Faculty Profiles - MORITA Hiroshi

Papers - MORITA Hiroshi

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Ion channel complex disease in long QT syndrome. International journal

Hiroshi Morita

Heart rhythm 10 ( 5 ) 738 - 9 2013.5

Brugada症候群の夜間・徐脈時の心室遅延電位の特徴の検討

寒川睦子, 森田宏, 永瀬聡, 西井伸洋, 河野晋久, 中村一文, 草野研吾, 伊藤浩, 亀井成美, 青木佐知子, 越智真金, 信定さおり, 川下隆二, 岡田健, 大江透

心電図 33 ( Suppl.2 ) S - 29 2013.5

メタボリックシンドローム患者におけるベザフィブラートの血管内皮機能への影響

大野佑子, 麻植浩樹, 三好亨, 杜徳尚, 河野晋久, 中村一文, 永瀬聡, 森田宏, 草野研吾, 伊藤浩

超音波医学 40 ( Suppl. ) S703 - S703 2013.4

Alogliptin ameliorates postprandial lipemia and postprandial endothelial dysfunction in non-diabetic subjects: a preliminary report Reviewed

Yoko Noda, Toru Miyoshi, Hiroki Oe, Yuko Ohno, Kazufumi Nakamura, Norihisa Toh, Kunihisa Kohno, Hiroshi Morita, Kengo Kusano, Hiroshi Ito

CARDIOVASCULAR DIABETOLOGY 12 8 2013.1

Language：English Publishing type：Research paper (scientific journal) Publisher：BIOMED CENTRAL LTD

Background: Postprandial hyperlipidemia impairs endothelial function and participates in the development of atherosclerosis. We investigated the postprandial effects of a dipeptidyl peptidase IV inhibitor, alogliptin, on endothelial dysfunction and the lipid profile.
Methods: A randomized cross-over trial design in 10 healthy volunteers (8 males and 2 females, 35 +/- 10 years) was performed. The postprandial effects before and after a 1-week treatment of 25 mg/day alogliptin on endothelial function were assessed with brachial artery flow-mediated dilation (FMD) and changing levels of lipids, apolipoprotein B48 (apoB-48), glucose, glucagon, insulin, and glucagon-like peptide-1 (GLP-1) during fasting and at 2, 4, 6, and 8 h after a standard meal loading test.
Results: Alogliptin treatment significantly suppressed the postprandial elevation in serum triglyceride (incremental area under the curve [AUC]; 279 +/- 31 vs. 182 +/- 32 mg h/dl, p = 0.01), apoB-48 (incremental AUC; 15.4 +/- 1.7 vs. 11.7 +/- 1.1 mu g h/ml, p = 0.04), and remnant lipoprotein cholesterol (RLP-C) (incremental AUC: 29.3 +/- 3.2 vs. 17.6 +/- 3.3 mg h/dl, p = 0.01). GLP-1 secretion was significantly increased after alogliptin treatment. Postprandial endothelial dysfunction (maximum decrease in% FMD, from -4.2 +/- 0.5% to -2.6 +/- 0.4%, p = 0.03) was significantly associated with the maximum change in apoB-48 (r = -0.46, p = 0.03) and RLP-C (r = -0.45, p = 0.04).
Conclusion: Alogliptin significantly improved postprandial endothelial dysfunction and postprandial lipemia, suggesting that alogliptin may be a promising anti-atherogenic agent.

DOI： 10.1186/1475-2840-12-8

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最大径40mmを越す心房中隔欠損症をいかにカテーテル閉鎖するか?利尿剤投与の効果

上岡亮, 木島康文, 赤木禎治, 杜徳尚, 中川晃志, 永瀬聡, 河野晋久, 森田宏, 草野研吾, 伊藤浩

日本成人先天性心疾患学会雑誌 2 ( 1 ) 70 - 70 2013.1

Increased passive stiffness of cardiomyocytes in the transverse direction and residual actin and myosin cross-bridge formation in hypertrophied rat hearts induced by chronic β-adrenergic stimulation.

Wakako Sumita Yoshikawa, Kazufumi Nakamura, Daiji Miura, Juichiro Shimizu, Ken Hashimoto, Noriyuki Kataoka, Hiroko Toyota, Hiroshi Okuyama, Toru Miyoshi, Hiroshi Morita, Kengo Fukushima Kusano, Tatsuhito Matsuo, Miyako Takaki, Fumihiko Kajiya, Naoto Yagi, Tohru Ohe, Hiroshi Ito

Circulation journal : official journal of the Japanese Circulation Society 77 ( 3 ) 741 - 8 2013

