Faculty Profiles - MORITA Hiroshi

Papers - MORITA Hiroshi

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宮地晃平, 森田宏, 多田毅, 平松茂樹, 村上正人, 西井伸洋, 永瀬聡, 中村一文, 草野研吾, 大江透

Journal of Arrhythmia 24 ( Suppl. ) 180 - 180 2008.4

Atrial fibrillation in patients with Brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds. International journal

Kengo F Kusano, Makiko Taniyama, Kazufumi Nakamura, Daiji Miura, Kimikazu Banba, Satoshi Nagase, Hiroshi Morita, Nobuhiro Nishii, Atsuyuki Watanabe, Takeshi Tada, Masato Murakami, Kohei Miyaji, Shigeki Hiramatsu, Koji Nakagawa, Masamichi Tanaka, Aya Miura, Hideo Kimura, Soichiro Fuke, Wakako Sumita, Satoru Sakuragi, Shigemi Urakawa, Jun Iwasaki, Tohru Ohe

Journal of the American College of Cardiology 51 ( 12 ) 1169 - 75 2008.3

Language：English Publishing type：Research paper (scientific journal)

OBJECTIVES: The goal of our work was to examine the relationships of atrial fibrillation (AF) with genetic, clinical, and electrophysiological backgrounds in Brugada syndrome (BrS). BACKGROUND: Atrial fibrillation is often observed in patients with BrS and indicates that electrical abnormality might exist in the atrium as well as in the ventricle. SCN5A, a gene encoding the cardiac sodium channel, has been reported to be causally related to BrS. However, little is known about the relationships of atrial arrhythmias with genetic, clinical, and electrophysiological backgrounds of BrS. METHODS: Seventy-three BrS patients (49 +/- 12 years of age, men/women = 72/1) were studied. The existence of SCN5A mutation and clinical variables (syncopal episode, documented ventricular fibrillation [VF], and family history of sudden death) were compared with spontaneous AF episodes. Genetic and clinical variables were also compared with electrophysiologic (EP) parameters: atrial refractory period, interatrial conduction time (CT), repetitive atrial firing, and AF induction by atrial extra-stimulus testing. RESULTS: Spontaneous AF occurred in 10 (13.7%) of the BrS patients and SCN5A mutation was detected in 15 patients. Spontaneous AF was associated with higher incidence of syncopal episodes (60.0% vs. 22.2%, p < 0.03) and documented VF (40.0% vs. 14.3%, p < 0.05). SCN5A mutation was associated with prolonged CT (p < 0.03) and AF induction (p < 0.05) in EP study, but not related to the spontaneous AF episode and other clinical variables. In patients with documented VF, higher incidence of spontaneous AF (30.8% vs. 10.0%, p < 0.05), AF induction (53.8% vs. 20.0%, p < 0.03), and prolonged CT was observed. CONCLUSIONS: Spontaneous AF and VF are closely linked clinically and electrophysiologically in BrS patients. Patients with spontaneous AF have more severe clinical backgrounds in BrS. SCN5A mutation is associated with electrical abnormality but not disease severity.

DOI： 10.1016/j.jacc.2007.10.060

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Longer repolarization in the epicardium at the right ventricular outflow tract causes type 1 electrocardiogram in patients with Brugada syndrome. International journal

Satoshi Nagase, Kengo Fukushima Kusano, Hiroshi Morita, Nobuhiro Nishii, Kimikazu Banba, Atsuyuki Watanabe, Shigeki Hiramatsu, Kazufumi Nakamura, Satoru Sakuragi, Tohru Ohe

Journal of the American College of Cardiology 51 ( 12 ) 1154 - 61 2008.3

Language：English Publishing type：Research paper (scientific journal)

