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  • 1
    Electronic Resource
    Electronic Resource
    Bepridil Prevents Paroxysmal Atrial Fibrillation by a Class III Antiarrhythmic Drug Effect (2003)
    350 Main Street , Malden , MA 02148-5018 , USA . : Blackwell Futura Publishing, Inc.
    Pacing and clinical electrophysiology 26 (2003), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: YOSHIDA, T., et al.: Bepridil Prevents Paroxysmal Atrial Fibrillation by a Class III Antiarrhythmic Drug Effect. Background: Bepridil, a multiple ion-channel blocker, has been reported to prevent paroxysmal atrial fibrillation (PAF). The f-f interval of PAF during treatment with bepridil versus class Ic antiarrhythmic drugs was compared. Methods: Fifty-two patients with PAF were randomized to bepridil, 200 mg/day (n = 14) versus flecainide, 100 to 200 mg/day (n = 15) or pilsicainide, 75 to 150 mg/day (n = 23) . The drug was considered effective when symptomatic episodes of PAF were decreased to 〈 50% during a follow-up of 2 to 6 months. The f-f interval was measured in 12-lead ECGs of initial PAF episodes. Results: Bepridil and Ic were effective in 10 of 14 (71.4%) and 24 of 38 patients (63.2%), respectively (ns). In the Ic group, the f-f interval was longer in successfully (114 ± 48  ms) than in unsuccessfully (68 ± 25  ms) treated patients (P = 0.002) . In the bepridil group, the f-f interval was shorter in successfully (84 ± 27  ms) than unsuccessfully (155 ± 68  ms) treated patients (P = 0.015) . When comparing unsuccessfully treated patients, the f-f interval in the bepridil group was significantly longer than in the Ic group (P = 0.007) . Conclusions: Bepridil was as effective as Ic drugs in the prevention of PAF. Because it was more effective in smaller (functional) than larger (anatomical) reentrant circuits, the effect of bepridil was considered to be mainly attributable to a class III antiarrhythmic action. (PACE 2003; 26[Pt. II]:314–317)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2003.00040.x
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  • 2
    Electronic Resource
    Electronic Resource
    Verapamil Suppresses the Inhomogeneity of Electrical Remodeling in a Canine Long-Term Rapid Atrial Stimulation Model (2003)
    350 Main Street , Malden , MA 02148-5018 , U.S.A . : Blackwell Publishing
    Pacing and clinical electrophysiology 26 (2003), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short-term atrial pacing, although the effect of a long-term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 ± 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 ± 4 ms in the control group and was larger than that in the verapamil group (31 ± 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (−19 ± 3 vs −5 ± 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged. (PACE 2003; 26:2072–2082)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2003.00323.x
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  • 3
    Electronic Resource
    Electronic Resource
    Measurement of Body Surface Energy Leakage of Defibrillation Shock by an Implantable Cardioverter Defibrillator (2002)
    Oxford, UK : Blackwell Futura Publishing, Inc.