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

BACKGROUND: Left ventricular (LV) hypertrophy is often present in patients with diastolic heart failure. However, stiffness of hypertrophied cardiomyocytes in the transverse direction has not been fully elucidated. The aim of this study was to assess passive cardiomyocyte stiffness of hypertrophied hearts in the transverse direction and the influence of actin-myosin cross-bridge formation on the stiffness. METHODS AND RESULTS: Wistar rats received a vehicle (control) or isoproterenol (ISO) subcutaneously. After 7 days, compared with the controls, ISO administration had significantly increased heart weight and LV wall thickness and had decreased peak early annular relaxation velocity (e') assessed by echocardiography. Elastic modulus of living cardiomyocytes in the transverse direction assessed by an atomic force microscope was significantly higher in the ISO group than in controls. We added butanedione monoxime (BDM), an inhibitor of actin-myosin interaction, and blebbistatin, a specific myosin II inhibitor, to the medium. BDM and blebbistatin significantly reduced the elastic modulus of cardiomyocytes in the ISO group. X-ray diffraction analysis showed that the reflection intensity ratio (I((1,0))/I((1,1))) at diastole was not different before and after treatment with BDM, which induces complete relaxation, in control hearts, but that I((1,0))/I((1,1)) was significantly increased after BDM treatment in the ISO group, indicating residual cross-bridge formation in hypertrophied hearts. CONCLUSIONS: Passive cardiomyocyte stiffness in the transverse direction is increased in hearts with ISO-induced hypertrophy and this is caused by residual actin-myosin cross-bridge formation.

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The compound mutation, a model for acquire long QT syndrome.

Hiroshi Morita

Journal of cardiology cases 6 ( 6 ) e187-e188 2012.12

Andersen-Tawil症候群に合併した心室性不整脈に対し各種薬効評価を行い得た1例

重歳正尚, 草野研吾, 武寛, 永瀬聡, 森田宏, 伊藤浩

心臓 44 ( Suppl.3 ) 29 - 35 2012.12

Language：Japanese Publisher：(公財)日本心臓財団

Andersen-Tawil症候群(ATS)は不整脈・周期性四肢麻痺・形態異常を特徴とする稀な遺伝性疾患である。今回、ATSに合併した心室性不整脈に対して各種薬物効果を確認したので報告する。症例は47歳の女性。幼少時より多源性・多発性の心室期外収縮による頻脈・失神歴があり、最近はピルジカイニド100mg/日を内服されていた。2011年動悸が悪化し他院へ入院。その際の遺伝子検査にてKCNJ2遺伝子に既報のミスセンス変異を認め、ATSと診断され、精査加療のため当院へ入院となった。フレカイニド、ピルジカイニド、フェントラミン、ベラパミル静脈投与で著明な心室期外収縮抑制効果を認めたが、β遮断薬は無効であった。心臓電気生理学的検査では持続性心室頻拍や心室細動は誘発されなかった。自然発生の心室期外収縮に対して良好なペースマップが得られた部位で通電したが、すぐに再発し、アブレーションの効果は乏しいと判断した。その後、スピロノラクトン、イコサペント酸、フレカイニド200mgの内服で著明に心室期外収縮数が減少し、症状の劇的な改善を認めた。(著者抄録)

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PDGF-BB Activates Inflammatory Signaling in Pulmonary Arterial Smooth Muscle Cells from Patients with Idiopathic Pulmonary Arterial Hypertension Reviewed

Kazufumi Nakamura, Satoshi Akagi, Hiromi Matsubara, Aiko Ogawa, Aya Miura, Daiji Miura, Toru Miyoshi, Satoshi Nagase, Hiroshi Morita, Kunihisa Kohno, Kengo F. Kusano, Hiroshi Ito

CIRCULATION 126 ( 21 ) 2012.11

Cardiac dysfunction and prolonged hemodynamic deterioration after implantable cardioverter-defibrillator shock in patients with systolic heart failure. International journal

Norihisa Toh, Nobuhiro Nishii, Kazufumi Nakamura, Takeshi Tada, Hiroki Oe, Satoshi Nagase, Kunihisa Kohno, Hiroshi Morita, Kengo F Kusano, Hiroshi Ito

