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J J Fenoglio

Publications and source records attributed to J J Fenoglio.

At least 19 recordsLinked to original sources
PubMed1989

Immunohistochemical characterization of fibrin(ogen)-related antigens in human tissues using monoclonal antibodies.

A new approach to study the distribution of fibrin(ogen)-related antigens was investigated using three different monoclonal antibodies (MAbs) and the avidin-biotin complex immunoperoxidase technique. MAb I8C6 recognizes B beta 1-42 peptide and can react with either fibrinogen or fibrin I; MAb T2G1 recognizes B beta 15-42 peptide and detects fibrin II but does not cross-react with fibrinogen; MAb GC4 reacts with Fragments D/DD derived from plasmin degradation of fibrinogen or fibrin but not with intact fibrinogen. The method can be applied to frozen or Bouin's fixed paraffin-embedded tissues obtained at biopsy, surgery, and autopsy. The distribution of the three antigens observed with the three MAbs was compared with that obtained with a polyclonal antiserum to fibrinogen and with the more conventional histochemical stains used in pathology to demonstrate fibrin deposits in tissues (Lendrum and PTAH). The staining observed with the three monoclonals clearly detected three different populations of fibrin(ogen)-related antigen in the tissues examined. The staining with MAb T2G1 specifically detected fibrin II with greater sensitivity than did conventional stains. The results of this study suggest that this method allows the molecular form of fibrin(ogen)-related deposits in tissues to be determined and this information may help to elucidate the role of fibrin in various disease states, such as atherosclerosis and renal disease, and in tumor growth and metastasis.

Antibodies, Monoclonal↗
PubMed1988

Biopsy diagnosis of myocarditis.

In closing, we can only note that none of the classification schemes for myocarditis has been perfect for clinicians, pathologists, and researchers alike. The definition and classification protocol offered by the "Dallas" group is based solely on histology, but we urge its use by physicians and other researchers as a means of imposing some standardization on the study of myocarditis. The question of optimum treatment, particularly immunosuppressive therapy, has never been definitively answered, but it is now clear that a large, multicenter randomized trial is the only proper method to search for such an answer. Standard nomenclature is a prerequisite for this study. In the meantime, the clinical correlates and prognostic utility of these histologic categories may be defined; these morphologic groupings will probably be shown to be clinically heterogeneous. In the end, we hope a hybrid clinical-pathologic scheme for the diagnosis and classification of myocarditis will be forged. Such a protocol, ideally, will allow the correlation of structure with function and also reliably predict clinical behavior and response to treatment so that someday we may be able to both counsel and cure persons with myocarditis.

Biopsy↗
PubMed1987

Myocarditis.

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Autoimmune Diseases↗
PubMed1987

Interobserver variability in the pathologic interpretation of endomyocardial biopsy results.

Controversy exists over the role of endomyocardial biopsy in evaluating patients with dilated cardiomyopathy, particularly in detecting myocarditis and in assessing prognosis. Interobserver variability, if high, could explain conflicting reports. To assess this possibility, we submitted biopsy specimens from 16 patients with dilated cardiomyopathy to seven cardiac pathologists. The same slides were independently reviewed by each and assessed for fibrosis, hypertrophy, nuclear changes on a 0 to 3+ scale, mean lymphocyte count per high-power field, and myocarditis. The prevalance of significant fibrosis ranged from 25% to 69%, hypertrophy from 19% to 88%, nuclear changes from 31% to 94%, and abnormal lymphocyte count from 0 to 38%. One or more pathologists diagnosed definite or possible myocarditis in 11 of the 16 patients. Of these 11 patients, three pathologists agreed about three and two pathologists agreed about five. Myocarditis was diagnosed by a single pathologist in three cases. We conclude that interobserver variability is high in interpreting biopsy specimens from patients with dilated cardiomyopathy and that quantitative and standardized methods are needed to increase diagnostic consistency.

Adult↗
PubMed1987

Circus movement in the canine atrium around the tricuspid ring during experimental atrial flutter and during reentry in vitro.

A Y-shaped lesion in the right atrium allows induction of atrial flutter in dogs. We recorded the activation sequence during this tachycardia from 96 endocardial bipolar electrodes using intracavitary electrode arrays during 12 separate episodes in three isolated perfused hearts. In each case a reentrant impulse circulated around the tricuspid valve orifice in either a clockwise or counter-clockwise direction. Cutting the pathway terminated the rhythm and prevented its reinduction. There was no discrete segment of markedly slow conduction in the reentrant circuit. The tachycardia cycle length was decreased by methacholine and increased by lidocaine. Reentry was also induced in atrial tissue around the tricuspid orifice when this structure was isolated and superfused in vitro. Tachycardia cycle lengths varied from 205 to 399 msec, depending on the circumference of the ring and temperature. Induction of tachycardia by premature stimulation depended on differences in the duration of the effective refractory period among parts of the ring. Conduction velocity was relatively uniform and was slower during tachycardias than during pacing at long cycle lengths. Analysis of the response to premature stimuli that reset the tachycardia provided evidence for incomplete recovery of excitability between depolarizations during the tachycardia. Fast-response action potentials were recorded throughout the pathway and up to six to eight cell layers deep. Histologic studies showed the supravalvular lamina, a circumferential band of fibers several cell layers below the endocardial surface, to be continuous around the tricuspid orifice. Propagation through this layer best explains the conduction velocities observed in the intact heart during flutter in this preparation.