    Pacing and clinical electrophysiology 25 (2002), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: NIWANO, S., et al.: Measurement of Body Surface Energy Leakage of Defibrillation Shock by an Implantable Cardioverter Defibrillator. Leakage of electrical current from the body surface during a defibrillation shock delivery by an ICD device was evaluated in 27 patients with life-threatening ventricular tachyarrhythmias. All patients underwent the implantation of the Medtronic Jewel Plus ICD system, and the defibrillation shocks were delivered between the active can implanted in the left subclavicular region and the endocardial lead placed in the right ventricle. At the time of measurement of the effect of electrical energy delivery for defibrillation, the shocks were delivered in a biphasic form at the energy level of 20 or 30 J. During each delivery of the defibrillation shock, the electrical current to the body surface was measured through large skin electrodes (6.2 cm2) that were pasted at the following positions: (1) parallel position: the electrodes were placed at the left shoulder and the right low-chest, and the direction of the electrode vector was parallel to the direction of the defibrillation energy flow, and (2) cross position: the electrodes were placed at the right shoulder and the left low-chest, and the vector of the electrodes was roughly perpendicular to the direction of the energy flow. The energy leakages were measured in 80 defibrillation shocks. The peak leakage current during the shock delivery at energy of 30 J was 48 ± 26 mA at the parallel position and 19 ± 15 mA at the cross position (P = 0.0002). The energy leakage at a 30-J shock was 7.4 ± 7.2 mJ at the parallel position and 1.4 ± 2.3 mJ at the cross position (P = 0.0002). The actual maximum energy leakage was 105 mA, 29 mJ, and 106 V that appeared at the parallel position. The body surface leakage of the defibrillation energy of the ICD device was evaluated. The power of the energy leakage strongly depended on the angle between the alignment of the recording electrodes and the direction of the energy flow. The highest current leakage to the body surface reached a considerable level, but the energy leakage was small because of the short duration of the defibrillation shock.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2002.01212.x
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  • 4
    Electronic Resource
    Electronic Resource
    Cardiac contractile proteins and autoimmune myocarditis (1993)
    Springer
    Molecular and cellular biochemistry 119 (1993), S. 67-71 
    Details
    ISSN: 1573-4919
    Keywords: myosin ; actin ; autoimmune myocarditis ; T-lymphocyte ; dendritic cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Concerning cardiac contractile proteins, antigenicity and myocarditogenicity were discussed. In normal states, these proteins are immunologically tolerant, and can not provoke any heart-specific disease. Why the proteins can provoke such lethal autoimmune myocarditis has not been completely elucidated. Shortly after cardiac infection or myocardial ischemia, these proteins may work as the antigen for the autoimmune myocardites. First of all, the role of cardiac myosin has been strongly emphasized. But, the antigen determinants: epitope proteins remain unclear. Either cross-activity to the streptococcal M protein and/or the α-helical coiled-coil protein may be an important factor to determine antigenicity. In this autoimmune myocarditis, the roles of T-lymphocyte and cardiac dendritic cell are noticeable. Through further study on the relation between antigen epitope and the infectious agents in the heart; on cardio-cytotoxity of the T-lymphocyte and on the precise contribution of cardiac dendritic cells, this autoimmune myocarditis will be more clarified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926855
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  • 5
    Electronic Resource
    Electronic Resource
    Preface (1998)
    Springer
    Molecular and cellular biochemistry 188 (1998), S. 1-1 
    Details
    ISSN: 1573-4919
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006807812593
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  • 6
    Electronic Resource
    Electronic Resource
    Experimental Autoimmune Myocarditis and Its Pathomechanism (2000)
    Springer
    Herz 25 (2000), S. 274-278 
    Details
    ISSN: 1615-6692
    Keywords: Key Words Autoimmune myocarditis ; Causative epitope ; Cardiac dentritic cell ; Autoreactive T cell ; Schlüsselwörter Autoimmunmyokarditis ; Auslösendes Epitop ; Kardiale dentritische Zelle ; Autoreaktive T-Zelle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Pathomechanismen einer Autoimmunmyokarditis unterscheiden sich von denen einer viralen Entzündung. Bei einer autoimmunen Myokarditis kommt kardialen Myosinfragmenten, dendritischen Zellen und autoreaktiven T-Zellen eine entscheidende Bedeutung für die Auslösung und das Fortestehen der Entzündung zu. Das auslösende Epitop befindet sich auf dem S2-Teil der schweren Kette von Myosin (MHC). Unsere rekombinanten Studien haben gezeigt, dass sich das Epitop auf der zweiten Hälfte der MHC-Aminosäuren 1070 bis 1165 befindet. Das Ausmaß der Antigenität der α- und β-Ketten war nicht verschieden. Die kardialen dendritischen Zellen haben eine charakteristische Morphologie mit großen mononukleären ineinander greifenden Fortsätzen. Diese Antigen präsentierende Zelle wird schnell durch das Antigen aktiviert und später supprimiert. Die autoreaktive T-Zelle ist entscheidend an der Zytokinproduktion beteiligt. Im initialen Stadium der Myokarditis sind die IL-2- und IL-12-Spiegel erhöht. Beim Fortbestehen der Entzündung werden große Mengen von IL-1b, INF-γ und TNF-α in der Randzone des entzündeten Gewebes und gleichzeitig NO durch infiltrierende Makrophagen freigesetzt. Die durch Entzündungsquellen freigesetzten Zytokine beschleunigen den T-Zell-Übergang von Th0 nach Th1. Im Ausheilungsstadium überwiegt die Produktion von TGF-β1 und IL-10 und führt zum Übergang von Th0- zu Th2-Lymphozyten.
