Cases reported "Cardiomyopathy, Dilated"

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1/111. A patient with hypertrophic cardiomyopathy accompanied by right ventricular dilation of unknown cause.

    Hypertrophic cardiomyopathy (HCM) is a disease characterized by an unknown cause of hypertrophy in the left or right ventricle. The dilated phase of HCM shows disease conditions resembling dilated cardiomyopathy, such as ventricular dilation, thin ventricular wall, and reduction of the ejection fraction. A patient presented with left ventricular concentric hypertrophy accompanied by right ventricular dilatation of unknown cause. Right ventricular endomyocardial biopsy specimens showed characteristic myocardial disarray. Therefore, there is the possibility that the patient had right and left ventricular HCM in the process toward the dilated phase, in which dilatation first occurred in the right ventricle.
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2/111. Acute clinical deterioration in a patient with end-stage dilated cardiomyopathy and left ventricular thrombus formation.

    The case of a 17-year-old male patient with severe end-stage dilated cardiomyopathy and a large thrombus formation within the cavum of the left ventricle is reported. After an acute thrombectomia combined with a partial left ventriculectomy (Batista procedure), the patient was successfully treated with an appropriate left ventricular assist device (LVAD) system using a centrifugal nonocclusive pump (Biomedicus, Medtronic, Anaheim, CA, U.S.A.). Mechanical support was removed on Day 9, and the patient was discharged from the hospital on Day 19. The effectiveness of emergency mechanical support in patients with very unfavorable prognoses is discussed.
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3/111. A female carrier of Duchenne muscular dystrophy complicated with cardiomyopathy.

    A 45-year-old female carrier of Duchenne muscular dystrophy (DMD) complicated with cardiomyopathy is described. She had no symptoms of muscle weakness or heart failure. Her chest x-ray film revealed marked cardiomegaly. Echocardiogram showed marked enlargement and severe hypokinesis of the left ventricle. In myocardial scintigraphic images, perfusion defects of the myocardium were revealed. dystrophin immunostaining of myocardial biopsy specimens showed a mosaic pattern of dystrophin-negative and -positive fibers. Cardiomyopathy is sometimes the only clinical symptom in female carriers of DMD. They are thought to be in a high risk group for developing heart failure.
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4/111. Dilated cardiomyopathy in Noonan's syndrome: a first autopsy case.

    The first autopsy case of dilated cardiomyopathy associated with Noonan's syndrome is described. A 9-month-old girl with Noonan's syndrome died from cardiac failure. autopsy showed biatrial and biventricular enlargement of the heart. The posterior half of the ventricular septum and right ventricular wall were remarkably thin. Other parts of the wall were nearly normal in thickness, but both ventricular cavities were dilated. Microscopically, the myocardium of both ventricles consisted of mainly abnormally thinned, elongated, and loosely arranged myocardial fibers lacking immunoreactivity to anti-dystrophin antibody. Myocardial disarray was not found except for where it normally existed. The abnormal changes of the myocardial fibers were considered to be primary. Common cardiomyopathy associated with Noonan's syndrome is a hypertrophic type. Various types of cardiovascular abnormality associated with Noonan's syndrome, including dilated cardiomyopathy, might be disclosed by further investigation and precise diagnosis of Noonan's syndrome.
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5/111. plasma exchange for hyperbilirubinemia following implantation of a left ventricle assist system: a case report.

    A 49-year-old patient with end-stage dilated cardiomyopathy underwent implantation of a left ventricular assist system (LVAS). Although the systemic circulation seemed to be improved, the serum total bilirubin (Tbili) level increased sharply in the early postoperative period (preoperative Tbili, 5.7 mg/dl; postoperative day 3, 33.6 mg/dl). plasma exchange (PE) was performed 7 times from postoperative day 4, and the Tbili level decreased to 16.3 mg/dl by postoperative day 11. Thereafter, serum Tbili normalized concomitant with improved circulatory condition. The cause of the hyperbilirubinemia was considered to be temporary right ventricular dysfunction or hepatic sinusoid endothelial dysfunction. The liver function was recoverable, so PE had been effective in this case. Unfortunately, the patient suffered a midbrain infarction and ultimately died. From this experience, PE is recommended if it is judged that liver function can be preserved and circulation is adequate, but its implementation should not be delayed. It is essential that LVAS is implanted before damage occurs to end-organ function and thus prevent hyperbilirubinemia.
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6/111. Dilated phase of hypertrophic cardiomyopathy with mid-ventricular obstruction after 20-year follow-up.

