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Biomedical subjects

R Subramanian

Publications and source records attributed to R Subramanian.

At least 73 records · Page 4Linked to original sources
PubMed1990

Primary left ventricular hemangiosarcoma diagnosed by endomyocardial biopsy in a dog.

An 8-year-old spayed Golden Retriever was examined because of recent onset of congestive heart failure complicated by ventricular arrhythmias. Echocardiography revealed a thickened, hypokinetic region of the left ventricular free wall. Fluoroscopically guided transarterial endomyocardial biopsy of the hypokinetic region of the left ventricle revealed infiltration of the endocradium by neoplastic cells consistent with hemangiosarcoma. The dog's clinical condition deteriorated 7 weeks later, and necropsy confirmed the diagnosis and primary site of origin of the tumor. This report describes the clinical use of an endomyocardial biopsy technique to diagnose an infiltrating myocardial tumor that was associated with signs mimicking canine dilated cardiomyopathy.

Animals↗
PubMed1990

Polymorphonuclear leucocytes as potential source of free radicals in the ischaemic-reperfused myocardium.

The feasibility of polymorphonuclear leucocytes as a potential source of free radicals during reperfusion of ischaemic myocardium was evaluated. Isolated rat heart was perfused in the presence of f-Met-Leu-Phe-activated and normal polymorphonuclear leucocytes for 30 min. To judge the degree of cellular injury which might result from activated polymorphonuclear leucocytes during perfusion, isolated hearts were also perfused with superoxide anions, hydroxyl radicals, and hypochlorous acid-generating systems in the absence or presence of their corresponding scavengers, superoxide dismutase plus catalase, dimethylthiourea, and allopurinol, respectively. Activated polymorphonuclear leucocytes stimulated the release of lactate dehydrogenase, a biological marker of cellular injury, and malondialdehyde, a presumptive marker for lipid peroxidation; increased tissue injury, as evidenced by morphologic examinations using light and electron microscopy; decreased dry/wet ratios of heart, signifying oedema formation; and reduced myocardial adenosine triphosphate and creatine phosphate content as well as coronary flow, indicating decreased myocardial performance. These biological, physiological, and morphologic parameters were reversed significantly, but not completely, by treating the heart with scavengers, superoxide dismutase plus catalase or allopurinol, but were reversed completely by simultaneous treatment with superoxide dismutase, catalase, and allopurinol. Comparable results were obtained when the hearts were treated with each of these free radical-generating systems and their corresponding scavengers. Generation of free radicals was confirmed either by cytochrome c reduction or by examining the chemiluminescence response using a luminometer. These results indicate that activated polymorphonuclear leucocytes can cause myocardial cellular injury equivalent to the damage caused by free radicals and oxidants which are present in an ischaemic-reperfused heart, suggesting that polymorphonuclear leucocytes may be a potential source of free radicals in the reperfused heart.

Animals↗
PubMed1990

Metabolism of indium chelates attached to monoclonal antibody: minimal transchelation of indium from benzyl-EDTA chelate in vivo.

The metabolism of radiolabeled antibodies is important for radioimmunoimaging and therapy. The loss of indium-111 (111In) from the chelate can pose problems in imaging and increases the radiation dose to normal tissues. We have evaluated the loss in vivo of 111In from Lym-1-benzyl-EDTA-111In (an antibody conjugated with isothiocyanato-benzyl-EDTA) in normal mice. A monoclonal antibody (CHA 255) that binds to benzyl-EDTA-indium chelates, but not to other forms of indium, was used to measure the percent of 111In remaining in the chelate. Four days after injection, 97.4 +/- 2.2% of the 111In in the liver was still in the benzyl-EDTA chelate, as was 99.4 +/- 0.7% of the 111In in the urine, and 99.1 +/- 0.7% of the 111In in the blood. Studies in vitro indicate that a benzyl-EDTA-111In-antibody-chelate conjugate is more stable in human serum than a benzyl-DTPA-111In conjugate, and that both benzyl-chelate conjugates are much more stable than an unsubstituted DTPA conjugate.