    Notes: Abstract The pathomechanisms of autoimmune myocarditis are quite different from viral infection. In this type of myocarditis, cardiac myosin fragments, proper dentritic cells and autoreactive T cells are the 3 major elements in initiating and promoting the inflammation. The causative epitope is locating on the S2 rod portion of the myosin heavy chain (MHC). Through our recombinant study, the peptide was found to be located on the latter half of MHC residues 1070 to 1165. Activity of antigenicity was not different between α and β chain. The cardiac dentritic cell presents a unique structure with large mononuclear and interdigitating process. This antigen presenter is quickly activated and suppressed by the antigen. The autoreactive T cell is closely linked with cytokine production. In the initial stage of myocarditis, IL-2 and IL-12 are increased. According to the progression of inflammatory changes, a great amount of IL-1b, INF-γ and TNF-α is released around the diseased tissue. At the same time, NO is massively produced from infiltrating macrophages. Cytokines secreted from inflammatory cells accelerate T cell induction from Th0 to Th1. In the convalescent stage, production of TGF-β1 and IL-10 become dominant. They contribute to cell induction from Th0 to Th2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000590050020
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  • 7
    Electronic Resource
    Electronic Resource
    Cardiomyopathy and myocarditis — A review of new aspects in research in West Germany (1985)
    Springer
    Heart and vessels 1 (1985), S. 8-13 
    Details
    ISSN: 1615-2573
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary New aspects in the research of myocarditis and dilated cardiomyopathy in West Germany have evolved from molecular biology, immunobiology of the mitochondrion, immunoserology, and immunohistology. Coxsackie B3 virus inoculated into fetal human myocytes induced myocytolysis in the absence of immunologic effector mechanisms. By pretreatment withβ-interferon, the virus yield from the myocytes was reduced significantly. In myocarditis and dilated cardiomyopathy, antibodies against an organ-specific autoantigen of cardiac mitochondria, the adenin nucleotide translocator, were demonstrated. Antibody titers roughly correlated with the ejection fraction using the Eliza technique. It could also be shown that in 13% of cases in myocarditis and 31% in dilated cardiomyopathy heart-associated antimitochondrial antibodies are found, called anti-M7. Most of the patients had an interfibrillary staining pattern in the immunofluorescence test. No correlation with the severity of heart disease could be established. In dilated cardiomyopathy and myocarditis, there has recently been controversy over low suppressor T-cell activity. Whereas other groups have demonstrated a low concanavaldin-A-induced suppressor T-cell activity in both diseases, we have not been able to confirm reduced Con-A-induced or spontaneous T-suppressor cell activity in the different indicator systems used in analysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02072351
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  • 8
    Electronic Resource
    Electronic Resource
    Efficacy of amoldipine besilate therapy for variant angina: Evaluation by 24-hour Holter monitoring (1993)
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 923-928 
    Details
    ISSN: 1573-7241
    Keywords: amlodipine ; variant angina ; ST elevation ; Holter electrocardiogram ; calcium antagonist
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The efficacy of amlodipine, a calcium antagonist, was investigated in 12 patients with variant angina. Amlodipine was administered at a dose of 5 mg once daily, and efficacy was assessed from the frequency of anginal attacks, the frequency of ST elevation or depression, and the extent of ST segment changes [ST segment elevation or depression (mm) × duration (seconds)] on the Holter ECG before and after treatment. The frequency of ST elevation during the observation period was 1.67 ± 0.33 times/day (symptomatic attacks: 1.17±0.21/day; asymptomatic attacks: 0.50±0.19/day), and this significantly decreased to zero per day (both symptomatic and asymptomatic attacks) after treatment (p〈0.05). The extent of ST segment elevation during the observation period was 507.5±156.6 mm·sec/day (symptomatic: 382.5±102.9 mm·sec/day; asymptomatic: 125.0±62.0 mm·sec/day), and such changes were completely suppressed (both symptomatic and asymptomatic) by