Faculty Profiles - MORITA Hiroshi

Papers - MORITA Hiroshi

Division display 281 - 300 of about 349 ／ All the affair displays >>

SCN5A遺伝子異常(R282H)を認めたBrugada症候群の一家系

中村一文, 三浦大志, 平松茂樹, 湯本晃久, 江森哲郎, 森田宏, 渡辺敦之, 永瀬聡, 齋藤博則, 草野研吾, 西井伸洋, 大江透, 長野仁, 神山憲王

Circulation Journal 69 ( Suppl.II ) 798 - 798 2005.4

カルシウム拮抗薬(CCB)の抗炎症作用についての検討

三浦龍志, 中村一文, 三浦大志, 三浦綾, 久松研一, 橋本克史, 永瀬聡, 森田宏, 草野研吾, 齋藤博則, 江森哲郎, 大江透

Circulation Journal 69 ( Suppl.II ) 805 - 805 2005.4

心室細動に対してキニジンが奏功したBrugada症候群の1例

渡辺敦之, 森田宏, 角田和歌子, 伴場主一, 西井伸洋, 永瀬聡, 中村一文, 齋藤博則, 草野研吾, 江森哲郎, 大江透

Circulation Journal 69 ( Suppl.II ) 797 - 797 2005.4

Brugada syndromeにおけるST上昇の日内変動性の検討 Holter心電図によるST変動測定の可能性

寒川睦子, 中津高明, 渡辺敦之, 豊永慎二, 草地省蔵, 森田宏, 草野研吾, 大江透

心電図 25 ( Suppl.1 ) S - 112 2005.3

Failure of disopyramide to improve right ventricular outflow tract obstruction after living-donor lobar lung transplantation.

Katsumasa Miyaji, Hiromi Matsubara, Masahito Kajiya, Yoshinori Tani, Kazufumi Nakamura, Hiroshi Morita, Tetsuro Emori, Hiroshi Date, Tohru Ohe

Circulation journal : official journal of the Japanese Circulation Society 68 ( 11 ) 1084 - 7 2004.11

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

Right ventricular (RV) outflow tract obstruction (RVOTO) is an uncommon complication of lung transplantation in patients with pulmonary hypertension (PH) and both medical management and surgical intervention are required. A 28-year-old female with primary PH was referred and because she did not respond to medical treatment, living-donor lobar lung transplantation was performed. The operation was successful, but dyspnea and exercise intolerance developed during rehabilitation and transthoracic echocardiography revealed RVOTO. Intravenous disopyramide during cardiac catheterization reduced the pressure gradient from 35 mmHg to 16 mmHg without decreasing RV systolic pressure. However, electrical and hemodynamic parameters were adversely affected by disopyramide and thus, after cardiac catheterization, administration of fluid and a low dose of atenolol was started, and her symptoms improved. Transthoracic echocardiography showed improvement in the RVOTO. This case suggests that disopyramide should be avoided for patients with RVOTO following lung transplantation and that other negative inotropic agents, such as beta-blockers, are more effective for relief of RVOTO.

PubMed

researchmap

Differences between flow profiles of pulmonary vein anastomoses affected by peripheral atelectasis in cadaveric and bilateral living-donor lobar lung transplantations. International journal

Katsumasa Miyaji, Hiromi Matsubara, Kazufumi Nakamura, Takeshi Maruo, Hiroshi Morita, Hironori Saito, Kengo F Kusano, Tetsuro Emori, Keiji Goto, Hiroshi Date, Tohru Ohe

Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography 17 ( 9 ) 1003 - 4 2004.9

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

We report two cases of peripheral atelectasis during cadaveric and living-donor lobar lung transplantation, which had different effects on the flow profile of pulmonary vein (PV) anastomoses. In the patient who underwent living-donor lobar lung transplantation, we detected the increase in the velocity of blood flow through the left PV anastomosis by intraoperative transesophageal echocardiography. Then peripheral atelectasis occurred in the transplanted left lung lobe. On the other hand, in the patient who underwent cadaveric bilateral lung transplantation, peripheral atelectasis occurred, but no changes in velocities of blood flow through PV anastomoses were detected by intraoperative transesophageal echocardiography. This difference may have been caused by the difference in sizes of pulmonary beds of transplanted grafts. These findings indicate the necessity of careful monitoring of PV anastomoses, especially in cases of living-donor lobar lung transplantation.

