Cases reported "Cardiomyopathies"

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1/10. Carboxyatractyloside poisoning in humans.

    OBJECTIVE: Cocklebur (xanthium strumarium) is an herbaceous annual plant with worldwide distribution. The seeds contain the glycoside carboxyatractyloside, which is highly toxic to animals. We describe nine cases of carboxyatractyloside poisoning in humans which, to our knowledge, has not previously been reported. The clinical, laboratory and histopathological findings and our therapeutic approach are also discussed. SUBJECTS AND methods: The patients presented with acute onset abdominal pain, nausea and vomiting, drowsiness, palpitations, sweating and dyspnoea. Three of them developed convulsions followed by loss of consciousness and death. RESULTS: Laboratory findings showed raised liver enzymes, indicating severe hepatocellular damage. BUN and creatinine levels were raised, especially in the fatal cases who also displayed findings of consumption coagulopathy. CPK-MB values indicative of myocardial injury were also raised, especially in the fatal cases. Three of the patients died within 48 hours of ingesting carboxyatractyloside. Post-mortem histopathology of the liver confirmed centrilobular hepatic necrosis and renal proximal tubular necrosis, secondary changes owing to increased permeability and microvascular haemorrhage in the cerebrum and cerebellum, and leucocytic infiltrates in the muscles and various organs including pancreas, lungs and myocardium. CONCLUSIONS: Carboxyatractyloside poisoning causes multiple organ dysfunction and can be fatal. Coagulation abnormalities, hyponatraemia, marked hypoglycaemia, icterus and hepatic and renal failure are signs of a poor prognosis. No antidote is available and supportive therapy is the mainstay of treatment.
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keywords = animal
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2/10. Secondary myocardial disease. Virus myocarditis and cardiomyopathy.

    In an attempt to prove the hypothesis that virus myocarditis may be a cause of idiopathic cardiomyopathy, clinical and experimental studies were performed. Eleven patients with a presumptive or proven diagnosis of virus myocarditis were followed for one and a half to 13 years after the acute illness. One patient died in the acute stage, six recovered completely and one continued to have bifascicular block without subjective symptoms. Three patients had exertional dyspnea, cardiomegaly and an abnormal ECG three to 13 years after the onset, and two of them had an enlarged LV cavity with reduced EF and histological changes in myocardial biopsies. The clinical picture in these three cases was similar to that seen in congestive cardiomyopathy. Clinical observations of the heart in an epidemic of coxsackie B 3 virus infection among school children revealed that 49 (19%) of 263 infected children had abnormal chest-X ray, electrocardiographic or echocardiographic findings one to 10 months after the onset, however none of them developed cardiomyopathy. In experimental infection of weanling golden hamsters with coxsackie B 3 virus (Nancy strain), all animals developed acute and severe myocarditis, and the virus was detected in the myocardium. Hemodynamic data suggested decreased contractility of the left ventricle in the acute stage. Histologically the heart showed focal myocardial necrosis and cellular infiltration without calcification, findings which resemble those in human doxsackie B virus myocarditi. Thus, the golden hamster is a better animal model than the mouse in studies on virus myocarditis and postcarditic cardiomyopathy.
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keywords = animal
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3/10. Primary cardiac echinococcosis: report of two cases with review of the literature.

    Two case reports of Saudi patients with primary cardiac hydatid cysts are presented. In the first case, a multilocular cyst was located in the wall of the left ventricle, whereas in the second case a cyst was located in the pericardial sac and another cyst in the left ventricular wall. The diagnosis was based on a history of animal contact, full clinical examination, serological tests and the use of plain radiography, including conventional tomogram, two-dimensional echocardiography, computed tomography and thallium perfusion isotope scan. This study has indicated that non-invasive radiological methods are sufficient to diagnose cardiac echinococcosis and could provide the same information as, or even more than if invasive techniques were used. Further screening of the two patients showed no involvement of other organs by hydatid cysts.
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ranking = 1
keywords = animal
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4/10. Fatal esorubicin-induced cardiomyopathy: report of a case and review of the literature.

    A case of fatal dilated cardiomyopathy induced by esorubicin (ESO) at a total dose of 740 mg/m2, given in 27 doses over 650 days, is reported. The sudden onset, rapid clinical deterioration, and fatal outcome are detailed. The outcome was not predicted by serial rest ejection fractions or clinical signs. The data from animal studies, phase 1 and phase 2 clinical testing, are reviewed, demonstrating the almost complete absence of reports of ESO-induced cardiotoxicity. Studies reviewing ejection fractions and myocardial biopsy scores show that ESO can be cardiotoxic and may produce fatal dilated cardiomyopathy.
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keywords = animal
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5/10. Cardiomyopathy in cystic fibrosis: lymphoedema of the heart with focal myocardial fibrosis.

