Cases reported "Cardiomyopathies"

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1/11. Evidence of cell-mediated cardiac myocyte injury involved in the heart failure of a patient with progressive systemic sclerosis.

    A 54-year-old woman with progressive systemic sclerosis (PSS) was admitted to hospital because of dyspnea and chest pain. Echocardiogram revealed diffuse hypokinesis of the left ventricle (ejection fraction 24%). methylprednisolone, heparin, and diuretics were administered, without benefit. anemia, thrombocytopenia, and renal dysfunction rapidly progressed, and she died of heart failure on the 14th hospital day. Immunohistochemical study of the myocardial tissue showed mild to moderate cell infiltration, mainly consisting of natural killer (NK) cells, macrophages, cytotoxic T lymphocytes (CTLs), and T helper cells. perforin, a cytolytic factor, was expressed in the infiltrating CTLs and NK cells, indicating that these cells were activated killer cells. Furthermore, human leukocyte antigen classes I and II, intercellular adhesion molecule-1, as well as costimulatory molecules B7-1, B7-2, and CD40, all of which are known not to be expressed in cardiac myocytes under normal conditions, were moderately to strongly expressed in cardiac myocytes. There was no detectable level of enterovirus genomes in the polymerase chain reaction products from the myocardial tissue of this patient. These findings strongly suggest that the infiltrating killer cells recognized cardiac myocytes as target cells and directly damaged them by releasing perforin. Enhanced expression of these antigens may have played an important role in the activation and cytotoxicity of the infiltrating killer cells. Absence of enterovirus genomes in the myocardial tissue may suggest that this autoimmune process is primarily induced by PSS.
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2/11. kerosene-induced severe acute respiratory failure in near drowning: reports on four cases and review of the literature.

    OBJECTIVE: The purpose of this study is to present an unusual respiratory and cardiovascular course after intoxication and near drowning in a river contaminated with kerosene. DESIGN: case reports and review of the literature. SETTING: intensive care unit of a university-affiliated hospital. patients: Four patients after near drowning. INTERVENTION: Supportive only. RESULTS: The four patients developed acute respiratory failure. Cardiomyopathy was present in three patients and a persistent hypokalemia in two patients. The onset of the symptoms was delayed, which led to underestimation of the severity of their illness. Two of the four patients died. The diagnosis of hydrocarbon intoxication was based on bronchoalveolar lavage results, neutrophilic alveolitis with the presence of lipid-laden macrophages, and evidence of lipoid pneumonia from the autopsy performed on one victim. One patient who clinically deteriorated and another who developed a severe restrictive pulmonary disorder were treated with corticosteroids, which were effective only in the latter patient. CONCLUSIONS: Acute kerosene intoxication in a near-drowning event often results in severe respiratory and cardiac failure, with a high fatality rate. Treatment with corticosteroids may lead to a rapid improvement in lung function.
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3/11. A case of hereditary amyloidosis transthyretin variant Met 30 with amyloid cardiomyopathy, less polyneuropathy, and the presence of giant cells.

    Transthyretin-Met 30 (TTR-Met 30) is a variant of transthyretin and is usually associated with familial amyloid polyneuropathy. It is rare that patients with TTR-Met 30 will primarily develop amyloid cardiomyopathy. This report presents a patient with late-onset TTR-Met 30 who primarily developed amyloid cardiomyopathy, with less amyloid polyneuropathy in the peripheral nervous system than is usually seen. An autopsy was performed, and histological examination revealed many foreign-body giant cells and macrophages in the area of amyloid deposition that was found in nearly all of the organs.
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4/11. An autopsy case of sudden death in a patient with giant cell myocarditis.

    We present a case of a 28-year-old male weight lifter who died suddenly while driving a bicycle. Forensic autopsy and histopathological examinations revealed granulomatous lesions in the myocardium and hilar lymph nodes. The latter had massive caseation necrosis, epithelioid granulomas and Langhans' giant cells suggestive of tuberculosis. However, the myocardium showed predominantly multinucleated foreign body and myogenic giant cells, lymphocytes, plasma cells, macrophages, eosinophils. Staining for acid-fast bacilli was negative. The present case highlights the difficulty in establishing whether the granulomatous lesions in the hilar lymph nodes and the myocardium are incidental findings or whether they are related by the same pathogenetic mechanisms.
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5/11. Takotsubo-shaped cardiomyopathy with type I CD36 deficiency.

    A transient left ventricular apical ballooning (so-called "ampulla" or "Takotsubo-shaped" cardiomyopathy) with type I CD36 deficiency is described in a 71-year-old woman. The patient was referred because of chest pain and worsening of dyspnea. Electrocardiogram showed T-wave inversions on the precordal leads, and acute coronary syndrome was suspected. Left ventricular apical ballooning was observed by echocardiogram and left ventriculography, and coronary arteriography did not reveal any significant stenosis. Left ventricular motion normalized at the follow-up period and there were no increases in specific markers for myocardial damage, such as myocardial band fraction of creatine kinase and troponin t, through out the admission. 123I-metaiodobengylguanidine myocardial single photon emission computed tomography (SPECT) revealed decreased accumulation areas at the apex, while 201Tl SPECT showed normal accumulation. An abnormal metabolism of cardiac free fatty acid was suggested by lack of accumulation of 123I beta-methyliodophenyl pentadecanoic acid (BMIPP) SPECT. No CD36 expression in either platelets or monocytes/macrophages was shown using flow cytometer analysis and type I CD36 deficiency was diagnosed. dna sequencing showed that the patient had compound heterozygosity of the CD36 gene (a nucleotide change in C478T and an adenine insertion at nucleotide 1159 in exon 10). Although CD36 deficiency is thought to be involved with many cardiovascular disease and metabolic abnormalities, Takotsubo-shaped cardiomyopathy with CD36 deficiency had not been reported. Further studies of Takotsubo-shaped cardiomyopathy and CD36 deficiency may reveal an association between this cardiomyopathy and specific genetic profiles.
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6/11. AL cardiac amyloidosis and arterial thromboembolic events.