Animals↗
PubMed1989

Mesothelioma of the atrioventricular node and congenital complete heart block.

Congenital complete heart block (CCHB) has heterogeneous etiologies. It may occur as an isolated entity with no associated congenital cardiac malformations and is difficult to diagnose even with modern technology. Mesothelioma of the atrioventricular (AV) node is a benign tumor that causes CCHB. The occurrence of this tumor is rare, and a definitive diagnosis of the entity is made only at autopsy. The conduction disturbance caused by the mesothelioma is potentially treatable and should be considered in the differential diagnosis of CCHB. We present a case report of a 38-year-old female with CCHB caused by such a tumor. Clinical diagnosis and treatment of CCHB are reviewed.

Adult↗
PubMed1987

Surgical pathology of the mitral valve: a study of 712 cases spanning 21 years.

The gross surgical pathologic features of the mitral valve were reviewed in 712 patients who had undergone mitral valve replacement at our institution during 1965, 1970, 1975, 1980, and 1985. Among the 452 cases of mitral stenosis, either with or without mitral insufficiency, 99% were attributable to postinflammatory disease and 1% were related to congenital mitral stenosis. Among the 260 cases of pure mitral regurgitation, the two most common causes were a floppy valve (38%) and postinflammatory disease (31%). Moreover, a floppy valve was observed in 73% of the 59 examples of chordal rupture and in 38% of the 16 cases of infective endocarditis. Women accounted for 73% of the 452 cases of mitral stenosis and for 72% of the 530 cases of postinflammatory disease. In contrast, men accounted for 58% of the 260 cases of pure mitral regurgitation, including 76% of the floppy valves and 69% of the infected valves. During the 21 years spanned by the study, the relative frequency of postinflammatory mitral insufficiency progressively decreased, whereas that of floppy mitral valves increased. It is unclear whether aging, heredity, environmental factors, changes in the frequency of acute rheumatic fever, or changes in patient referral practices may account for this observation.

Adolescent↗
PubMed1987

Modulation of adenine nucleotide translocase activity during myocardial ischemia.

Preliminary studies have shown that high levels of free fatty acids, which elevate LCACAE and lower levels of free carnitine, are much more harmful to the heart after repeated periods of ischemia and reperfusion than after exposure to continuous ischemia and reperfusion. These observations appear to support our hypothesis that LCACAE inhibition of the mitochondrial ANT during ischemia potentiates free radical mediated damage to the inner mitochondrial membrane during reperfusion. These and related findings by others have led us to hypothesize that the mechanisms of ischemic injury to the heart involve the following sequence of events: (1) exposure to high levels of FFA during ischemia and reperfusion results in permanently elevated LCACAE and low free carnitine levels; (2) LCACAE-ANT binding increases and ANT activity decreases; (3) mitochondrial swelling occurs because of decreased ADP/ATP transport and oxidative phosphorylation; (4) complex III activity is altered (superoxide formation increases), and swelling of mitochondrial membranes exposes C = C bonds that are required for lipid peroxidation, which can lead to inner mitochondrial membrane damage. We further hypothesize that LCACAE-ANT inhibition-induced free radical damage causes the loss of mitochondrial matrix components (22), eventually leading to lesions of the sarcolemmal membrane and cell necrosis (22). Studies now in progress support this hypothesis and indicate that inhibition of ANT in isolated rat heart mitochondria by carboxyatractyloside or palmitoyl CoA stimulates free radical formation, probably at the complex III loci.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Free radical-mediated damage during myocardial ischemia and reperfusion and protection by carnitine esters.

