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  • 1
    Electronic Resource
    Electronic Resource
    Prevalence and Clinical Course of the Juveniles with Brugada-Type ECG in Japanese Population (2005)
    350 Main Street , Malden , MA 02148-5018 , USA and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Pacing and clinical electrophysiology 28 (2005), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Although many studies on Brugada syndrome have been done, with many reports of genetic findings and clinical features, little evidence exists to support the role of this syndrome in sudden cardiac death in a juvenile population. We sought to determine the prevalence and clinical course in children exhibiting Brugada-type ECG in a community-based population. Methods: Our study population comprised 21,944 subjects (11,282 boys and 10,662 girls) who underwent ECG during their first-year elementary school health examinations between 1992 and 2001 in Izumi City, Osaka. Brugada-type ECG was defined as demonstrating ST-segment elevation (coved or saddle-back type, J wave amplitude ≥0.2 mV) in the right precordial leads. We also divided Brugada-type ECGs into three types according to a consensus report. Type 1: coved ST-segment elevation displaying high J wave amplitude followed by a negative T wave; Type 2: high take-off and gradually descending ST-segment elevation (remaining ≥1 mm) followed by a positive or biphasic T wave; and Type 3: ST-segment elevation of 〈1 mm of both types. Results: Four subjects showed Brugada-type ECG (0.02%) (2 boys and 2 girls). Only one subject, a girl, met Type 1 criteria (0.005%). No history of structural heart disease was documented in these four subjects. During 6.8 ± 1.0 years of follow-up, no episode of unexpected sudden death, syncopal attack, and fatal arrhythmia occurred. Conclusions: The prevalence of Brugada-type ECG in a juvenile population was extremely low. To investigate when the typical Brugada-type ECG might be manifested, it could be necessary to check ECGs after adolescence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.2005.40020.x
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  • 2
    Electronic Resource
    Electronic Resource
    Differences in time course of myocardial mRNA expression in non-infarcted myocardium after myocardial infarction (2000)
    Springer
    Basic research in cardiology 95 (2000), S. 316-323 
    Details
    ISSN: 1435-1803
    Keywords: Key words Cardiac remodeling – Doppler echocardiography – myocardial infarction – mRNA – Sarcoplasmic reticulum Ca2+-ATPase – Na+-Ca2+ exchanger
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In non-infarcted myocardium after myocardial infarction, the change of cardiac phenotypic modulation of contractile protein, extracellular matrix and intracellular Ca2+ transport protein, such as sarcoplasmic reticulum Ca2+(SR-Ca2+)-ATPase, Na+-Ca2+ exchanger, have a important role during cardiac remodeling. However, the time course in this gene expression in the adjacent and remote left ventricular, or right ventricular myocardium after myocardial infarction has not been well examined. The purpose of this study was to examine the left ventricular function and regional cardiac gene expression after myocardial infarction. Myocardial infarction was produced in Wistar rats by the ligation of the left anterior descending coronary artery. After 3 weeks, 2 months and 4 months from myocardial infarction, we performed Doppler echocardiography and measured the systolic and diastolic function. Then, we analyzed the contractile protein, extracellular matrix and intracellular Ca 2+ transport protein mRNAs of cardiac tissues in the adjacent and the remote noninfarcted myocardium, and right ventricular myocardium by Northern blot hybridization. Fractional shortening of infarcted heart progressively decreased. Peak early diastolic filling wave (E wave) velocity increased, and the deceleration rate of the E wave velocity was more rapid in myocardial infarction areas. Atrial filling wave (A wave) velocity decreased, resulting in a marked increase in the ration of E wave to A wave velocity. Expression of myocardial α-skeletal actin, β-MHC and ANP mRNA, or collagen I and III mRNA were higher at 3 weeks after myocardial infarction. SR Ca2+-ATPase mRNA in the adjacent non-infarcted myocardium was decreased at 2 months, and that in remote myocardium was decreased at 4 months after infarction. Na+-Ca2+ exchanger mRNA levels were increased at 3 weeks, but was decreased at 2 months in the adjacent non-infarcted myocardium and at 4 months in the remote myocardium. These findings suggest that the compensation for myocardial infarction by myocardial gene expression in non-infarcted myocardium may occur at an early phase after myocardial infarction, and myocardial dysfunction may begin from adjacent to remote non-infarcted myocardium during progressive cardiac remodeling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950070051
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  • 3
    Electronic Resource
    Electronic Resource
    Endomyocardial biopsy findings in patients with atrioventricular block in the absence of apparent heart disease (1999)
    Springer
    Heart and vessels 14 (1999), S. 170-176 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF02482303
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of Diltiazem on Cardiac Remodeling in Rats Assessed by Doppler Echocardiography and mRNA Expression (1999)
    Springer
    Cardiovascular drugs and therapy 13 (1999), S. 249-258 
    Details
    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
    URL: http://dx.doi.org/10.1023/A:1007752310881