PubMed

researchmap

Effect of a kink in unilateral pulmonary artery anastomosis on velocities of blood flow through bilateral pulmonary vein anastomoses in living-donor lobar lung transplantation. International journal

Katsumasa Miyaji, Kazufumi Nakamura, Takeshi Maruo, Hiroshi Morita, Hironori Saito, Tetsuro Emori, Keiji Goto, Hiroshi Date, Tohru Ohe

Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography 17 ( 9 ) 998 - 9 2004.9

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

Intraoperative transesophageal echocardiography is generally performed to detect vascular complications during lung transplantation. We report a case with a kink in pulmonary artery (PA) anastomosis suggested by an abnormal flow profile of pulmonary vein (PV) anastomoses during living-donor lobar lung transplantation. During the transplantation, velocity of blood flow through the right PV anastomosis showed abnormal elevation. Then, the patient's PA pressure elevated abnormally and a kink in the left PA anastomosis was found. Careful monitoring of PV anastomoses may enable detection of not only an abnormality of PV anastomoses but also that of PA anastomoses, especially in living-donor lobar lung transplantation.

PubMed

researchmap

Relationships between depolarization abnormality and repolarization abnormality in patients with Brugada syndrome: using body surface signal-averaged electrocardiography and body surface maps. International journal

Kenichi Hisamatsu, Kengo Fukushima Kusano, Hiroshi Morita, Shiho Takenaka, Satoshi Nagase, Kazufumi Nakamura, Tetsuro Emori, Hiromi Matsubara, Hiroshi Mikouchi, Yoshitomo Nishizaki, Tohru Ohe

Journal of cardiovascular electrophysiology 15 ( 8 ) 870 - 6 2004.8

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

INTRODUCTION: Repolarization and depolarization abnormalities have been reported to be related to Brugada syndrome. METHODS AND RESULTS: We evaluated the relationships between repolarization abnormality and depolarization abnormality using 48-lead unipolar signal-averaged electrocardiograms and 87-lead unipolar body surface maps in 15 patients with Brugada-type ECGs. Data were compared with those from healthy control subjects (n = 5) and within subgroups of Brugada syndrome with (n = 8) and without (n = 7) ventricular arrhythmias (VA) induced by programmed electrical stimulation (PES). Eighty-seven-lead body surface maps were recorded, and potential maps were constructed to evaluate elevation of the ST segment 20 ms after the J point. Forty-eight-lead signal-averaged ECGs were recorded, and isochronal maps of duration of the delayed potential (dDP) were constructed to evaluate the dDP in each lead. Potential maps showed that patients with Brugada-type ECG, especially those with VA induced by programmed electrical stimulation, had greater elevation of the ST segment in the right ventricular outflow tract, especially at E5. Isochronal maps of dDP in the Brugada-type ECG group showed that maximum dDP was located at E5 and that the area with long dDP was larger than that in the control subjects. The dDPs at E7, E5, F7, and F5 in the VA-inducible group were significantly longer than those in the VA-noninducible group. These results showed that the location of greater elevation in the ST segment coincided with the location of longer dDP. CONCLUSION: Repolarization abnormality and depolarization abnormality in the walls of both ventricles, especially in the right ventricular outflow tract, are related to the VA of Brugada syndrome.

