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Relationship between arrhythmogenesis and disease activity in cardiac sarcoidosis

Kimikazu Banba, Kengo Fukushima Kusano, Kazufumi Nakamura, Hiroshi Morita, Aiko Ogawa, Fuyo Ohtsuka, Keiko Ohta Ogo, Nobuhiro Nishii, Atsuyuki Watanabe, Satoshi Nagase, Satoru Sakuragi, Tohru Ohe

HEART RHYTHM 4 ( 10 ) 1292 - 1299 2007年10月

記述言語：英語出版者・発行元：ELSEVIER SCIENCE INC

BACKGROUND In patients with cardiac sarcoidosis, ventricular arrhythmias and/or conduction disturbances are frequently observed and sometimes fatal. However, few reports on disease activity and arrhythmic events in cardiac sarcoidosis are available.
OBJECTIVE The purpose of this study was to investigate the relationship between disease activity and arrhythmic events in cardiac sarcoidosis and the effect of corticosteroid therapy.
METHODS The study population consisted of 15 cardiac sarcoidosis patients with new-onset symptomatic arrhythmia, including eight patients admitted once for complete atrioventricular block (CAVB), five patients admitted once for sustained ventricular tachycardia (VT), and two patients admitted twice for two arrhythmic events (one for CAVB and the other for sustained VT). Disease activity was evaluated by gallium-67 citrate (Ga) scintigraphy. All patients with positive Ga uptake were treated with corticosteroids, and arrhythmic events were evaluated by repeat Hotter recordings.
RESULTS Positive uptake of Ga was observed in 8 (80%) of the 10 CAVB events and in 1 (14%) of the 7 sustained VT events (80% vs 14%, P =.02). Corticosteroids abolished myocardial Ga uptake in all nine patients with positive Ga uptake. After corticosteroid therapy was started, AV conduction improved in 5 of 9 CAVB patients (including 8 patients with new-onset CAVB and one patient with history of CAVB). However, ventricular arrhythmias were not improved after corticosteroid therapy.
CONCLUSION In cardiac sarcoidosis patients, CAVB develops mainly during the active phase of the disease. Early treatment with corticosteroids might improve AV conduction disturbance. However, sustained VT is not closely linked with disease activity and frequently develops in the advanced stage of disease.

DOI： 10.1016/j.hrthm.2007.06.006

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

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 - 1809 2007年10月

T75M-KCNJ2 mutation causing Andersen-Tawil syndrome enhances inward rectification by changing Mg2+ sensitivity

Yoshinori Tani, Daiji Miura, Junko Kurokawa, Kazufumi Nakamura, Mamoru Ouchida, Kenji Shimizu, Tohru Ohe, Tetsushi Furukawa

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 43 ( 2 ) 187 - 196 2007年8月

記述言語：英語出版者・発行元：ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD

Andersen-Tawil syndrome (ATS) is a multisystem inherited disease exhibiting periodic paralysis, cardiac arrhythmias, and dysmorphic features. In this study, we characterized the KCNJ2 channels with an ATS mutation (T75M) which is associated with cardiac phenotypes of bidirectional ventricular tachycardia, syncope, and QT(c) prolongation. Confocal imaging of GFP-KCNJ2 fusion proteins showed that the T75M mutation impaired membrane localization of the channel protein, which was restored by co-expression of WT channels with T75M channels. Whole-cell patch-clamp experiments in CHO-K1 cells showed that the T75M mutation produced a loss-of-function of the channel. When both WT and the T75M were co-expressed, the T75M mutation showed dominant-negative effects on inward rectifier K+ current densities, with prominent suppression of outward currents at potentials between 0 mV and + 80 mV over the E-K. Inside-out patch experiments in HEK293T cells revealed that co-expression of WT and the T75M channels enhanced voltage-dependent block of the channels by internal Mg2+, resulting in enhanced inward rectification at potentials 50 mV more positive than the EK. We suggest that the T75M mutation causes dominant-negative suppression of the co-expressed WT KCNJ2 channels. In addition, the T75M mutation caused alteration of gating kinetics of the mutated KCNJ2 channels, i.e., increased sensitivity to intracellular Mg2+ and resultant enhancement of inward rectification. The data presented suggest that the mutation may influence clinical features, but it does not directly show this. (c) 2007 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.yjmcc.2007.05.005

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Brugada 症候群と自律神経との関わり : 歴史・診断・臨床的意義・治療について

寒川睦子, 中津高明, 豊永慎二, 間島圭一, 草地省蔵, 渡辺敦之, 伴場主一, 西井伸洋, 多田毅, 永瀬聡, 森田宏, 中村一文, 草野研吾, 大江透

自律神経 = The Autonomic nervous system 44 ( 3 ) 156 - 165 2007年6月

71)WPW症候群を合併した家族性肥大型心筋症の一例(第89回日本循環器学会中国地方会)

赤木達, 大田恵子, 中川晃志, 多田毅, 永瀬聡, 中村一文, 桜木悟, 草野研吾, 大江透

Circulation journal : official journal of the Japanese Circulation Society 71 858 - 858 2007年4月