Ischemic injury may be exacerbated by readmission of oxygen into the myocardium, probably due to the formation of free radicals and their interaction with membrane lipids. We tested the hypothesis that ischemic myocardial damage is potentiated during reperfusion with excess free fatty acids in the globally ischemic rat heart, and in parallel studies, we investigated the protective effects of carnitine derivatives. Intermittent ischemia, i.e. three 20 min periods of ischemia followed by 10 min reperfusion each, was induced in isolated working rat hearts perfused with either glucose (11 mM) alone or glucose with palmitate (11 mM and 1.2 mM). The ischemic coronary flow was reduced to 1.1 ml/min in a low-flow group and equalled 0 ml/min in a no-flow group. Loss of functional recovery in the low-flow and no-flow group was more pronounced when palmitate was present in the perfusate. This was associated with increased levels of long-chain acyl-CoA esters in the palmitate perfused hearts. Malondialdehyde, an indicator of free radical formation, was elevated in both low-flow and no-flow groups when either substrate was used. We therefore suggest that free radical formation contributes to myocardial injury in intermittent ischemia. The mechanism of free radical formation and their sites of action have not yet been completely elucidated - the peroxidation of membrane lipids is probably involved, particularly in the presence of high palmitate. The protective effect of the carnitine derivatives D-propionylcarnitine, L-propionylcarnitine and propionylcarnitine taurine amide was studied in the no-flow hearts (Table 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Acute cardiac events temporally related to cocaine abuse.

The increasingly widespread use of cocaine in the United States has been accompanied and perhaps exacerbated by the misconception that the drug is not associated with serious medical complications. In particular, the potential for cocaine to precipitate life-threatening cardiac events needs to be reemphasized. We report the clinical and pathological findings in seven people in whom nonintravenous "recreational" use of cocaine was temporally related to acute myocardial infarction, ventricular tachycardia and fibrillation, myocarditis, sudden death, or a combination of these events. We also review data on 19 previously reported cases of cocaine-related cardiovascular disorders. Analysis of all 26 patients indicated the following findings: the cardiac consequences of cocaine abuse are not unique to parenteral use of the drug, since nearly all the patients took the drug intranasally; underlying heart disease is not a prerequisite for cocaine-related cardiac disorders; seizure activity, a well-documented noncardiac complication of cocaine abuse, is neither a prerequisite for, nor an accompanying feature of, cardiac toxicity of cocaine; and the cardiac consequences of cocaine are not limited to massive doses of the drug. Although the pathogenesis of cardiac toxicity of cocaine remains incompletely defined, available circumstantial evidence suggests that cocaine has medical consequences that are equal in importance to its well-documented psychosocial consequences.

Administration, Inhalation↗
PubMed1986

Diagnosis of intrapericardial tumor in an infant by two-dimensional echocardiography.

Two-dimensional echocardiography is a useful noninvasive tool for diagnosing intrapericardial tumors as a cause of respiratory distress or abnormal cardiomediastinal shadow on chest x-ray. Early recognition of these tumors within the pericardium is important since surgical removal is often curative. Cardiac cineangiography is unnecessary to delineate further the tumor and should be reserved for those in which associated intracardiac defects are suspected.

Cysts↗
PubMed1986

Peripartum cardiomyopathy: clinical, hemodynamic, histologic and prognostic characteristics.

Peripartum cardiomyopathy is defined as left ventricular dilation and failure, first developing during the third trimester of pregnancy or in the first 6 months postpartum. In an effort to characterize this syndrome in a middle class population, 14 consecutive patients with peripartum cardiomyopathy underwent a detailed history and physical examination, right heart catheterization, M-mode and two-dimensional echocardiography, radionuclide ventriculography and right ventricular endomyocardial biopsy. These patients were then observed with sequential noninvasive studies to determine prognostic indicators. Eight (57%) of these 14 patients were primiparous and an equal number first presented with heart failure concomitant with or immediately before the onset of labor. When these women were compared with 55 patients with idiopathic dilated cardiomyopathy, only mean age at onset of symptoms (28.7 +/- 5.7 versus 48.2 +/- 13.6 years, p less than 0.001) and symptom duration (4.1 +/- 7.7 versus 19.0 +/- 18.4 months, p less than 0.001) differed between the groups. There was no difference in ventricular arrhythmia, left ventricular chamber size, ejection fraction or hemodynamics. Myocyte histologic findings were similar; however, myocarditis was identified in 29% of patients with peripartum cardiomyopathy and in only 9% of those with idiopathic dilated cardiomyopathy. In all patients with peripartum cardiomyopathy and myocarditis, the myocardial biopsy was performed within 1 week of onset of symptoms. Seven (50%) of the patients with peripartum cardiomyopathy had dramatic improvement within 6 weeks of follow-up, and 6 (43%) died.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Postoperative evaluation of endomyocardial fibrosis.