OBJECTIVES: We examined the relationship between repolarization abnormality and coved-type ST-segment elevation with terminal inverted T-wave (type 1 electrocardiogram [ECG]) in patients with Brugada syndrome (BrS). BACKGROUND: Recent experimental studies have suggested that accentuation of the right ventricular action potential (AP) notch preferentially prolongs epicardial AP causing inversion of the T-wave. METHODS: In 19 patients with BrS and 3 control subjects, activation-recovery intervals (ARIs) and repolarization times (RTs) in the epicardium and endocardium were directly examined with the use of local unipolar electrograms at the right ventricular outflow tract. Surface ECG, ARI, and RT were examined before and after administration of pilsicainide. RESULTS: Type 1 ECG was observed in 10 of the 19 BrS patients before the administration of pilsicainide and in all of the 19 patients after the administration of pilsicainide. We found that ARI and RT in the epicardium were shorter than those in the endocardium in all 9 BrS patients without type 1 ECG under baseline conditions and in all control subjects regardless of pilsicainide administration. However, longer epicardial ARI than endocardial ARI was observed in 8 of the 10 BrS patients manifesting type 1 ECG under baseline conditions and in all of the BrS patients after the administration of pilsicainide. Also, epicardial RT was longer than endocardial RT in all patients manifesting type 1 ECG regardless of pilsicainide administration. CONCLUSIONS: Our data provide support for the hypothesis that the negative T-wave associated with type 1 BrS ECG is due to a preferential prolongation of the epicardial AP secondary to accentuation of the AP notch in the region of the right ventricular outflow tract.

DOI： 10.1016/j.jacc.2007.10.059

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Clinical significance of macroscopic T-wave alternans after sodium channel blocker administration in patients with Brugada syndrome. International journal

Takeshi Tada, Kengo Fukushima Kusano, Satoshi Nagase, Kimikazu Banba, Daiji Miura, Nobuhiro Nishii, Atsuyuki Watanabe, Kazufumi Nakamura, Hiroshi Morita, Tohru Ohe

Journal of cardiovascular electrophysiology 19 ( 1 ) 56 - 61 2008.1

Language：English Publishing type：Research paper (scientific journal)

INTRODUCTION: Macroscopic T-wave alternans (TWA) is sometimes observed after sodium channel blocker administration in patients with Brugada syndrome (BS), but little is known about the association between occurrence of TWA and clinical characteristics in BS patients. We investigated the association between spontaneous ventricular fibrillation (VF) occurrence and TWA after pilsicainide, a sodium channel blocker administration in BS patients. METHODS AND RESULTS: We administered pilsicainide at a dose of 1 mg/kg to 77 BS patients (76 males and one female; mean age, 48.4 years) and examined the association between TWA after pilsicainide administration and clinical characteristics, including age, spontaneous VF, syncope, family history of sudden death, spontaneous coved ST elevation, late potentials (LP), induction of VF by programmed electrical stimulation, and SCN5A mutation. None of the patients had TWA before pilsicainide administration, but TWA became apparent in 17 (22.1%) of the patients after pilsicainide administration. Patients with TWA had a significantly higher incidence of spontaneous VF (52.9% vs 8.3%, P < 0.001) and syncope (58.8% vs 26.7%, P < 0.05) than did patients without TWA. Then, we focused on the association between spontaneous VF and clinical characteristics. Patients with spontaneous VF had a significantly higher incidence of TWA (64.3% vs 12.7%, P < 0.001) and LP positive (92.9% vs 56.5%, P < 0.01) than did patients without spontaneous VF. In multivariate analysis, TWA (P = 0.001) and LP (P = 0.047) appeared as the independent predictor for spontaneous VF. CONCLUSION: TWA after pilsicainide administration is associated with a high risk of clinical VF in patients with BS.

