Cases reported "Myocarditis"

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1/13. Evidence for early vessel involvement in the dysfunctional myocardium of Takayasu's arteritis.

    A 15-year-old girl presented with persistent fevers, night sweats, leukocytosis, an elevated erythrocyte sedimentation rate, and a 13-pound weight loss over 2 months. Duplex Doppler scans, computed tomographic scan, and magnetic resonance imaging studies were suggestive of Takayasu's arteritis. Left ventricular dysfunction occurred during the episode of active disease, and an endomyocardial biopsy demonstrated increased HLA-DR (human leukocyte antigen-DR) on the endothelium and evidence of immune complex deposition in the walls of small vessels. One year later, after treatment with corticosteroids and resolution of clinical symptoms, repeat endomyocardial biopsy revealed focal interstitial fibrosis and persistent immune complex deposition. These results indicate that the inflammatory, vasculitic process affecting the large vessels in Takayasu's arteritis may also involve the endomyocardium and its small vessels resulting in ventricular dysfunction.
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2/13. coronary artery disease obscuring giant cell myocarditis--a case report.

    A case in which the diagnosis of idiopathic giant cell myocarditis was obscured by the presence of severe coronary artery disease is described. A 47-year-old man presented with recurrent inferior myocardial infarction and complete heart block. cardiac catheterization confirmed severe 2-vessel disease and left ventricular dysfunction. Incessant ventricular arrhythmia rapidly ensued, which did not respond to anti-arrhythmic therapy and overdrive pacing despite complete surgical revascularization. He eventually died. autopsy revealed giant cell myocarditis superimposed on coronary artery disease. Acute myocarditis masquerading as myocardial infarction has been well known, but virtually all reported cases had normal coronary arteries. This case illustrated the fact that even in the presence of obvious coronary artery disease the remote possibility of myocarditis should not be entirely disregarded. Although giant cell myocarditis is a rare and frequently fatal disorder, recent studies suggest that combined immunosuppressive therapy may improve the prognosis.
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3/13. Late bleeding from right internal mammary artery after HeartMate left ventricular assist device implantation.

    Postoperative bleeding is one of the major complications after implantation of left ventricular assist devices. We experienced 5 unusual cases, which had bleeding from the right internal mammary artery between 5 and 69 days after implantation of a HeartMate (Thoratec Corporation, Pleasanton, CA) device. It was evident that the outflow graft had eroded through the vessel. Sudden decreases in device flow, hypotension, bleeding from the driveline or chest tube sites, and a drop in hematocrit were the initial manifestations. Chest roentgenogram and transthoracic echocardiography were effective in identifying hemothorax and cardiac tamponade. Four out of 5 patients survived to heart transplantation and were discharged from the hospital. When identified and treated appropriately, this complication does not impair patient outcome.
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4/13. Accelerated arteriosclerosis in heart transplant recipients is associated with a T-lymphocyte-mediated endothelialitis.

    Accelerated arteriosclerosis has emerged as a major life-threatening complication in long-term survivors of heart transplantation. It has been proposed that accelerated arteriosclerosis is an immune-mediated complication of rejection. We observed a striking endothelialitis in the coronary arteries of two explanted hearts obtained from patients with severe transplant-related accelerated arteriosclerosis. This finding prompted us to review the pathologic changes in the coronary arteries of 23 autopsied patients who had received heart transplants. The infiltrate in these vessels was characterized using immunohistochemical stains for lymphocytes (CD45), macrophages (MAC-387), T lymphocytes (CD45RO), B lymphocytes (L-26), and smooth muscle cells (actin). In addition, a full panel of monoclonal antibodies was used on the fresh-frozen tissue available from one of the two explanted hearts. Ten of the eleven recipients with accelerated arteriosclerosis had a moderate to marked lymphocytic endothelialitis compared to 3 of 14 without transplant-related arteriosclerosis (P less than 0.005). Immunohistochemical staining of the paraffin-embedded material demonstrated that most of the lymphocytes in the subendothelial space of these vessels were T lymphocytes and that this infiltrate was associated with an accumulation of macrophages and a proliferation of smooth muscle cells in the intima. In the explanted heart from which fresh-frozen tissue was available for more detailed cell typing, the T cells marked predominantly as cytotoxic T lymphocytes (CD8 , CD2 ). These results suggest that accelerated arteriosclerosis may be mediated, in part, by a cytotoxic T-lymphocyte-directed endothelialitis.
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5/13. myocarditis in adult Still's disease.