25 patients with angiographic features suggestive of endomyocardial fibrosis underwent endocardiectomy and atrioventricular valve replacement. There were 8 deaths. 17 survivors were reevaluated after a mean follow-up of 13.5 months. 8 had right ventricular endomyocardial fibrosis (RVEMF) 5 had left ventricular endomyocardial fibrosis (LVEMF) and 4 had biventricular disease (BVEMF). The survivors showed a significant improvement in their clinical features and functional status. There was a significant reduction in atrial size in X-ray. Hemodynamic data showed a significant fall in right heart filling pressure, right ventricular systolic pressure and pulmonary artery mean pressure, and a significant fall in left heart filling pressure in patients with left ventricular disease either alone or as a part of biventricular disease. In ventriculogram, while there was no change in right ventricular shape after endocardiectomy, left ventricular shape was restored to near normal. The significant improvement is mostly due to the correction of the regurgitant lesion and to some extent due to restoration of ventricular compliance.

Adolescent↗
PubMed1986

Dilated cardiomyopathy: emerging role of endomyocardial biopsy.

The development of safe techniques of endomyocardial biopsy has led to a significant increase in our understanding of the etiology and pathogenesis of dilated cardiomyopathy. The scope of patients for whom this technique is absolutely clinically indicated, however, remains quite narrow and should be restricted to those centers with active cardiac transplant programs, large oncology practices, or those involved with active research into the etiology and treatment of patients with heart muscle disease. The most exciting concept to emerge from the use of EMB is the role of myocarditis in the development of dilated cardiomyopathy. It can accurately be stated that a subset of patients with the clinical presentation of dilated cardiomyopathy may in fact have histologic evidence of myocarditis. Although there is a suspicion that immunosuppressive therapy may be helpful, a randomized trial of large numbers of patients is necessary before definitive conclusions may be drawn. If immunosuppressive therapy proves to be efficacious in active myocarditis, then one could argue that all patients with heart failure of unknown cause with no evidence of valvular or coronary artery disease should undergo endomyocardial biopsy as part of the routine diagnostic workup. However, this recommendation must be considered premature. Since routine histologic findings are nonspecific in dilated cardiomyopathy, biochemical, pharmacologic, and cell culture techniques may provide more definitive information regarding the functional state of the heart muscle. In conclusion, endomyocardial biopsy is rapidly emerging as a useful diagnostic tool in the evaluation of patients with heart failure of unknown cause.

Biopsy, Needle↗
PubMed1985

Photo-induced nicking of deoxyribonucleic acid by ruthenium(II)-bleomycin in the presence of air.

A new metallobleomycin, ruthenium(II)-bleomycin A2 was prepared. When irradiated at 366 nm the ruthenium complex (1-10 microM) was found to break a 121-base pair DNA restriction fragment at specific sites (usually the pyrimidine residues located at the 3'-side of guanine). Care was taken to rule out complications due to the presence of trace amounts of iron. Photo-induced damage by cobalt-bleomycin in the presence of light, and redox-mediated damage by bleomycin and iron produced DNA cleavage at sites similar to ruthenium-bleomycin. In contrast to cobalt-bleomycin, ruthenium-bleomycin required oxygen as well as light to cause significant damage to DNA.

Air↗