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Simvastatin Inhibits Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells from Patients with Idiopathic Pulmonary Arterial Hypertension

Miura Daiji, Nakamura Kazufumi, Ikeda Tetsuya, Nagase Satoshi, Morita Hiroshi, Fuke Soichiro, Oka Tekefumi, Mohri Satohi, Kusano Kengo, Matsubara Hiromi, Date Hiroshi, Ohe Tohru

Proceedings of Annual Meeting of the Physiological Society of Japan 2008 189 - 189 2008

Publisher：PHYSIOLOGICAL SOCIETY OF JAPAN

Background: Idiopathic pulmonary arterial hypertension (IPAH) is a progressive disease characterized by inappropriate increase of pulmonary artery smooth muscle cells (PASMCs) leading to occlusion of pulmonary arterioles. In this study, we assessed the inhibitory effects of simvastatin, an HMG-CoA reductase inhibitor, on proliferation and migration of PASMCs obtained from patients with IPAH. Methods and Results: PASMCs were obtained from 6 patients with IPAH who underwent lung transplantation. Platelet-derived growth factor (PDGF) (10 ng/mL) stimulation caused a significantly higher growth rate of PASMCs from patients with IPAH than that of control cells assessed by 3H-thymidine incorporation (P<0.05). Simvastatin at 0.1 μmol/L significantly inhibited PDGF-induced cell proliferation of PASMCs from IPAH patients but did not inhibit proliferation of control cells at the same concentration. Simvastatin at 1 μmol/L also inhibited PDGF-induced migration of PASMCs from IPAH patients assessed by a transwell migration assay (P<0.05) and a time-lapse microscopy assay with a dish that has micro-lithographed squared pattern (Kuraray, Japan) (P<0.0001). Conclusions: Simvastatin may be useful for treatment of patients with IPAH. [J Physiol Sci. 2008;58 Suppl:S189]

DOI： 10.14849/psjproc.2008.0_189_3

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Controlled Proliferation of Rat Cardiomyocytes Mediated by Retroviral transfer and Site-specific Recombination

Nakamura Kazufumi, Kobayashi Naoya, Shimizu Juichiro, Miura Daiji, Kono Yasuyuki, Nagase Satoshi, Oka Takefumi, Morita Hiroshi, Kusano Kengo, Ohe Tohru

Proceedings of Annual Meeting of the Physiological Society of Japan 2008 189 - 189 2008

Publisher：PHYSIOLOGICAL SOCIETY OF JAPAN

Background: Cardiomyocytes lose their capacity to proliferate soon after birth. Therefore, we can not obtain large amount of cardiomyocytes in vitro. Here, we report the amplification of the cardiomyocyte population using retrovirus-mediated transfer of simian virus 40 large T (SV40T) antigen. SV40T was subsequently removed by Cre-loxP-based site-specific recombination.Methods and Results: Cultured neonatal rat cardiomyocytes were transduced with a retroviral vector expressing SV40T which is flanked by a pair of loxP recombination targets. Transduced cardiomyocytes yielded clones with greatly extended life spans up to population doubling level 142. Laser scanning cytometry analysis revealed that the transduction caused an induction of cell cycle progression. Complete elimination of the transferred SV40T gene was achieved after infection with a recombinant adenovirus expressing the Cre recombinase. Loss of SV40T caused G1-phase cell cycle arrest and discontinuance of cellular proliferation. DNA microarray analysis of cells that had lost SV40T showed increases in expression levels of cardiomyocyte-specific genes (cardiac actin alpha, Troponin T, myosin light chain and actinin alpha2)Conclusion: This study provides a means to obtain large numbers of well-differentiated and safe cardiomyocytes. [J Physiol Sci. 2008;58 Suppl:S189]

DOI： 10.14849/psjproc.2008.0.189.1

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働き盛りの突然死突然あの世に行かないために突然死をきたす不整脈と対策

大江透, 草野研吾, 永瀬聡, 森田宏, 中村一文

日本医学会総会会誌 27回 ( 学術講演要旨 ) 243 - 243 2007.12

Anti-KCNH2 antibody-induced long QT syndrome: novel acquired form of long QT syndrome. International journal

