FullText URL J_Cardiology_70_1_23.pdf Fig.pdf
Author Tachibana, Motomi| Nishii, Nobuhiro| Morimoto, Yoshimasa| Kawada, Satoshi| Miyoshi, Akihito| Sugiyama, Hiroyasu| Nakagawa, Koji| Watanabe, Atsuyuki| Nakamura, Kazufumi| Morita, Hiroshi| Ito, Hiroshi|
Keywords Implantable cardioverter-defibrillator Sudden cardiac death Ventricular arrhythmia
Note This is an Accepted Manuscript of an article published by Elsevier|
Published Date 2017-07
Publication Title Journal of Cardiology
Volume volume70
Issue issue1
Publisher Japanese College of Cardiology
Start Page 23
End Page 28
ISSN 0914-5087
NCID AN10070473
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
File Version author
PubMed ID 28034575
DOI 10.1016/j.jjcc.2016.11.014
Web of Science KeyUT 000408601100004
Related Url isVersionOf https://doi.org/10.1016/j.jjcc.2016.11.014
Author Morita, Hiroshi|
Published Date 2011-08
Publication Title Heart Rhythm
Volume volume8
Issue issue8
Content Type Journal Article
JaLCDOI 10.18926/AMO/32121
FullText URL fulltext.pdf
Author Hisamatsu, Kenichi| Kusano, Kengo Fukushima| Morita, Hiroshi| Takenaka, Shiho| Nagase, Satoshi| Nakamura, Kazufumi| Emori, Tetsuro| Matsubara, Hiromi| Ohe, Tohru|
Abstract <p>We attempted to determine the usefulness of body surface mapping (BSM) for differentiating patients with Brugada syndrome (BS) from patients with asymptomatic Brugada syndrome (ABS). Electrocardiograms (ECG) and BSM were recorded in 7 patients with BS and 35 patients with ABS. Following the administration of Ic antiarrhythmic drugs, BSM was recorded in 5 patients with BS and 16 patients with ABS. The maximum amplitudes at J0, J20, J40 and J60 were compared between the 2 groups, as were 3-dimensional maps. The maximum amplitudes at J0, J20 and J60 under control conditions were larger in patients with BS than in patients with ABS (P < 0.05). A three-dimensional map of the ST segments under control conditions in patients with BS showed a higher peak of ST elevation in the median precordium compared to that for patients with ABS. Increases in ST elevation at J20, J40 and J60 following drug administration were greater in patients with BS than in patients with ABS (P < 0.05). Evaluation of the change in amplitude of the ST segment at E5 caused by Ic drug administration was also useful for differentiating between the 2 groups. In conclusion, BSM was useful for differentiating patients with BS from those with ABS.</p>
Keywords body surface map Brugada syndrome asymptomatic Brugada syndrome Ic antiarrhythmic drugs
Amo Type Article
Published Date 2004-02
Publication Title Acta Medica Okayama
Volume volume58
Issue issue1
Publisher Okayama University Medical School
Start Page 29
End Page 35
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 15157009
Web of Sience KeyUT 000189271100005
JaLCDOI 10.18926/AMO/31636
FullText URL fulltext.pdf
Author Hong, Kui| Kusano, Kengo Fukushima| Morita, Hiroshi| Fujimoto, Yoshihisa| Wang, Xian| Yamanari, Hiroshi| Ohe, Tohru|
Abstract <p>Ischemic preconditioning has been acknowledged as a powerful method of decreasing ischemic injury. However, the antiarrhythmic mechanism of ischemic preconditioning during ischemia is unclear. We studied the effects of ischemic preconditioning on arrhythmias and cardiac electrophysiology during ischemia in Langendorff rat hearts (n = 44). In the non-preconditioned group (PC(-); n = 24), the hearts underwent 5-min zero-flow global ischemia without any prior ischemic preconditioning. In the preconditioned group (PC(+); n = 20), the hearts were preconditioned by three cycles of 3-min zero-flow global ischemia and 5-min reperfusion before undergoing 5-min global ischemia. Ischemic preconditioning reduced the incidence of ischemia-induced arrhythmias (PC(-); 38.9%, PC(+): 8.3%, p < 0.05), shortened monophasic action potential duration (MAPD, P < 0.05), attenuated conduction delay (conduction time; PC(-): 234.2%, PC(+): 173.4%, P < 0.05) and increased the ventricular fibrillation threshold. Although the shortening of MAPD in PC(-) hearts was not influenced by the presence or absence of arrhythmias, conduction time prolongation at 3-min was more obvious in PC(-) hearts with arrhythmia than in PC(-) hearts without arrhythmia (PC(-) with arrhythmia: 220.2%, PC(-) without arrhythmia: 190.7%, P < 0.05). We concluded that ischemic preconditioning could protect the rat hearts from ischemia-induced arrhythmias and postulated that attenuation of conduction delay during ischemia might be an important factor in the antiarrhythmic action of ischemic preconditioning.</p>
Keywords preconditioning ischemia arrhythmia
Amo Type Article
Published Date 1999-10
Publication Title Acta Medica Okayama
Volume volume53
Issue issue5
Publisher Okayama University Medical School
Start Page 233
End Page 238
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 10561732
Web of Science KeyUT 000083427100005