    An original case study of a myocardial involvement in a patient with adult Still's disease is presented. The fibrinoid necrosis appearance of a myocardial vessel is an unusual finding at histology.
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6/13. Autoimmune myocarditis: a clinical entity.

    In a case of myocarditis electron microscopic and immunoflourescent studies of a transmural myocardial biopsy specimen indicated an autoimmune process. Extensive inflammatory cell infiltration, immunoglobulin and complement deposition along the sarcolemma and in the interstitium, and capillary endothelial injury were found. After a short course of immunosuppressive therapy the inflammatory process was replaced by collagenous scarring and lymphocytic depletion; the blood vessels were then normal. Earlier therapy in such cases may be lifesaving.
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7/13. hepatitis b virus and myocarditis.

    myocarditis may be a serious extrahepatic complication of hepatitis. In this fatal case of serologically documented hepatitis B viral hepatitis, acute myocarditis was present, with histologic features consistent with a viral pathogenesis. Hepatitis B surface antigen was demonstrated by immunoperoxidase methods in small intramyocardial vessels, suggesting that hepatitis b virus infected the heart. The resulting inflammatory heart disease may have been caused either directly, by virus infecting the myocardium, or indirectly, by an immune-mediated mechanism.
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8/13. An autopsied case of a two-month-old infant with granulomatous pancarditis having severe vasculitis and valvulitis.

    A 2-month-old female infant with pancarditis was reported. The patient died after a 26-day clinical course. The autopsy showed pancarditis, including inflammation in all 4 valves and chordae, fibrinoid vasculitis, pharyngolaryngitis and atrophy of the lymph nodes. Microscopic examination revealed proliferative inflammation in the endocardium, valve, myocardium, epicardium and coronary vessels. The histological findings suggested the etiology to be a rheumatic-type reaction at an extremely young age.
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9/13. IgA2-alveolitis and eosinophilic pneumonia--a possibly virus-triggered allergy.

    A case of severe therapy-resistant asthma in a young girl with a duration of two years prior to death is reported. At autopsy antibodies of the IgA2-subtype were demonstrated in the lungs on the alveolar basement membranes. We were able to demonstrate intracellular virus-like structures by electron microscopy; this virus infection is taken to be the cause of antibody production. Following antigen-antibody reaction a non-complement-mediated eosinophilic pneumonia with numerous macrophages developed. This inflammatory reaction showed the injurious effect of eosinophilic granulocytes causing fibrinoid necrosis; this is confirmed by the pronounced depletion of the Charcot-Leyden-granules, equivalent to the release of the major basic protein and the Charcot-Leyden crystal protein. death was caused by IgA2 deposition in the myocardial vessels with consequent eosinophilic myocarditis.
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10/13. endocardial fibroelastosis: myocardial and vascular alterations associated with viral-like nuclear particles.

    Although clinical, immunologic, and experimental evidence exists implicating in utero viral infection of the myocardium in the development of primary endocardial fibroelastosis, the infectious etiology of this condition remains somewhat controversial. To date, specific features of viral myocarditis and morphological demonstration of viral particles have not been described in EFE. The present case is the first in which extensive light microscopic and ultrastructural analysis of the myocardium revealed abnormalities consistent with a primary viral myocarditis associated with typical EFE. These alterations consisted of chronic myocardial inflammation, extensive interstitial fibrosis, severe degenerative changes in myocardial cells, and a marked proliferation of endothelial cells in large nad small intramyocardial vessels leading to vascular occlusions. In support of the infectious etiology of this disease, similar features were noted in skeletal muscle. Most interestingly, viral-like particles were observed in many myocardial and endothelial nuclei. Although we are not absolutely certain of the viral nature of these particles, their appearance suggests viral assoicated material. We propose that the presence of these particles in this case in association with the other morphological alterations in support for the viral etiology of EFE. The prominent vascular occlusion observed in the myocardium may be an important clue to the pathogenesis of fibroelastosis as either a primary or secondary disease.
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