Kazufumi Nakamura, Yusuke Katayama, Kengo F Kusano, Kayo Haraoka, Yoshinori Tani, Satoshi Nagase, Hiroshi Morita, Daiji Miura, Yoshihisa Fujimoto, Tetsushi Furukawa, Kazuo Ueda, Yoshiyasu Aizawa, Akinori Kimura, Yoshihisa Kurachi, Tohru Ohe

Journal of the American College of Cardiology 50 ( 18 ) 1808 - 9 2007.10

Anti-KCNH2 antibody-induced long QT syndrome - Novel acquired form of LQT syndrome Reviewed

Kazufumi Nakamura, Yusuke Katayama, Kaye Haraoka, Yoshinori Tani, Daiji Miura, Hiroshi Morita, Kengo F. Kusano, Tetsushi Furukawa, Akinori Kimura, Yoshihisa Kurachi, Satoshi Nagase, Tohru Ohe

CIRCULATION 116 ( 16 ) 477 - 477 2007.10

Brugada症候群における右室流出路再分極相のばらつき基礎および臨床的知見

森田宏, 草野研吾, 永瀬聡, 大江透, Zipes Douglas P., Wu Jiashin

心電図 27 ( 5 ) 499 - 499 2007.9

Mechanism of U wave and polymorphic ventricular tachycardia in a canine tissue model of Andersen-Tawil syndrome. International journal

Hiroshi Morita, Douglas P Zipes, Shiho T Morita, Jiashin Wu

Cardiovascular research 75 ( 3 ) 510 - 8 2007.8

Language：English Publishing type：Research paper (scientific journal)

OBJECTIVE: Andersen-Tawil syndrome (ATS) is a channelopathy affecting inward rectifier potassium I(K1) with QT prolongation, large U waves, and frequent ventricular tachycardia (VT). Although ATS is clinically defined and genetically identified, its electrophysiological mechanism is still unclear, and thus, was the subject of the current study. METHODS AND RESULTS: We replicated the major electrophysiological features of ATS with cesium chloride (CsCl, at I(K1) blockade concentration of 5-10 mmol/l) in 23 isolated canine left ventricular tissues perfused arterially with Tyrode's solution having normal or low potassium concentrations, [K(+)](o). We mapped action potentials (APs) on the cut-exposed transmural surface of the wedges in control, after CsCl, and CsCl with 0.15 mumol/l isoproterenol (CsCl+ISP). CsCl delayed late phase 3 repolarization and prolonged the duration of the AP, more so during low [K(+)](o) perfusion. Rapid pacing induced delayed afterdepolarizations (DADs) in all low [K(+)](o) and in 71% of normal [K(+)](o) preparations after CsCl treatment. Addition of ISP induced DADs in all preparations. DADs originated in mid-to-endocardium, and initiated VT after CsCl+ISP. Migration of DAD-VT foci resulted in multifocal VT. Alternating DADs at 2 foci resulted in bidirectional VT. There were more foci and longer durations of VT at low [K(+)](o) than at normal [K(+)](o). Delayed late phase 3 repolarization of APs and DADs generated U waves. Verapamil abolished all DADs and VT. CONCLUSIONS: CsCl blockade of I(K1) produced a ventricular wedge model of ATS. Suppressing I(K1) generated U waves by delaying late repolarization of APs and creating DADs, and promoted polymorphic VT by triggering DADs at multiple shifting sites.

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Brugada Syndrome:from gene to bedside Brugada症候群における電気的異常についての検討

草野研吾, 永瀬聡, 森田宏, 中村一文, 伴場主一, 西井伸洋, 大江透

Journal of Cardiology 50 ( Suppl.I ) 133 - 133 2007.8

Analysis of action potentials in the canine ventricular septum: no phenotypic expression of M cells. International journal

Shiho T Morita, Douglas P Zipes, Hiroshi Morita, Jiashin Wu

Cardiovascular research 74 ( 1 ) 96 - 103 2007.4

Language：English Publishing type：Research paper (scientific journal)

