0.001). This study demonstrates that selective administration of adenosine after reperfusion significantly attenuates functional and structural abnormalities in the microvasculature after prolonged (2 hours) regional ischemia in the canine model. Prevention of microvascular injury and the non-reflow phenomenon by adenosine may preserve reversibly injured myocytes following restoration of blood flow to previously ischemic myocardium.

Adenosine↗
PubMed1988

Frequency of myocarditis, left ventricular dysfunction and ventricular tachycardia in the acquired immune deficiency syndrome.

To evaluate possible relations between clinical and histopathologic cardiac findings in patients with the acquired immune deficiency syndrome (AIDS), 58 consecutively autopsied AIDS patients were reviewed retrospectively. Twenty-six (45%) had histopathologic myocarditis. Fifteen of these 26 (58%) had greater than or equal to 1 clinical cardiac abnormalities: 6 had congestive heart failure or left ventricular (LV) dysfunction, or both, 4 had ventricular tachycardia (VT), 10 had electrocardiographic abnormalities and 4 had pericardial abnormalities. Of the 32 patients without myocarditis, 6 (19%) had pericardial or electrocardiographic abnormalities, or both, but none had congestive heart failure, LV dysfunction or VT. Overall, clinical cardiac abnormalities were found in 21 patients (36%). Patients with myocarditis had a significantly higher incidence of clinical cardiac abnormalities than patients without myocarditis (58 vs 19%, p less than 0.01). All patients with congestive heart failure, LV dysfunction or VT had myocarditis. Thus, serious clinical cardiac abnormalities were common in patients with AIDS and were associated with myocarditis.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Serial electrocardiographic changes in idiopathic dilated cardiomyopathy confirmed at necropsy.

Serial electrocardiographic changes in necropsy-proven idiopathic dilated cardiomyopathy are evaluated and a method of predicting heart weight using QRS amplitudes is described. In 34 patients with multiple electrocardiograms (mean 3/patient) progressive prolongation of PR interval (0.18 +/- 0.03 to 0.21 +/- 0.03, p less than 0.001) and QRS duration (0.10 +/- 0.02 to 0.13 +/- 0.03, p less than 0.0001) was noted. Progressive conduction abnormalities were common (82%). QTc interval and QRS- and T-wave axes did not change. In 50 patients with electrocardiograms within 60 days of death, total 12-lead QRS and V1 through V6 QRS amplitude correlated better with heart weight (r = 0.51, p less than 0.0001 and r = 0.55, p less than 0.0001) than the Estes-Romhilt score did. The mean total 12-lead QRS amplitude was 138 mm with a mean of 106 for V1 through V6. In 31 patients cardiac mass index was calculated and showed significant correlation with 12-lead and V1 through V6 QRS amplitudes (r = 0.68, p less than 0.0001 and r = 0.75, p less than 0.0001, respectively). The QRS amplitudes remained constant during the illness. By using total 12-lead QRS or frontal plane QRS amplitude, heart weight can be predicted as early as 2 years before death. Use of body surface area and QRS amplitude criteria increases the accuracy of heart weight prediction. Thus, progressive electrocardiographic changes are common in patients with idiopathic dilated cardiomyopathy and QRS amplitude criteria are more accurate in the prediction of left ventricular hypertrophy than standard criteria.

Adolescent↗
PubMed1988

Laser angioplasty: an atherosclerotic swine model.

Rapid production of occlusive, atherosclerotic iliac artery lesions was achieved in 25 of 27 (93%) Yucatan miniature swine, using a combination of high cholesterol diet and mechanical endothelial denudation. Animals were fed a diet with 2% of their calories as raw cholesterol 2 weeks prior to balloon denudation of iliac arteries, which resulted in atherosclerotic lesions within 8 weeks. Early after denudation we have demonstrated total occlusion of arteries by fibrin thrombi, which in time organize and ultimately result in fibrotic occlusive disease. The arterial walls and intima show varying degrees of foam cell infiltration with destruction of the internal elastic lamina and calcification. Totally occluded lesions show fibrointimal proliferation, fibrosis, and multiluminal channels, which are probably secondary to organized thrombus. Our model of occlusive iliac artery disease involving vessels of 1 to 3 mm in diameter allows the development of catheter systems suitable for use in human peripheral and coronary arteries. This model is useful for the study of angioplasty, whether mechanical, balloon, or laser-mediated.

Angioplasty, Balloon↗
PubMed1988

Cardiovascular effects of cocaine: an autopsy study of 40 patients.