PubMed

researchmap

肺高血圧患者の肺移植前後における心電図変化の検討

藤尾栄起, 森田宏, 松原広己, 宮地克維, 中村一文, 斎藤博則, 草野研吾, 江森哲郎, 大江透

心電図 24 ( 5 ) 368 - 368 2004.8

院内の自動体外式除細動器にて除細動された2症例

斎藤博則, 藤尾栄起, 宮地克維, 中村一文, 森田宏, 草野研吾, 江森哲郎, 大江透, 林峰栄, 氏家良人

心電図 24 ( 5 ) 343 - 343 2004.8

Brugada症候群患者でのイソプレナリンの治療効果

渡辺敦之, 森田宏, 西井伸洋, 伴場主一, 永瀬聡, 中村一文, 斎藤博則, 草野研吾, 江森哲郎, 大江透

心電図 24 ( 5 ) 345 - 345 2004.8

不整脈治療とその効果 QOLと予後の改善をめざして Brugada症候群に対する植込み型除細動器による治療予後とQOLの観点からの検討

江森哲郎, 森田宏, 永瀬聡, 西井伸洋, 伴場主一, 渡辺敦之, 中村一文, 斉藤博則, 草野研吾, 大江透

心電図 24 ( 5 ) 293 - 293 2004.8

非虚血性心筋症患者の生命予後と心室頻拍に対する治療戦略について

西井伸洋, 江森哲郎, 宮地克維, 永瀬聡, 中村一文, 森田宏, 斎藤博則, 草野研吾, 大江透

心電図 24 ( 5 ) 382 - 382 2004.8

不整脈治療とその効果 QOLと予後の改善をめざして Brugada症候群に対する植込み型除細動器による治療予後とQOLの観点からの検討

江森哲郎, 森田宏, 永瀬聡, 西井伸洋, 伴場主一, 渡辺敦之, 中村一文, 斉藤博則, 草野研吾, 大江透

Journal of Cardiology 44 ( Suppl.I ) 194 - 194 2004.8

Brugada症候群に対するキニジンの効果

渡辺敦之, 森田宏, 角田和歌子, 西井伸洋, 伴場主一, 永瀬聡, 中村一文, 斎藤博則, 草野研吾, 江森哲郎, 大江透

心電図 24 ( 5 ) 346 - 346 2004.8

Significance of the level of monocyte chemoattractant protein-1 in human atherosclerosis.

Kengo Fukushima Kusano, Kazufumi Nakamura, Hitoshi Kusano, Nobuhiro Nishii, Kimikazu Banba, Tetsuya Ikeda, Katsushi Hashimoto, Mika Yamamoto, Hideki Fujio, Aya Miura, Keiko Ohta, Hiroshi Morita, Hironori Saito, Tetsuro Emori, Yoichi Nakamura, Isao Kusano, Tohru Ohe

Circulation journal : official journal of the Japanese Circulation Society 68 ( 7 ) 671 - 6 2004.7

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

BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1), a potent chemoattractant for monocytes, plays an important role in the earliest events of atherogenesis. However, direct evidence of the effects of MCP-1 on atherosclerosis in chronic hemodialysis (HD) patients has not been reported. METHODS AND RESULTS: The serum MCP-1 concentrations and the intimal - medial thickness (IMT) in the carotid arteries were measured in 42 non-diabetic chronic HD patients and 20 age-matched controls. The expression of MCP-1 was examined immunohistochemically in radial arterial tissues obtained from the HD patients. IMT and the serum concentration of MCP-1 in the HD patients were both significantly greater than in controls. Multiple regression analysis revealed that the serum concentration of MCP-1 was an independent factor influencing IMT. Tissue immunostaining showed that MCP-1 is expressed in both endothelial and smooth muscle cells and that its level of expression correlates with the serum concentration of MCP-1. CONCLUSIONS: An increase in MCP-1 may be an important factor in the progression of atherosclerosis in non-diabetic HD patients.