    This paper reports a case of dilated phase in hypertrophic cardiomyopathy with mid-ventricular obstruction. Following the first cardiac catheterization and endomyocardial biopsy, the patient was diagnosed as having hypertrophic cardiomyopathy (HCM) with mid-ventricular obstruction. He had been first diagnosed at the age of 38 years and was subsequently followed for 20 years. Echocardiogram revealed gradually progressive dilatation of the left ventricle, associated with disappearance of the mid-ventricular obstruction. The second cardiac catheterization and endomyocardial biopsy performed at the age of 58 disclosed that the patient was in the dilated phase of HCM with a dip-and-plateau pattern diastolic pressure trace.
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7/111. Implantation of a cardiac resynchronization system for idiopathic dilated cardiomyopathy in a patient with persistent left superior vena cava using an experimental lead for left ventricular stimulation.

    A persistent left superior vena cava (PLSVC) was discovered at the implantation of a cardiac resynchronization system in a woman with an idiopathic dilated cardiomyopathy. Standard leads were used to obtain right ventricular and right atrial (RA) stimulation according to a formerly described technique. The left ventricle was stimulated through the posterolateral vein of the heart by a novel lead design to be used over a guidewire for placement. Despite expected difficulties in this anatomic situation, the research lead was positioned in 23 minutes.
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8/111. Partial left ventriculectomy in a 3-year-old boy with dilated cardiomyopathy.

    A 3-year-old boy suffered severe heart failure 2 months after ventricular septal defect repair. The cardiothoracic ratio was 67% and the ejection fraction 13%. echocardiography showed a dilated left ventricle and thin myocardium. After thorough study, we made a diagnosis of dilated cardiomyopathy. Because conventional therapy was unsuccessful, we conducted partial left ventriculectomy with Alfieri repair of the mitral valve. The postoperative cardiothoracic ratio was 57% at 1 year of follow-up and the ejection fraction 40%. The new york Heart association functional class improved from IV to I. In conclusion, the role of partial left ventriculectomy is both as a bridge to transplantation and as a definitive repair in dilated cardiomyopathy during childhood.
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9/111. Doppler-sonographic evidence of cerebral microembolism originating from a biventricular assist device.

    The use of extracorporeal assist devices in heart failure is associated with the risk of thromboembolic complications [1]. Prove of thromboembolic material in the ventricles and tubes of the assist devices is difficult, and the clinical relevance of thrombotic material in the tubes is not clear. Here, we report on a patient with severe heart failure caused by endstage dilated cardiomyopathy who was bridged to transplantation using a biventricular assist device (BVAD). Five weeks after implantation, transcranial Doppler sonography (TCD) revealed high intensity transient signals (HITS) in basal cerebral arteries, suggesting continued cerebral microembolism. Apart from a correlation of these Doppler sonographic findings with neurological symptoms, macroscopic evidence of fibrin thrombi in the artificial ventricle, and post mortem confirmation of cerebral infarction could be proved.
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10/111. 3-methylcrotonyl-CoA carboxylase deficiency in an infant with cardiomyopathy, in her brother with developmental delay and in their asymptomatic father.

    Three affected members of one family, each with a different clinical presentation of isolated biotin-resistant 3-methylcrotonyl-CoA carboxylase (MCC) deficiency are described. The index patient presented at 7 weeks of age with feeding difficulties, sweating and tachypnoea. echocardiography showed a severely dilated left ventricle with minimal contractility. MCC deficiency was suspected on the basis of elevated urinary excretion of 3-hydroxyisovalerate and 3-methylcrotonylglycine. Deficiency of MCC activity was found in lymphocytes and fibroblasts (ca. 2% of mean normal). serum carnitine was low (free 10 micromol/l). Some other possible causes of cardiomyopathy were excluded. Cardiomyopathy was not improved by carnitine therapy. The healthy father and a developmentally delayed brother also had MCC deficiency. Both also had decreased serum carnitine concentrations, but without cardiac involvement. Dilatative cardiomyopathy as predominant symptom in isolated MCC deficiency has not been described before, although severe carnitine deficiency is a common finding in MCC deficiency. It is not clear whether this is a coincidental association. CONCLUSION: In order to understand the phenotypic spectrum of this rare disorder, cardiac evaluation should be made in patients with 3-methylcrotonyl-CoA carboxylase deficiency. Biochemical and clinical investigations have also to be performed in their parents and siblings. In addition, 3-methylcrotonyl-CoA carboxylase deficiency should be included in the differential diagnosis of dilatative cardiomyopathy.
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