Circulation. Arrhythmia and electrophysiology 5 ( 5 ) 898 - 905 2012.10

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

BACKGROUND: We investigated the acute effects of implantable cardioverter-defibrillator shock on myocardium, cardiac function, and hemodynamics in relation to left ventricular systolic function. METHODS AND RESULTS: We studied 50 patients who underwent implantable cardioverter-defibrillator implantation and defibrillation threshold (DFT) testing: 25 patients with left ventricular ejection fraction (LVEF) ≥ 45% and 25 patients with LVEF <45%. We measured cardiac biomarkers (creatine kinase, creatine kinase-MB, myoglobin, cardiac troponin T and I, and N-terminal probrain natriuretic peptide). Left ventricular relaxation was assessed by global longitudinal strain rate during the isovolumetric relaxation period using speckle-tracking echocardiography. Blood sampling and echocardiography were performed before, immediately after, and 5 minutes and 4 hours after DFT testing. Mean arterial pressure was measured directly during DFT testing. Cardiac biomarkers showed no significant changes in either group. LVEF was decreased until 5 minutes after DFT testing and had recovered to the baseline at 4 hours in the group with reduced LVEF (P<0.001), whereas LVEF reduction was not observed in the group with preserved LVEF (P=0.637). Global isovolumetric relaxation period was decreased until 5 minutes after DFT testing and had recovered to the baseline at 4 hours in both groups (preserved LVEF: 0.39 ± 0.14 versus 0.23 ± 0.13* versus 0.23 ± 0.13* versus 0.40 ± 0.13 s(-1), *P<0.001 versus baseline; reduced LVEF: 0.15 ± 0.05 versus 0.08 ± 0.04† versus 0.09 ± 0.04† versus 0.15 ± 0.05 s(-1), †P<0.001 versus baseline, repeated-measures ANOVA). Time to recovery of mean arterial pressure to the baseline was prolonged in the group with reduced LVEF (P<0.001). CONCLUSIONS: Implantable cardioverter-defibrillator shock transiently impairs cardiac function and hemodynamics especially in patients with systolic dysfunction, although significant tissue injury is not observed.

DOI： 10.1161/CIRCEP.111.970285

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完全房室ブロックでペースメーカー植え込み後4年の経過を経て心サルコイドーシスと診断し得た一例

内藤優佳, 三好章仁, 高谷陽一, 永瀬聡, 河野晋久, 森田宏, 草野研吾, 伊藤浩

日本サルコイドーシス/肉芽腫性疾患学会雑誌 32 ( サプリメント号 ) 43 - 43 2012.9

Fragmented QRS: What Is The Meaning? International journal

Yutaka Take, Hiroshi Morita

Indian pacing and electrophysiology journal 12 ( 5 ) 213 - 25 2012.9

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

Fragmented QRS (fQRS) is a convenient marker of myocardial scar evaluated by 12-lead electrocardiogram (ECG) recording. fQRS is defined as additional spikes within the QRS complex. In patients with CAD, fQRS was associated with myocardial scar detected by single photon emission tomography and was a predictor of cardiac events. fQRS was also a predictor of mortality and arrhythmic events in patients with reduced left ventricular function. The usefulness of fQRS for detecting myocardial scar and for identifying high-risk patients has been expanded to various cardiac diseases, such as cardiac sarcoidosis, arrhythmogenic right ventricular cardiomyopathy, acute coronary syndrome, Brugada syndrome, and acquired long QT syndrome. fQRS can be applied to patients with wide QRS complexes and is associated with myocardial scar and prognosis. Myocardial scar detected by fQRS is associated with subsequent ventricular dysfunction and heart failure and is a substrate for reentrant ventricular tachyarrhythmias.

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24時間ホルター心電図を用いた、Brugada症候群、特発性心室細動、健常者の心室遅延電位(LP)の特徴の検討

寒川睦子, 森田宏, 永瀬聡, 西井伸洋, 河野晋久, 中村一文, 草野研吾, 伊藤浩, 大江透

心電図 32 ( Suppl.5 ) S - 180 2012.9

Brugada症候群におけるspontaneous type1波形を呈さないハイリスク群の検討

和田匡史, 森田宏, 三好亨, 西井伸洋, 橋本克史, 永瀬聡, 中村一文, 河野晋久, 草野研吾, 伊藤浩

心電図 32 ( Suppl.5 ) S - 156 2012.9

Brugada症候群患者における心室細動のリスクとしての下壁側壁誘導の早期再分極(ER)とFragmented QRS

時岡浩二, 草野研吾, 森田宏, 永瀬聡, 西井伸洋, 中村一文, 河野晋久, 伊藤浩

心電図 32 ( Suppl.5 ) S - 158 2012.9

左室拡張不全のリスクマーカーとしての冠動脈石灰化スコア冠動脈有意狭窄を認めない例での検討

三好亨, 大澤和宏, 麻植浩樹, 杜徳尚, 永瀬聡, 河野晋久, 中村一文, 森田宏, 草野研吾, 伊藤浩

日本高血圧学会総会プログラム・抄録集 35回 471 - 471 2012.9

Pro-apoptotic effects of imatinib on PDGF-stimulated pulmonary artery smooth muscle cells from patients with idiopathic pulmonary arterial hypertension. International journal

Kazufumi Nakamura, Satoshi Akagi, Aiko Ogawa, Kengo F Kusano, Hiromi Matsubara, Daiji Miura, Soichiro Fuke, Nobuhiro Nishii, Satoshi Nagase, Kunihisa Kohno, Hiroshi Morita, Takahiro Oto, Ryutaro Yamanaka, Fumio Otsuka, Aya Miura, Chikao Yutani, Tohru Ohe, Hiroshi Ito