    OBJECTIVE: To study the prevalence and characteristics of arterial thromboembolic events (ATEE) in the course of AL amyloidosis. methods: We report the case of a non-anticoagulated patient with AL amyloidosis restrictive cardiomyopathy who developed acute lower limb ischaemia. We then prospectively determined the prevalence of ATEE in all patients with AL amyloidosis who were evaluated in our institution for autologous peripheral stem cell transplantation. RESULTS: Nine out of 15 non-anticoagulated patients (60%) developed ATEE: ischaemic stroke (3), transient cerebral ischaemic attack (2), multiple peripheral arterial emboli (1), bilateral iliac artery thrombosis (1), bilateral optic nerve ischaemia (1), and mesenteric ischaemia (1). Haemodynamic stasis seemed to play a leading role in the pathophysiology of ATEE, in that all patients were on sinus rhythm and only one had a thrombus on echocardiography. We identified possible contributing factors to ATEE occurrence: concomitant treatments with oestroprogestogen regimen, thalidomide, granulocyte-macrophage colony-stimulating factor (GM-CSF) and extracellular volume disturbances related to the cytapheresis procedure. CONCLUSION: We report on an unusual frequency of ATEE among patients with AL cardiac amyloidosis. Despite its theoretical risks, anticoagulation should be discussed for patients with amyloid cardiomyopathy.
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7/11. Acute idiopathic interstitial myocarditis: case report with special reference to morphological characteristics of giant cells.

    Necropsy findings of an acute fatal case of idiopathic interstitial myocarditis were reported. The patient was a 33 year old housewife who had acute cardiac failure on the sixteenth day after the onset of the disease. Necropsy showed important pathological changes confined to the heart. Both ventricles were affected by confluent granulomas with an ill defined patchy appearance. Histologically these lesions consisted of round cells, histiocytes, eosinophils and myogenic giant cells. The findings were compatible with those of interstitial myocarditis associated with a proliferation of giant cells. Both atriums were also affected to a minor extent, detectable only by histological examination. Electron microscopy and cytochemistry showed that most giant cells noted in the lesion showed myofibrils and primary lysosomes in the cytoplasm. giant cells were positive for myoglobin. Though the macrophage origin of the giant cell in this disorder has been emphasised in a recent report, these cytological results suggest that giant cells observed in the cardiac granulomatous lesions of this case were mainly myogenic in origin.
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8/11. Cardiovascular amyloidosis with giant cell reaction.--Two autopsy cases.

    Two autopsy cases, a 77-year-old man and a 66-year-old woman, of cardiovascular amyloidosis with many giant cells were reported. These cells were always found adjacent to amyloid masses which were deposited mainly in small arteries and arterioles, and some of them contained amyloid substance in their cytoplasms. The incidence of these cells was high in the heart and in the kidneys of both cases, and in the latter case the cells were found in the majority of the organs varying in degree. The significance of the giant cells, which probably originated from macrophages, were discussed and that giant cells might appear as a foreign body reaction to amyloid substance was presumed.
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9/11. Mesothelial/monocytic incidental cardiac excrescences: cardiac mice.

    We have identified four new cases of the cardiac lesion resembling a histiocytoid (epithelioid) hemangioma from the consultation and surgical pathology files of the Mayo Clinic from 1979 to 1992. The lesions occurred in two men and two women, mean age 60 yr (range, 55 to 63), three of whom had undergone previous cardiac catheterization. All were found incidentally, two as separate tissue fragments obtained by right ventricular endomyocardial biopsy during investigations for dilated cardiomyopathy, and two during mitral valve replacement (one free floating in the left atrium and the other attached to the mitral valve). The latter two lesions measured 1.0 and 0.8 cm. All were composed of histiocytes (macrophages) focally admixed with cuboidal cells which formed strips and tubular arrays in three cases. immunohistochemistry (two cases) confirmed their biphasic nature with cytokeratin positivity of the cuboidal cells and CD68 (KP-1) positivity (macrophage-myeloid lineage) of the histiocytes. carcinoembryonic antigen and Leu-M1 were negative for both cell types. Transmission electron microscopy (two cases) showed macrophage-like cells and cuboidal cells with intracytoplasmic intermediate filaments, desmosome-like cellular junctions, and rough endoplasmic reticulum consistent with mesothelial cells. All four patients had a benign clinical course (range, 2 mo to 13 yr). This mesothelial and monocytic (histiocytic) process is postulated to relate to previous cardiac catheterization (applicable in three of our patients). The importance of these nodules, which are likely reactive, is their potential confusion with metastatic adenocarcinoma. We propose the name mesothelial/monocytic incidental cardiac excresences (cardiac mice) for these lesions.
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10/11. necrobiotic xanthogranuloma with cardiac involvement.

    A patient with necrobiotic xanthogranuloma (NXG) and paraproteinaemia, who was followed-up for several years, and treated with low-dose chlorambucil, died as a result of a respiratory illness. The significant findings at autopsy were a xanthogranuloma of the spleen and giant cell myocarditis. The myocardial lesions were composed of macrophages, giant cells and lymphocytes. This finding is important because four of five known autopsied patients with NXG have had giant cell myocardial disease, and an effort at antemortem diagnosis should be made.
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