36)心臓再同期療法後より頻発する心室頻拍に対し高周波カテーテルアブレーションを施行した一例(第89回日本循環器学会中国地方会)

二階堂暁, 酒井芳昭, 赤木進, 福家聡一郎, 西井伸洋, 永瀬聡, 中村一文, 桜木悟, 草野研吾, 大江透

Circulation journal : official journal of the Japanese Circulation Society 71 854 - 854 2007年4月

89)原発性肺高血圧症の心房中隔欠損合併例にepoprostenolを導入した2症例(第89回日本循環器学会中国地方会)

福家聡一郎, 二階堂暁, 圓光賢希, 赤木達, 溝口博喜, 永瀬聡, 中村一文, 桜木悟, 草野研吾, 大江透

Circulation journal : official journal of the Japanese Circulation Society 71 860 - 860 2007年4月

68)ステロイド投与が有用であった好酸球性心筋炎の一症例(第89回日本循環器学会中国地方会)

圓光賢希, 桜木悟, 大郷恵子, 永瀬聡, 中村一文, 草野研吾, 大江透

Circulation journal : official journal of the Japanese Circulation Society 71 857 - 857 2007年4月

3)ヒト冠動脈平滑筋細胞におけるPioglitazoneの効果 : 遊走・増殖・活性酸素発生の抑制効果の検討(第89回日本循環器学会中国地方会)

吉川昌樹, 中村一文, 永瀬聡, 桜木悟, 草野研吾, 大江透

Circulation journal : official journal of the Japanese Circulation Society 71 850 - 850 2007年4月

FRS-087 Relationship between SCN5A Mutation and Atrial Vulnerability in Brugada Syndrome(Arrhythmia (clinical) ; Pathophysiology of Atrial Fibrillation, The 71st Annual Scientific Meeting of the Japanese Circulation Society)

Taniyama Makiko, Kusano Kengo, Banba Kimikazu, Morita Hiroshi, Nishii Nobuhiro, Watanabe Atsuyuki, Miura Daiji, Sumida Wakako, Iwasaki Jun, Urakawa Shigemi, Kimura Hideo, Miura Aya, Kobayashi Kaoru, Nagase Satoshi, Nakamura Kazufumi, Ohe Toru

Circulation journal : official journal of the Japanese Circulation Society 71 141 - 141 2007年3月

心不全(下）－最新の基礎・臨床研究の進歩－XXIII 心不全での合併症－成因・病態・治療－不整脈心不全に用いられる抗不整脈薬

中村一文, 西井伸洋, 大江透

日本臨床 65 ( 5 ) 369 - 374 2007年

Efficacy and safety of the additional bepridil treatment in patients with atrial fibrillation refractory to class I antiarrhythmic drugs.

Miyaji K, Tada H, Fukushima Kusano K, Hashimoto T, Kaseno K, Hiramatsu S, Tadokoro K, Naito S, Nakamura K, Oshima S, Taniguchi K, Ohe T

Circ J 71 ( 8 ) 1250 - 1257 2007年

異常Purkinje線維の興奮と多源性心室性不整脈の発生機序に関し検討を行った特発性心室細動の1例

伴場主一, 草野研吾, 永瀬聡, 西井伸洋, 渡邊敦之, 平松茂樹, 多田毅, 村上正人, 大郷恵子, 酒井芳昭, 中村一文, 櫻木悟, 大江透

臨床心臓電気生理 30 237 - 245 2007年

記述言語：日本語出版者・発行元：臨床心臓電気生理研究会

29歳の女性。Short-coupled variant of torsade de pointesとして植込み型除細動器(ICD)植込みをされている。電気生理学的検査開始時より心室期外収縮はさまざまな連結期で出現し、波形もさまざまであった。この多源性の心室期外収縮は、左室内中部中隔に配置した多極カテーテルからの記録によって常にPurkinje電位(PP)が同じ場所で同じ興奮順序で記録された。興味あることにこのPPが出現する周期を検討すると、副収縮を呈していた。PPの連結期とPP-心室期外収縮間隔について検討を行うとPP-心室期外収縮間の興奮伝導様式には遅延伝導と減衰伝導特性が存在し、Purkinje network内あるいはPurkinje-心筋間でのブロックの変化によって多源性の心室期外収縮様のQRS波形を呈しているものと考えられた。心室期外収縮連発時も各々のQRS波形に先行してPPが記録され、PPを標的に高周波アブレーションを施行し、心室期外収縮は消失した。(著者抄録)