    Cardiomyopathy in cystic fibrosis (CF) is an unusual heart disease, mainly characterized by a multifocal fibrosis of the left ventricle. The disorder chiefly occurs in the age group of 1-2 years and leads to fatal cardiac failure. The causal pathogenesis of the disease has not been discovered up to now. In two cases of CF-associated cardiomyopathy we found an oedema (mainly lymphoedema) of the myo- and epicardium and a lymph stasis in lymph vessels and lymph nodes of the heart. Based on a comparative study using animal models we speculate that a) CF may be complicated by a disorder of cardiac lymph circulation, and b) chronic cardiac lymphoedema of the heart in CF can cause focal myocardial damage with fibrosis.
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keywords = animal
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6/10. Future directions for clinical investigation in thrombolytic therapy.

    Experiments in animals have shown that coronary artery reperfusion limits the extent of myocardial damage and brings about late return of regional contraction and overall left ventricular function over a period of several weeks. Such studies provide a basis for optimism that similar effects can be demonstrated after thrombolytic treatment in man, and such functional contractile recovery should provide an important end point in clinical investigations. However, before the initiation of a large-scale clinical trial, adequate methods for determining salvage of myocardium must be identified, and since changes in such measures may be small, the use of mortality as an end point should also be considered. In addition, the possibility of having two treatment groups to compare intracoronary and intravenous modes of therapy should be examined. Based on the growing number of uncontrolled clinical reports concerned with the success of intracoronary thrombolysis in restoring vessel patency and preliminary data on morbidity, mortality and potential improvement in left ventricular function with this procedure, planning for a randomized clinical trial sponsored by the National Institutes of health is warranted.
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keywords = animal
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7/10. Morphologic effects of defibrillation: a preliminary report.

    A 72-yr-old man receiving more than 300 separate DC countershocks in 2 wk exhibited morphologic heart changes, including areas of coagulation necrosis in the subepicardium and areas of frank hemorrhage. In other sites the myocytes were pathologically contracted, a finding previously demonstrated in experimental animals as a result of defibrillation but not seen in man. We suggest that these changes may occur more often than has been previously supposed and thus may be of clinical importance.
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ranking = 1
keywords = animal
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8/10. selenium deficiency and fatal cardiomyopathy in a patient on home parenteral nutrition.

    An adult patient with chronic idiopathic intestinal pseudo-obstruction maintained on home parenteral nutrition for 6 consecutive years died from cardiomyopathy and ventricular fibrillation. Postmortem examination of the heart revealed widespread myocytolysis and replacement fibrosis similar to that seen in the selenium deficient cardiomyopathy in china (Keshan disease) and animal models. selenium deficiency in this patient was documented with extremely low concentrations of selenium and decreased activity of the selenoprotein, glutathione peroxidase, in blood, heart, liver, and skeletal muscle. Reports of selenium deficient diets causing myocardial damage in humans and animals and the findings in our patient strongly suggest that his fatal cardiomyopathy was caused by selenium deficiency.
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ranking = 2
keywords = animal
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9/10. Reversible cardiopathy after accidental overdose of mitoxantrone.

    mitoxantrone is an anthraquinone structurally related to the anthracycline drugs doxorubicin and daunorubicin. In animal tumor models, it was equally cytotoxic as but less cardiotoxic than the parent compounds. We here describe the clinical course of a 9-year old girl who inadvertently received 100 mg/m2 of mitoxantrone as a bolus injection. hemoperfusion carried out twice with the objective of increasing the drug clearance was totally inefficient. Severe but transient myelotoxicity was induced. Sequential echocardiograms demonstrated a reversible decrease of the shortening fraction of the left ventricle.
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ranking = 1
keywords = animal
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10/10. Human stress cardiomyopathy mimicking acute myocardial syndrome.

    Two cases of transient acute cardiomyopathy occurring in the immediate aftermath of intense emotional stress and without any identified aetiology are described. These two cases reports, mimicking cases of acute cardiomyopathy described in patients with pheochromocytoma, suggest the possibility in man of acute catecholamine induced cardiomyopathy related to major emotional stress alone, a phenomenon so far reported only in animal experimental models.
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keywords = animal
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