PubMed

researchmap

Functional characterization of a trafficking-defective HCN4 mutation, D553N, associated with cardiac arrhythmia. International journal

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

The Journal of biological chemistry 279 ( 26 ) 27194 - 8 2004.6

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

Hyperpolarization-activated cyclic nucleotide-gated channel 4 gene HCN4 is a pacemaker channel that plays a key role in automaticity of sinus node in the heart, and an HCN4 mutation was reported in a patient with sinus node dysfunction. Expression of HCN4 in the heart is, however, not confined to the sinus node cells but is found in other tissues, including cells of the conduction system. On the other hand, mutations in another cardiac ion channel gene, SCN5A, also cause sinus node dysfunction as well as other cardiac arrhythmias, including long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation, and progressive cardiac conduction disturbance. These observations imply that HCN4 abnormalities may be involved in the pathogenesis of various arrhythmias, similar to the SCN5A mutations. In this study, we analyzed patients suffering from sinus node dysfunction, progressive cardiac conduction disease, and idiopathic ventricular fibrillation for mutations in HCN4. A missense mutation, D553N, was found in a patient with sinus node dysfunction who showed recurrent syncope, QT prolongation in electrocardiogram, and polymorphic ventricular tachycardia, torsade de pointes. In vitro functional study of the D553N mutation showed a reduced membranous expression associated with decreased If currents because of a trafficking defect of the HCN4 channel in a dominant-negative manner. These data suggest that the loss of function of HCN4 is associated with sinus nodal dysfunction and that a consequence of pacemaker channel abnormality might underlie clinical features of QT prolongation and polymorphic ventricular tachycardia developed under certain conditions.

PubMed

researchmap

Sinus node function in patients with Brugada-type ECG.

Hiroshi Morita, Kengo Fukushima-Kusano, Satoshi Nagase, Kohei Miyaji, Shigeki Hiramatsu, Kimikazu Banba, Nobuhiro Nishii, Atsuyuki Watanabe, Mikio Kakishita, Shiho Takenaka-Morita, Kazufumi Nakamura, Hironori Saito, Tetsuro Emori, Tohru Ohe

Circulation journal : official journal of the Japanese Circulation Society 68 ( 5 ) 473 - 6 2004.5

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

BACKGROUND: Some studies have shown that patients with Brugada syndrome (BS) have atrioventricular conduction disturbance, but their sinus node function has not been evaluated. METHODS AND RESULTS: The patients group consisted of 59 male patients and 1 female patient with BS. Supraventricular and ventricular programmed electrical stimulation (PES) was performed. Ventricular fibrillation (VF) or sustained polymorphic ventricular tachycardia was induced by ventricular PES in 26 patients with BS (VF group), but was not induced in the other 34 patients (non-VF group). Sinus node function and conduction of the atrioventricular (AV) node in the control group, non-VF group and VF group were evaluated. Sinus node function was attenuated and the His - ventricle interval was prolonged in the VF group (corrected sinus node recovery time: 452+/-126 ms (VF group), 324+/-146 ms (non-VF group), Sino-atrial conduction time: 179+/-60 ms (VF group), 127+/-60 ms (non-VF group), His-ventricle interval: 41+/-9 ms (VF group), 35+/-8 ms (non-VF group)). CONCLUSION: The function of both the sinus node and AV node are attenuated in patients with PES-induced VF.

PubMed

researchmap

右室心尖部以外に留置された植込み型除細動器の心室リードの安全性について

西井伸洋, 森田宏, 渡辺敦之, 伴場主一, 永瀬聡, 斉藤博則, 草野研吾, 江森哲郎, 大江透

不整脈 20 ( 2 ) 215 - 215 2004.4

特発性心室細動と考えられた2症例 Short coupled variant of Torsades de pointesとBrugada症候群との比較検討

渡邊敦之, 森田宏, 伴場主一, 西井伸洋, 永瀬聡, 斉藤博則, 草野研吾, 江森哲郎, 大江透

不整脈 20 ( 2 ) 258 - 258 2004.4

　 PREV - NEXT 　

< MORITA Hiroshi >

Papers - MORITA Hiroshi