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of Cilazapril on Ventricular Remodeling Assessed by Doppler-Echocardiographic Assessment and Cardiac Gene Expression (1998)
    Springer
    Cardiovascular drugs and therapy 12 (1998), S. 57-70 
    Details
    ISSN: 1573-7241
    Keywords: ventricular remodeling ; myocardial infarction ; angiotensin converting enzyme inhibitor ; echocardiography ; gene expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study is to determine whether the administration of the ACE inhibitor cilazapril can lessen the adverse effects of ventricular remodeling, including systolic and diastolic dysfunction, modulation of fetal gene expression, increase of collagen genes, and depression of the sarcoplasmic reticulum (SR) Ca2+ ATPase gene in a myocardial infarcted (MI) rat model. At 1 day after MI, the animals were randomly assigned to cilazapril treatment or no treatment. We performed Doppler-echocardiographic examinations and measured cardiac mRNA in rats at 1 month and 3 months after MI (each group n = 8). The weights of the right (RV) and left ventricles (LV) in 1- and 3-month MI rats were significantly larger than those of the control rats. Cilazapril significantly prevented the increase. The MI rats showed systolic dysfunction, as evidenced by decreased fractional shortening (control, 34 ± 3% vs. MI, 17 ± 3%; P 〈0.01) and ejection fraction measured by the modified Simpson’s method (control, 61 ± 2% vs. MI, 36 ± 3%; P 〈 0.01) in rats at 1 month after operation. MI rats showed diastolic dysfunction, defined as increased peak early filling velocity, increased deceleration rate of the early filling wave, decreased late filling velocity, and an increase in the ratio of early filling to late filling velocity. Cilazapril significantly prevented systolic and diastolic dysfunction in rats after MI. The increases in β-MHC, α-skeletal actin, ANP, and collagen I and III mRNAs in the nonischemic LV and RV were significantly suppressed by treatment with cilazapril. Depressed SR Ca2+-ATPase mRNA (nonischemic LV, 0.7-fold, P 〈 0.05 vs. control; RV, 0.5-fold, P 〈 0.05 vs. control) at 3 months after MI was significantly restored to normal levels by cilazapril. Cilazapril improved the adverse remodeling process by attenuating the progression of systolic and diastolic dysfunction, and prevented abnormal cardiac gene expression following MI.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007789519005
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  • 6
    Electronic Resource
    Electronic Resource
    Long-acting calcium channel antagonist pranidipine prevents ventricular remodeling after myocardial infarction in rats (1999)
    Springer
    Heart and vessels 14 (1999), S. 111-119 
    Details
    ISSN: 1615-2573
    Keywords: Ventricular remodeling ; Myocardial infarction ; Calcium channel antagonist ; Echocardiography ; Gene expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this study was to examine the effects of the long-acting calcium channel antagonist pranidipine on ventricular remodeling, systolic and diastolic cardiac function, circulating humoral factors, and cardiac mRNA expression in myocardial infarcted rats. Myocardial infarction (MI) was produced by ligation of the coronary artery in Wistar rats. Three mg/kg per day of pranidipine was randomly administered to the infarcted rats. Hemodynamic measurements, Doppler echocardiographic examinations, analyses of the plasma levels of humoral factors, and myocardial mRNA expression were performed at 4 weeks after myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 24.2 ± 1.2mmHg and 5.4 ± 0.6mmHg. Pranidipine reduced LVEDP and CVP to 13.6 ± 1.4mmHg (P 〈 0.01) and 2.5 ± 0.4mmHg (P 〈 0.01). The weight of the left and right ventricles in MI was significantly higher than in the sham-operated rats (sham, 2.02 ± 0.04 and 0.47 ± 0.02g/kg; MI, 2.18 ± 0.05 and 0.79 ± 0.04g/kg;P 〈 0.01). Left ventricular end-diastolic dimension (LVDd) in MI increased to 10.3 ± 0.3mm (P 〈 0.01) (sham, 6.4 ± 0.3mm). Pranidipine prevented an increase in the weight of the left and right ventricles (2.02 ± 0.04 and 0.6 ± 0.03g/kg,P 〈 0.01) and LVDd (7.9 ± 0.2mm,P 〈 0.01 to MI). Plasma renin activity (PRA), and plasma epinephrine, norepinephrine, and dopamine concentrations in MI were higher than those of the sham-operated rats. Pranidipine decreased the PRA and plasma cathecolamine levels of the myocardial infarcted rats to the level of the sham-operated rats. Moreover, the rats in MI showed systolic dysfunction, shown by decreased fractional shortening (sham, 31 ± 2% vs MI, 15 ± 1%;P 〈 0.01) and diastolic dysfunction shown by the E-wave deceleration rate (sham, 12.8 ± 1.1 m/s2; MI, 32.6 ± 2.1m/s2;P 〈 0.01). Pranidipine significantly prevented systolic and diastolic dysfunction. The increases in β-myosin heavy chain (MHC), α-skeletal actin, and atrial natriuretic polypeptide mRNAs in the noninfarcted left ventricle and right ventricle at 4 weeks after the myocardial infarction were significantly suppressed by the treatment with pranidipine. On the other hand, depressed α-MHC was restored to normal levels by pranidipine in both regions. In conclusion, pranidipine prevents the left ventricular remodeling process accompanied by systolic and diastolic dysfunction, and inhibits abnormal cardiac gene expression after myocardial infarction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02482294
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  • 7
    Electronic Resource
    Electronic Resource
    Point mutations in mitochondrial DNA of patients with alcoholic cardiomyopathy (2000)
    Springer
    Heart and vessels 15 (2000), S. 172-175 
    Details
    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
    URL: http://dx.doi.org/10.1007/PL00007268
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