OBJECTIVE: Transmural heterogeneity in the ventricular free wall, enhanced by the midmyocardial long action potential duration (APD) of M cells, plays an important role in the arrhythmogenesis of long QT syndrome. Although we observed dynamic expression of M cell phenotypes in the canine ventricular free wall, it is still unclear whether similar phenomena are present in the interventricular septum. This study evaluated transmural heterogeneity of APD in the septum. METHODS: We isolated and perfused 22 canine septal preparations through the septal branch of the anterior descending coronary artery, and optically mapped 256 channels of action potentials on their cut-exposed transseptal surfaces before and after treatment with sotalol (I(Kr) blocker), anemone toxin II (ATX-II, which slows the inactivation of I(Na)), or drug-free state in 6, 9, and 22 preparations, respectively. The preparations were paced from the left ventricular endocardium at cycle lengths of 500, 1000, 2000, and 4000 ms. RESULTS: We observed progressively lengthening of APD across the septum from the right ventricular to the left ventricular endocardium without a midmyocardial maximum under all conditions. All action potentials had minor phase-1 notches, resembling the endocardial action potential in the ventricular free wall. Increasing cycle lengths and concentrations of sotalol and ATX-II prolonged APD without midmyocardial preference and increased the transseptal dispersion of APDs. CONCLUSIONS: Canine interventricular septal action potentials are similar in shape to the endocardial action potentials in the ventricular free wall, with smooth transseptal transition in APD. We found no phenotypical expression of M cells in the canine interventricular septum.

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Temperature modulation of ventricular arrhythmogenicity in a canine tissue model of Brugada syndrome. International journal

Hiroshi Morita, Douglas P Zipes, Shiho T Morita, Jiashin Wu

Heart rhythm 4 ( 2 ) 188 - 97 2007.2

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Fever promotes ventricular arrhythmias in Brugada syndrome (BrS). Hypothermia can induce BrS electrocardiogram (ECG) and arrhythmia. However, the mechanisms are unclear. OBJECTIVE: We evaluated the hypothesis that pathological temperatures promoted arrhythmogenesis by modulating the spatial heterogeneity and functional dynamics of right ventricular electrophysiological activity. METHODS: We mapped action potentials (APs) on the epicardial or cut-exposed transmural surfaces and recorded transmural ECGs in 27 arterially perfused canine right ventricular preparations before and after inducing BrS at 32 degrees C, 36.5 degrees C, and 40 degrees C. RESULTS: We observed major intraepicardial dispersion of AP duration (APD) and reversal of transmural gradient of APD in association with manifestation of BrS at 36.5 degrees C. Reducing the temperature to 32 degrees C prolonged APDs and enhanced the phase 1 notch of epicardial APs, while 40 degrees C caused opposite changes. Prominent phase 2 domes of APs frequently led to spontaneous premature ventricular activations (PVAs), which conducted to surrounding regions having shorter APDs. Longer APDs at 32 degrees C and 36.5 degrees C frequently blocked reentry, although they promoted PVA, while shortened APDs at 40 degrees C facilitated reentrant ventricular tachycardia. During bradycardia (2,000 ms), the J-ST elevation in the ECG was enhanced at 32 degrees C and attenuated at 40 degrees C. Rapid pacing (500 ms) eliminated the dome of epicardial APs and enhanced J-ST elevation at each temperature. Blocking the transient outward current, I(to), with 4-aminopyridine reduced J-ST elevation and eliminated the PVA and reentry. CONCLUSIONS: In this BrS model, prolongation and increased dispersion of APDs promoted spontaneous activation during hypothermia, while APD abbreviation facilitated reentry during hyperthermia. I(to) mediated the arrhythmogenicity.