treatment (p〈0.05). The frequency of ST depression was 2.08±0.42 times/day (symptomatic: 0.25±0.13/day; asymptomatic: 1.83±0.37/day) during the observation period, while it was 1.50±0.36 times/day (symptomatic: 0.25±0.13/day; asymptomatic: 1.25±0.30/day) after treatment. Although anginal attacks remained unchanged, asymptomatic attacks tended to decrease (p=0.07). The extent of ST depression during the observation period was 632.5±239.4 mm·sec/day (symptomatic: 105.0±64.4 mm·sec/day; asymptomatic: 527.5±189.5 mm·sec/day), and this significantly decreased to 333.8±111.4 mm·sec/day (symptomatic: 50.0±31.2 mm·sec/day; asymptomatic: 283.8±102.6 mm·sec/day) after treatment (p〈0.05). The frequency of anginal attacks during the observation period was 1.27±0.18 times/day, and this significantly decreased to 0.40±0.12/day after 1 week of treatment and to 0.22±0.07/day after 2 weeks of treatment (p〈0.05). These results suggest that amlodipine is effective for treating variant angina at a daily dose of 5 mg.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00877728
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  • 9
    Electronic Resource
    Electronic Resource
    Experimental rat model representing both acute and chronic heart failure related to autoimmune myocarditis (1995)
    Springer
    Cardiovascular drugs and therapy 9 (1995), S. 701-707 
    Details
    ISSN: 1573-7241
    Keywords: autoimmune myocarditis ; heart failure ; hemodynamics ; dobutamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The most important clinical manifestation of myocarditis is congestive heart failure. The precise mechanisms of heart failure during myocarditis have not been elucidated because no animal model that would permit in vivo study of hemodynamics in severe active myocarditis has been available. We monitored hemodynamics and left ventricular function in a rat model of experimental autoimmune myocarditis to determine if this model could be useful for the study of in vivo hemodynamics in severe active myocarditis. Lewis rats were immunized with human cardiac myosin suspended in complete Freund's adjuvant. Baseline hemodynamics were measured using an ultraminiature catheter pressure transducer via the right internal carotid artery, 4 weeks after immunization in one group of rats (acute phase) and 3 months after immunization in another group (chronic phase). Untreated rats served as the control group. Hemodynamic measurements were also obtained after infusion of dobutamine in the acute-phase and chronic-phase groups. The heart weight-to-body weight ratios were significantly higher in both the acute-phase group and the chronic-phase group compared with normal control rats. The baseline left ventricular systolic pressure was significantly lower in the chronic phase group than in the control group. Peak dP/dt and peak -dP/dt were significantly lower in both the acute-phase group and the chronic-phase group compared with the control group. Dobutamine significantly increased left ventricular systolic pressure, peak dP/dt, and peak -dP/dt in the chronic-phase group but caused only minor changes in hemodynamic variables in the acute-phase group. In vivo measurements of hemodynamic variables indicated the presence of left ventricular dysfunction in rats with experimental autoimmune myocarditis. This animal model may be useful for the study of both acute heart failure related to acute myocarditis and chronic heart failure due to diffuse myocardial fibrosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00878553
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  • 10
    Electronic Resource
    Electronic Resource
    Infiltrates in experimental autoimmune myocarditis (1994)
    Springer
    Medical molecular morphology 27 (1994), S. 243-245 
    Details
    ISSN: 1860-1499
    Keywords: Autoimmune myocarditis ; Giant cell ; Macrophage ; Dendritic cell ; T cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Unique features of experimental aut oimmune myocarditis were investigated ultrastructurally and immuno-histologically. The characteristic multinuclear giant cell is not syncytial, but singular in nature. The cell must be derived from macrophage. Large mononuclear cells, dominant infiltrates in this model, are classified into three forms: macrophage, cardiac dendritic cell and cells which have both surface antigens. These three cells occur according to inflammatory changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02349665
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