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原発性肺高血圧症の進行メカニズムの解明と治療薬の開発

小川愛子, 中村一文, 松原広己, 藤尾栄起, 池田哲也, 宮地克維, 三浦大志, 三浦綾, 永瀬聡, 草野研吾, 伊達洋至, 大江透

岡山医学会雑誌 118 ( 3 ) 187 - 192 2007年

循環器症候群（第2版）Ⅰ－その他の循環器疾患を含めて－Ⅲ. 不整脈二次性QT延長症候群

原岡佳代, 中村一文, 大江透

別冊日本臨床新領域別症候群シリーズ 4 221 - 224 2007年

イオン感応性電界効果トランジスタ（ISFET）を用いた迅速・簡便な細胞活性測定システムの開発

合田典子, 中村通宏, 山本尚武, 中村一文

中谷電子計測技術振興財団年報 21 53 - 57 2007年

救命しえた劇症型好酸球性心筋炎の1例

大郷恵子, 圓光賢希, 草野研吾, 櫻木悟, 永瀬聡, 中村一文, 柳井広之, 大森昌子, 大家政志, 難波靖治, 津田佳穂, 大江透

心臓 39 ( 3 ) 112 - 117 2007年

記述言語：日本語出版者・発行元：(公財)日本心臓財団

症例は19歳、男性。主訴は胸苦・胸痛。2006年4月29日午前2時ころ、胸苦・胸痛のため近医を受診、心電図上広範囲のST-T変化を認め急性心膜炎の疑いで入院となった。30日午前4時ころより血圧低下がみられたためdopamine点滴を開始され当科転院となった。転院時、血圧80mmHg、脈拍130/分で、奇脈、III音、頸静脈怒張を認めた。心エコーでの左室壁厚増大とびまん性の高度壁運動低下(左室駆出率23.8%)、多量の心嚢液貯留、CPKの上昇などから劇症型心筋炎による心原性ショックと診断した。機械的循環補助を行った上で、心臓カテーテル検査により冠動脈疾患を否定し、右室心内膜心筋生検を施行した。5月2日好酸球性心筋炎との組織診断によりステロイド投与を開始した。そのころより心機能の急速な回復がみられ、補助循環が離脱可能となった(離脱時に脳出血を合併)。その後ステロイドを漸減中止したが好酸球性心筋炎の再発やLoeffler心内膜炎への移行は認めていない。原因検索の結果、イヌ回虫に対する抗体が陽性であり、寄生虫感染に関連した好酸球性心筋炎と考えられた。今回著者等は劇症型心筋炎がイヌ回虫感染に伴う好酸球性心筋炎によるという稀な1例を経験し、ステロイド投与と機械的循環補助により救命しえたので報告する。(著者抄録)

DOI： 10.11281/shinzo1969.39.Supplement3_112

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その他リンク： https://search.jamas.or.jp/default/link?pub_year=2007&ichushi_jid=J00679&link_issn=&doc_id=20070820320022&doc_link_id=10.11281%2Fshinzo1969.39.Supplement3_112&url=https%3A%2F%2Fdoi.org%2F10.11281%2Fshinzo1969.39.Supplement3_112&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

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 ( Supplement 1 ) 2007年

4-hydroxy-2-nonenal induces calcium overload via NADPH oxidase-derived reactive oxygen species in isolated rat cardiac myocytes

Kazufumi Nakamura, Daiji Miura, Hiromi Matsubara, Wakako Sumita, Satoshi Nagase, Satoru Sakuragi, Kengo F. Kusano, Tohru Ohe

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 41 ( 6 ) 1050 - 1050 2006年12月

Aldosterone synthesis and cytokine production in human peripheral blood mononuclear cells

Ryuzea Miura, Kazufumi Nakamura, Daiji Miura, Aya Miura, Kenichi Hisamatsu, Masahito Kajiya, Katsushi Hashimoto, Satoshi Nagase, Hiroshi Morita, Kengo Fukushima Kusano, Tetsuro Emori, Kazuhiko Ishihara, Tohru Ohe

JOURNAL OF PHARMACOLOGICAL SCIENCES 102 ( 3 ) 288 - 295 2006年11月

記述言語：英語出版者・発行元：JAPANESE PHARMACOLOGICAL SOC

Previously, we reported that spironolactone reduced cytokine production in cultured human peripheral blood mononuclear cells (PBMCs) with angiotensin (Ang) II stimulation. To address the mechanisms underlying this effect, we examined the contribution of aldosterone to cytokine production in cultured human PBMCs with Ang II stimulation. PBMCs expressed the messenger RNA (mRNA) of Ang II type I receptor (ATIR) and mineralocorticoid receptor (MR) both spontaneously and after Ang II stimulation, but expressed Ang II type 2 receptor (AT2R) under neither condition. After 24 h of incubation, exogenous Ang II induced the expression of CYP11B2 (a key enzyme of aldosterone synthesis) mRNA and caused aldosterone synthesis. CV-11974 (an AT1R antagonist) reduced Ang II-induced aldosterone synthesis, whereas PD-123319 (an AT2R antagonist) had no effect. The concentration of aldosterone peaked earlier than those of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha). After 48 h of incubation (under the influence of synthesized aldosterone), CV-11974 and spironolactone significantly reduced the Ang II-enhanced production of MCP-1 and TNF-alpha, whereas PD-123319 also had no effect. In conclusion, Ang II induces aldosterone synthesis through AT1R and enhances cytokine production through an AT1R-dependent mechanism and, at least partly, through a MR-dependent mechanism in human PBMCs.

DOI： 10.1254/jphs.FP0060801

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