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Differences in arrhythmogenicity between the canine right ventricular outflow tract and anteroinferior right ventricle in a model of Brugada syndrome. International journal

Hiroshi Morita, Douglas P Zipes, Shiho T Morita, Jiashin Wu

Heart rhythm 4 ( 1 ) 66 - 74 2007.1

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: The Brugada syndrome is characterized by ST-segment elevation on the ECG, especially in the right precordial leads sensitive to the right ventricular outflow tract (RVOT). OBJECTIVES: The purpose of this study was to evaluate the hypothesis that right ventricular electrophysiologic heterogeneity caused arrhythmogenicity in the Brugada syndrome. METHODS: Action potentials (APs) were mapped on the epicardium of 14 RVOT preparations and on the transmural surfaces of 15 pairs of RVOT and right ventricular anteroinferior (RVAI) preparations isolated from canine hearts. Brugada ECG and arrhythmias were induced with pilsicainide (2.5-12.5 micromol/L), pinacidil (1.25-12.5 micromol/L), and terfenadine (2.0 micromol/L). RESULTS: Low doses of drugs elevated the J-ST segment and induced APs with both short and long action potential durations (APDs) in contiguous RVOT epicardial regions. In addition, APs in the RVOT had a larger phase 1 notch and longer APD than in RVAI. The longest APDs were in the epicardium in RVOT but in the endocardium in RVAI regions. High doses of drugs eliminated the phase 2 dome of the AP and abbreviated APDs in the epicardium but not in endocardium and reduced the epicardial heterogeneity of APs but increased the transmural gradient of APD in 14 (93%) of the RVOT preparations. In contrast, abbreviations of epicardial APDs occurred in only 4 (27%) of the RVAI preparations. Ventricular tachycardia occurred more frequently in the RVOT (47%) than in paired RVAI preparations (7%). Blocking the transient outward current reduced the heterogeneity of APs and eliminated arrhythmogenicity in all preparations. CONCLUSION: Compared with the RVAI region, the RVOT has greater electrophysiologic heterogeneity that contributes to arrhythmogenicity in this model of Brugada syndrome.

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Steroid therapy improves atrioventricular conduction disturbance but not ventricular arrhythmia in active phase of cardiac sarcoidosis Reviewed

Kimikazu Banba, Kengo Kusano, Kazufumi Nakamura, Hiroshi Morita, Aiko Ogawa, Atsuyuki Watanabe, Nobuhiro Nishii, Satoshi Nagase, Satoru Sakuragi, Tohru Ohe

CIRCULATION 114 ( 18 ) 469 - 469 2006.10

T wave alternans in an in vitro canine tissue model of Brugada syndrome. International journal

Hiroshi Morita, Douglas P Zipes, John Lopshire, Shiho T Morita, Jiashin Wu

American journal of physiology. Heart and circulatory physiology 291 ( 1 ) H421-8 2006.7

Language：English Publishing type：Research paper (scientific journal)

Macroscopic T wave alternans (TWA) associated with increased occurrence of ventricular arrhythmias has been reported in patients with Brugada syndrome. However, the mechanisms in this syndrome are still unclear. We evaluated the hypothesis that TWA in Brugada syndrome was caused by the dynamic instability and heterogeneity of action potentials (APs) in the right ventricle. Using an optical mapping system, we mapped APs on the epicardium or transmural surfaces of 28 isolated and arterially perfused canine right ventricular preparations having drug-induced Brugada syndrome (in micromol/l: 2.5-15 pinacidil, 5.0 terfenadine, and 5.0-13 pilsicainide). Bradycardia at cycle length (CL) of 2,632 +/- 496 ms (n = 19) induced alternating deep and shallow T waves in the transmural electrocardiogram. Compared with the shallow T waves, deep T waves were associated with epicardial APs having longer durations and larger domes. Adjacent regions having APs with alternating domes, with constant domes, and without domes coexisted simultaneously in the epicardium and caused TWA. In contrast to the alternating epicardial APs, midmyocardial and endocardial APs did not change during TWA. Alternans could be terminated by rapid (CL: 529 +/- 168 ms, n = 7) or very slow (CL: 3,000 ms, n = 7) pacing. The heterogeneic APs during TWA augmented the dispersion of repolarization both within the epicardium and from the epicardium to the endocardium and caused phase 2 reentry. In this drug-induced model of Brugada syndrome, heterogeneic AP contours and dynamic alternans in the dome of right ventricular epicardial, but not midmyocardial or endocardial, APs caused TWA and heightened arrhythmogenicity in part by increasing the dispersion of repolarization.