International journal of cardiology 159 ( 2 ) 100 - 6 2012.8

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

BACKGROUND: Remodeling of the pulmonary artery by an inappropriate increase of pulmonary artery smooth muscle cells (PASMCs) is problematic in the treatment of idiopathic pulmonary arterial hypertension (IPAH). Effective treatment that achieves reverse remodeling is required. The aim of this study was to assess the pro-apoptotic effects of imatinib, a platelet-derived growth factor (PDGF)-receptor tyrosine kinase inhibitor, on PASMCs obtained from patients with IPAH. METHODS: PASMCs were obtained from 8 patients with IPAH undergoing lung transplantation. Cellular proliferation was assessed by (3)H-thymidine incorporation. Pro-apoptotic effects of imatinib were examined using TUNEL and caspase-3,7 assays and using transmission electron microscopy. RESULTS: Treatment with imatinib (0.1 to 10 μg/mL) significantly inhibited PDGF-BB (10 ng/mL)-induced proliferation of PASMCs from IPAH patients. Imatinib (1 μg/mL) did not induce apoptosis in quiescent IPAH-PASMCs, but it had a pro-apoptotic effect on IPAH-PASMCs stimulated with PDGF-BB. Imatinib did not induce apoptosis in normal control PASMCs with or without PDGF-BB stimulation. PDGF-BB induced phosphorylation of Akt at 15 min, and Akt phosphorylation was inhibited by imatinib in IPAH-PASMCs. Akt-I-1/2 (1 μmol/L), an Akt inhibitor, in the presence of PDGF-BB significantly increased apoptotic cells compared with the control condition. Thus, Akt-I-1/2 could mimic the effects of imatinib on PASMCs. CONCLUSION: Imatinib has anti-proliferative and pro-apoptotic effects on IPAH-PASMCs stimulated with PDGF. The inhibitory effect of imatinib on Akt phosphorylation induced by PDGF plays an important role in the pro-apoptotic effect.

DOI： 10.1016/j.ijcard.2011.02.024

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不整脈と心臓病理形態学器質的心疾患に伴う心室性不整脈の特徴と対策

草野研吾, 永瀬聡, 森田宏, 中村一文, 伊藤浩, 大江透

日本心臓病学会誌 7 ( Suppl.I ) 219 - 219 2012.8

Identification of high-risk syncope related to ventricular fibrillation in patients with Brugada syndrome. International journal

Yutaka Take, Hiroshi Morita, Norihisa Toh, Nobuhiro Nishii, Satoshi Nagase, Kazufumi Nakamura, Kengo F Kusano, Tohru Ohe, Hiroshi Ito

Heart rhythm 9 ( 5 ) 752 - 9 2012.5

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

BACKGROUND: Syncope in patients with Brugada syndrome is usually associated with ventricular tachyarrhythmia, but some episodes of syncope can be related to autonomic disorders. OBJECTIVE: The purpose of this study was to investigate the characteristics of syncope to differentiate high-risk syncope episodes from low-risk events in patients with Brugada syndrome. METHODS: We studied 84 patients with type 1 electrocardiogram and syncope. Patients were divided into 2 groups: patients with prodrome (prodromal group; n = 41) and patients without prodrome (nonprodromal group; n = 43). RESULTS: Ventricular fibrillation (VF) was documented at index event in 19 patients: 4 patients (21%) with documented VF experienced a prodrome prior to the onset of VF, whereas 15 patients (79%) did not have symptoms prior to documented VF (P <.01). Twenty-seven patients in the prodromal group and 7 patients in the nonprodromal group were considered to have syncope related to autonomic dysfunction. Syncope in other patients was defined as unexplained syncope. During the follow-up period (48 ± 48 months), recurrent syncope due to VF occurred in 13 patients among patients with only unexplained syncope and was more frequent in the nonprodromal group (n = 10) than in the prodromal group (n = 3; P = .044). In multivariate analysis, blurred vision (hazard ratio [HR] 0.20) and abnormal respiration (HR 2.18) and fragmented QRS (HR 2.39) were independently associated with the occurrence of VF. CONCLUSION: Syncope with prodrome, especially blurred vision, suggests a benign etiology of syncope in patients with Brugada syndrome.

DOI： 10.1016/j.hrthm.2011.11.045

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電気的ストームの実態と対処 Brugada症候群における植込み型除細動器頻回作動に対する抗不整脈薬の長期的効果

草野研吾, 永瀬聡, 森田宏, 中村一文, 西井伸洋, 田中正道, 中川晃司, 三浦大治, 伊藤浩

Journal of Arrhythmia 28 ( Suppl. ) 160 - 160 2012.5

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Papers - MORITA Hiroshi