Action Potentials↗
PubMed1986

Arteriovenous malformation of the bladder presenting as gross hematuria.

Arteriovenous malformation, in which direct communication is present between arterioles and venules, are reflected histologically by abrupt changes in the thickness of the medial and elastin layers of the vessels. Another result of the lack of the interposed capillary bed is abnormal dilation and, often, advanced small vessel disease, which is due to the increased intravascular pressures as well as to the basic defects in the blood vessel walls. The diversion of arterial flow and small vessel disease may lead to ischemia, which is postulated to stimulate proliferation of the vascular channels in these lesions. Hence, they tend to grow slowly with time. The ischemia, increased pressure, and small vessel disease predispose to ulceration and hemorrhage, which is a common mode of presentation for these lesions. Common sites for arteriovenous malformations are the intestine, central nervous system, lungs, and extremities. The lesion has not been reported in the urinary bladder. The present case of massive hematuria was found at autopsy to be due to an arteriovenous malformation of the bladder neck.

Aged↗
PubMed1986

Utility of endomyocardial biopsy in the diagnosis of cardiac sarcoidosis.

Cardiac involvement in sarcoidosis can be demonstrated in about 25 percent of autopsied cases, but antemortem diagnosis is uncommon. To evaluate the usefulness of the endomyocardial biopsy in detecting cardiac sarcoid disease, the medical records of ten patients with sarcoidosis who underwent endomyocardial biopsy for routine clinical indications were reviewed. The patients fell into two groups: patients with known sarcoidosis and presumed cardiac involvement (n = 8), and patients in whom the biopsy finding of sarcoid disease was unexpected (n = 2). Four patients in the first group had positive endomyocardial biopsy results (granulomas and/or marked mononuclear cell infiltrate) and were treated with glucocorticoid therapy with improvement in three; the fourth was disabled with lung disease. The diagnoses of three other patients were revised on the basis of the biopsy results; their therapy was tailored accordingly. The remaining patient may represent a false-negative biopsy result, based on clinical criteria. The two patients in the second group presented with symptomatic ventricular tachycardia and restrictive cardiomyopathy respectively, and in neither case was sarcoidosis considered prior to biopsy results. Overall, a change in treatment strategy based on biopsy results occurred in eight of ten cases. Thus, endomyocardial biopsy is useful for the diagnosis of cardiac sarcoidosis; treatment strategies may be affected by biopsy findings; and rarely, endomyocardial biopsy can provide the first clinical evidence of sarcoid disease that is otherwise occult.

Adrenal Cortex Hormones↗
PubMed1985

Monoclonal antibody identification of mononuclear cells in endomyocardial biopsy specimens from a patient with rheumatic carditis.

A 17-year-old woman with rheumatic carditis underwent endomyocardial biopsy both prior to and following treatment with prednisone and aspirin. Frozen sections from the endomyocardial biopsy specimens were studied with monoclonal antibodies by an indirect immunofluorescence technique to define the composition of the inflammatory infiltrate in the myocardium and to determine whether the composition of the infiltrate is distinctive and diagnostically useful. The specimen from the initial biopsy contained a heterogeneous infiltrate composed of T lymphocytes, macrophages, B lymphocytes, and mast cells. T lymphocytes predominated, and the ratio of T-helper to T-cytotoxic/suppressor cells was 2.0. Following treatment the overall cellularity of the infiltrate was diminished, but the infiltrate remained heterogeneous; T cells predominated, and the T-helper to T-cytotoxic/suppressor ratio was reversed, to 0.59. The composition of the inflammatory infiltrate in this case of rheumatic carditis distinguishes it immunologically from other "idiopathic," presumably virus-associated, forms of myocarditis.

Adolescent↗
PubMed1985

Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts.