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Low-dose isoproterenol for repetitive ventricular arrhythmia in patients with Brugada syndrome. International journal

Atsuyuki Watanabe, Kengo Fukushima Kusano, Hiroshi Morita, Daiji Miura, Wakako Sumida, Shigeki Hiramatsu, Kimikazu Banba, Nobuhiro Nishii, Satoshi Nagase, Kazufumi Nakamura, Satoru Sakuragi, Tohru Ohe

European heart journal 27 ( 13 ) 1579 - 83 2006.7

Language：English Publishing type：Research paper (scientific journal)

AIMS: Arrhythmic storm or repetitive ventricular arrhythmia (VA) has been occasionally observed in Brugada syndrome (BS). A beta-adrenergic stimulator [isoproterenol (ISP)] has been reported to suppress this arrhythmic storm in sporadic cases. Accordingly, we investigated the antiarrhythmic effects of ISP infusion in consecutive BS patients with arrhythmic storm or repetitive VA. METHODS AND RESULTS: Seven BS patients with arrhythmic storm were studied. Intravenous ISP was administered as a bolus injection (1-2 microg), followed by continuous infusion (0.15 microg/min). Arrhythmic storm or repetitive VA was suppressed immediately after the bolus administration of ISP, which was followed by continuous infusion of low-dose ISP for 1-3 days. In all patients, ST-elevation decreased in right precordial leads. In six of the seven patients, VA subsided after the discontinuance of ISP. RR interval was shortened and ST-elevation in right precordial leads was decreased after ISP bolus injection. ST-elevation in right precordial leads remained decreased during continuous ISP infusion, whereas the RR interval returned to the control level. CONCLUSION: Continuous administration of low-dose ISP may be effective for the suppression of repetitive VA occurrence in patients with BS.

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不整脈を合併する輸送欠陥HCN43変異であるD553Nの機能的特性(Functional Characterization of a Trafficking-defective HCN4 Mutation, D553N, Associated with Cardiac Arrhythmia)

Ueda Kazuo, Nakamura Kazufumi, Hayashi Takeharu, Inagaki Natsuko, Takahashi Megumi, Arimura Takuro, Morita Hiroshi, Higashiuesato Yasushi, Hirano Yuji, Yasunami Michio, Takishita Shuichi, Yamashina Akira, Ohe Tohru, Sunamori Makoto, Hiraoka Masayasu, Kimura Akinori

心電図 25 ( 5 ) 373 - 373 2005.9

[Long QT syndrome].

Atsuyuki Watanabe, Kazufumi Nakamura, Hiroshi Morita, Kengo Fukushima Kusano, Tohru Ohe

Nihon rinsho. Japanese journal of clinical medicine 63 ( 7 ) 1171 - 7 2005.7

Language：Japanese Publishing type：Research paper (scientific journal)

The long QT syndrome (LQTS) is characterized by prolongation of the QT interval, causing torsade de pointes and sudden cardiac death. This syndrome can be divided into idiopathic (congenital) and acquired forms. The idiopathic form is a familial disorder that can be associated with sensorineural deafness (Jervell and Lange--Nielsen syndrome, autosomal recessive) or normal hearing (Romano--Ward syndrome, autosomal dominant). The acquired form has a long QT interval caused by various drugs such as quinidine sotalol and dofetilide, also by noncardiovascular drugs such as antihistamine, antibiotics, antipsychotics and others. Also, the QT interval is prolonged by electrolyte abnormalities such as hypokalemia and hypomagnesemia, central nervous system lesions, significant bradyarrhythmias, cardiac ganglionitis, mitral valve prolapse and probucol. DNA variants appearing to predispose to drug-associated acquired long QT syndrome have been reported in congenital long QT.

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