From September 1983 through November 1986, autopsies were performed on 6810 patients at the Office of the Maryland Medical Examiners; of these 40 had detectable cocaine, its metabolites, or both in body fluids. These patients were divided into two groups: natural cocaine-associated deaths (31 patients, mean age 28 +/- 5 years, blood level of cocaine 5.3 +/- 8.1 mg/L) and homicide deaths with detectable cocaine (nine patients, mean age 33 +/- 8 years, blood level of cocaine 0.3 +/- 0.3 mg/L). Cocaine-associated deaths were compared to a control group of 27 victims of sudden traumatic death (mean age 34 +/- 5 years). Total thrombotic occlusion of the left anterior descending coronary artery overlying mild coronary atherosclerosis occurred in one patient with cocaine-associated death. Results of histologic examination showed myocarditis (mononuclear infiltrate) in 8 of 40 (20%) patients dying with detectable cocaine in body fluids compared to 1 of 27 victims of sudden traumatic death (3.7%, p less than or equal to 0.05). Contraction band necrosis occurred in 25% of cocaine-associated deaths compared to a 41% incidence among victims of sudden traumatic death. We conclude that myocarditis occurs frequently in patients dying of cocaine abuse and may represent microvascular injury.

Adult↗
PubMed1988

Myocardial protection by perfluorochemical infusion during transient ischemia produced by balloon coronary occlusion.

To assess the efficacy of the perfluorochemical Fluosol-DA 20% for myocardial protection during repeated periods of balloon occlusion of the left circumflex coronary artery, 25 anesthetized dogs were randomized to receive either oxygenated perfluorochemical, (Fluosol-DA [F]; n = 10) or oxygenated Ringer's lactate (R; n = 6), at the rate of 30 ml/min, during inflation of the balloon. A control group (C; n = 9) received no infusion. A total of eight inflations were performed, each lasting 90 seconds, followed by an equivalent deflation time. Hemodynamics, ECGs, regional myocardial function, and biochemical parameters were studied. Significant differences were noted in ST segment elevation at 90 seconds of inflation in the F (1.5 mm +/- 0.6), C (3.7 mm +/- 0.75), and R (2.9 mm +/- 0.75) groups (F vs C or R p less than 0.05). This was associated with significant improvement in radial shortening in the jeopardized zone at 45 seconds into occlusion in the F group compared to the C and R groups (F = 21.1% +/- 5.1 vs C = 3.5% +/- 4.5 or R = 1.1% +/- 3.2; p less than 0.05). Results of electron microscopy showed reversible changes of ischemia within the mitochondria, and these were most marked in the C and R groups compared to the F group. Endothelial swelling was mild and was present only focally in the R and C groups. Thus perfluorochemicals may enhance the safety and efficacy of balloon angioplasty.

Adenine Nucleotides↗
PubMed1988

A comparison of morphologic and angiographic findings in long-term internal mammary artery and saphenous vein bypass grafts.

Internal mammary artery grafts are currently considered the conduits of choice for myocardial revascularization. Comparisons of long-term morphologic changes in internal mammary artery grafts and saphenous vein grafts and correlation with premortem angiography have not been reported. Eighteen internal mammary artery and 15 saphenous vein grafts that had been in place for 12 to 118 months (mean 56) in 18 patients were removed either surgically or at necropsy and examined histologically. Premortem angiograms were performed within 1 month of histologic study in 15 of these patients. Fibrointimal proliferation was more frequent in internal mammary artery than in saphenous vein grafts 8 [( 44%] of 18 versus 4 [27%] of 15; p = NS). In contrast, atherosclerosis was common in saphenous vein grafts but was extremely rare in internal mammary artery grafts (10 of 15 versus 1 of 18; p = 0.01). A good correlation was noted between the degree of narrowing estimated by angiographic and histologic measurements in both internal mammary artery grafts (d = 0.90) and saphenous vein grafts (d = 0.71). Accelerated atherosclerosis did not occur in internal mammary artery grafts, but was common in saphenous vein grafts. Fibrointimal proliferation was commonly associated with graft narrowing in internal mammary artery grafts and may be an important factor in late graft closure. This study also confirms that internal mammary artery grafts have greater longevity compared with saphenous vein grafts.

Adult↗
PubMed1988

Prevalent myocarditis at necropsy in the acquired immunodeficiency syndrome.

The prevalence of myocarditis was retrospectively evaluated in 71 consecutive necropsy patients who died from acquired immunodeficiency syndrome (AIDS) between 1982 and 1986. Myocarditis was found in 37 cases (52%). Biventricular dilation at necropsy was present in seven cases (10%) and was accompanied by myocarditis in each case; fatal congestive heart failure occurred in four of these seven cases. Although viral, protozoan, bacterial, fungal and mycobacterial opportunistic pathogens were present in myocardial sections of 7 of 37 myocarditis cases, the etiology of myocarditis in the majority of these patients with AIDS remained idiopathic. Thus, myocarditis is a frequent finding at necropsy in patients with AIDS and may contribute to the development of biventricular dilation.

Acquired Immunodeficiency Syndrome↗