The electrophysiologic and anatomic basis for fractionated electrograms were investigated in superfused epicardial preparations from infarcted canine hearts. Fractionated bipolar electrograms were frequently recorded in preparations from infarcts 2 weeks to 18 months old but only rarely in preparations from 5-day-old infarcts. The fractionated electrograms were not caused by movement artifacts. They were not associated with depressed transmembrane resting or action potentials (which were found in the 5-day-old infarcts), but rather transmembrane potentials recorded in the vicinity of the bipolar electrodes were normal. Despite the normal transmembrane potentials, activation time in regions where fractionated electrograms occurred was prolonged. However, prolonged activation time by itself did not cause fractionation, since fractionated electrograms were not recorded from normal preparations in which conduction was markedly slowed by a superfusate containing 16 mM potassium and epinephrine. Unipolar electrograms recorded with glass microelectrodes (tip size 1 to 5 microns) showed that activation in regions where fractionated electrograms were recorded was inhomogeneous. Prepotentials were found preceding the upstrokes of some action potentials in regions where double potentials were recorded, suggesting the possibility of electrotonic transmission across high resistance or inexcitable gaps, but no electrotonic potentials were seen in regions with multicomponent fractionated electrograms. Fractionated electrograms were recorded in regions where infarct healing caused wide separation of individual myocardial fibers while distorting their orientation. The anatomic changes probably caused slow and inhomogeneous activation.

Action Potentials↗
PubMed1985

Structural and electrophysiological changes in the epicardial border zone of canine myocardial infarcts during infarct healing.

Structural and electrophysiological properties of the epicardial muscle which survives on the surface of transmural infarcts of the canine heart (epicardial border zone) were studied at different times after occlusion of the left anterior coronary artery (LAD). Isolated preparations were superfused in vitro, transmembrane potentials recorded, and impulse propagation mapped. In preparations from subacute infarcts (1 and 5 days), resting potential, action potential amplitude, upstroke velocity, and duration were all significantly reduced. Well-defined directional differences in propagation occurred. Propagation was more rapid in the direction perpendicular to the left anterior coronary artery than in the direction perpendicular to the base of the heart, because of the uniform anisotropic structure of the surviving muscle fibers which were arranged in tightly packed bundles oriented perpendicular to the left anterior coronary artery. The only ultrastructural abnormalities found in these muscle fibers was an accumulation of large amounts of lipid droplets. As the infarcts healed, resting potential, action potential amplitude, and upstroke velocity returned to normal by 2 weeks, although action potential duration decreased further. Lipid droplets had disappeared, and connective tissue had invaded the epicardial border zone, separating the muscle bundles. By 2 months, action potentials were normal, but the muscle fibers were widely separated and disoriented by the connective tissue (parallel bundles no longer were found). In these regions with a nonuniform anisotropic structure, the well-defined directional differences in impulse propagation were lost. However, activation was very slow, perhaps because of diminished connections between cells. The persistence of slow conduction in healed infarcts may contribute to the occurrence of chronic arrhythmias.

Animals↗
PubMed1979

Right atrial ultrastructure in congenital heart disease. II. Atrial septal defect: effects of volume overload.

Portions of operatively resected right atrium from 15 patients with atrial septal defect were studied ultrastructurally to determine whether the cell hypertrophy in the right atrium of patients with increased right atrial blood flow and increased right atrial pressure is caused by the increased blood flow. In 12 patients with normal right atrial mean pressure but increased right atrial blood flow the atrium was dilated but no atrial arrhythmias were noted clinically. Ultrastructurally, the atrial myocardial cells in these patients were normal, measuring 6 to 10 mu in diameter, and there was no evidence of cell hypertrophy or degeneration. The remaining three patients had elevated right atrial mean pressure and increased right atrial blood flow. Ultrastructurally, the atrial myocardial cells in all three patients were hypertrophied, and two patients had evidence of focal cell degeneration; the atrium was markedly dilated, but atrial arrhythmias were not noted. The lack of cell hypertrophy in the right atrium of the 12 patients with increased blood flow but normal mean pressure suggests that in congenital heart disease volume overload alone does not lead to cell hypertrophy of the right atrial myocardium.

Adult↗
PubMed1979

Drug related vasculitis. Clinicopathologic correlations in 30 patients.

Drug related vasculitis has variously been described as necrotizing hypersensitivity or allergic angiitis or microscopic panarteritis nodosa. We reviewed tissue sections from 30 patients with validated drug hypersensitivity and vasculitis in order to precisely define this entity. No evidence of necrotizing vascular lesions or of fibrinoid associated with necrosis was found. The vascular lesions in all 30 patients involved small arteries, arterioles, capillaries, and venules. The inflammatory infiltrate consisted primarily of mononuclear cells and prominent numbers of eosinophils and was present in all three layers of the involved vessel walls. Clinically the patients developed either localized or systemic vasculitis, which could not be predicted on the basis of the associated drug. The findings of a skin rash, fever, or eosinophilia and the development of symptoms consistent with a hypersensitivity reaction while medication was being taken were all suggestive of the diagnosis of drug related vasculitis.

Adolescent↗