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  • 1
    ISSN: 1615-2573
    Keywords: Endomyocardial biopsy ; Electrophysiological testing ; Atrioventricular block
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this study was to examine the histopathological findings of right ventricular endomyocardial biopsies from ten patients less than 60 years of age (47 ± 9.8 (mean ± SD) years) with documented atrioventricular block but without apparent heart disease. They underwent electrophysiological testing, echocardiography, coronary angiography, and right ventricular endomyocardial biopsy. Biopsy specimens were assessed for morphologic changes in myocyte diameter, fibrosis, disarray, and degeneration. Electrophysiological testing demonstrated atrioventricular nodal block in 2, intra-His bundle block in 2, and infra-His bundle block in 6 patients. Histology revealed evidence of myocardial fibrosis with either myocyte hypertrophy or disarray in 7 of the 10 patients. The results of electrophysiological testing did not correlate with the histopathological findings or severity. In one patient, heart failure appeared during the follow-up period. We conclude that patients with atrioventricular block of unknown etiology have histological abnormalities of the ventricular endomyocardium in addition to the conduction system disturbances. We consider such cases as constituting one of the disease groups of cardiomyopathy, and suggest that it is necessary to follow up the clinical course in these patients.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1615-2573
    Keywords: Key words Mitochondrial disease ; Biopsy ; Congestive heart failure ; Dilated cardiomyopathy ; Alcohol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathogenesis of alcoholic cardiomyopathy (ACM) is not well understood. However, recent reports have shown that mutations in mitochondrial DNA (mtDNA) were associated with mitochondrial encephalomyopathy and cardiomyopathy. Our objective was to explore point mutations in mtDNA and the pathogenesis of ACM. We obtained heart biopsy specimens from ten male habitual drinkers with congestive heart failure. We amplified the total mtDNA obtained from these specimens using a two-step polymerase chain reaction method and analyzed the products using automated fluorescence-based direct sequencing. The sequences were compared with those of controls. MtDNA from the ACM patients contained multiple point mutations. Specifically, four of the ten patients carried five point mutations that had been detected previously in several other mitochondrial diseases. These point mutations were not observed in controls. These results suggest that mtDNA abnormalities are involved in the pathogenesis of ACM.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-7241
    Keywords: ventricular remodeling ; myocardial infarction ; diltiazem ; Doppler echocardiography ; gene expression ; cardiac function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Summary. The purpose of this study was to examine the effect of diltiazem on cardiac dysfunction and the change in cardiac gene expression after myocardial infarction in rats. On the first day after myocardial infarction, rats were randomly assigned to a diltiazem treatment (Dil, n = 7) or an untreated group (MI, n = 8). We then performed Doppler-echocardiographic examinations on the rats and measured their hemodynamics at 4 weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. Diltiazem decreased the mean aortic pressure and heart rate. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 18 ± 2 mmHg and 5 ± 1 mmHg (P 〈 0.01). Diltiazem reduced LVEDP to 14 ± 1 mmHg (P 〈 0.05), but it did not change CVP. The weight of the right ventricle in MI was significantly larger than in the control rats (control, n = 7, 0.46 ± 0.02 g/kg vs. MI, 0.81 ± 0.06 g/kg; P 〈 0.01). The left ventricular end-diastolic dimension (LVDd) in MI increased to 8.8 ± 0.3 mm (P 〈 0.01, control, 6.1 ± 0.3 mm). Diltiazem prevented an increase in the weight of the right ventricle (0.69 ± 0.03 g/kg, P 〈 0.05) and LVDd (7.7 ±6 0.2 mm, P 〈 0.05 to MI). The rats within MI showed systolic dysfunction, defined by a decreased ejection fraction (control, 67 ± 2% vs. MI, 36 ± 3%, P 〈 0.01), and diastolic dysfunction, defined by the E-wave deceleration rate (control, 13.4 ± 1.6 m/s2 vs. MI, 30.4 ± 3.4 m/s2 P 〈 0.01). Diltiazem significantly prevented systolic and diastolic dysfunction. The increases in β-MHC, ANP, and collagen type I and III mRNAs in the noninfarcted left ventricle and right ventricle were significantly suppressed by treatment with diltiazem. α-Skeletal actin increased in MI, and α-skeletal actin was more increased with Dil. In conclusion, diltiazem prevents cardiac dysfunction and morphological change due to left ventricular remodeling after experimental myocardial infarction.
    Type of Medium: Electronic Resource
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