基本情報
研究分野
1学歴
2-
- 2006年
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- 2006年
受賞
2-
2011年
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2006年
論文
14-
Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 25(9) 2023年8月2日AIMS: The relationship between local unipolar voltage (UV) in the pulmonary vein (PV)-ostia and left atrial wall thickness (LAWT) and the utility of these parameters as indices of outcome after atrial fibrillation (AF) ablation remain unclear. METHODS AND RESULTS: Two-hundred seventy-two AF patients who underwent AF ablation were enrolled. Unipolar voltage of PV-ostia was measured using a CARTO system, and LAWT was measured using computed tomography. The primary endpoint was atrial tachyarrhythmia (ATA) recurrence including AF. The ATA recurrence was documented in 74 patients (ATA-Rec group). The UV and LAWT of the bilateral superior PV roof to posterior and around the right-inferior PV in the ATA-Rec group were significantly greater than in patients without ATA recurrence (ATA-Free group) (P < 0.001). The UV had a strong positive correlation with LAWT (R2 = 0.446, P < 0.001). The UV 2.7 mV and the corresponding LAWT 1.6 mm were determined as the cut-off values for ATA recurrence (P < 0.001, respectively). Multisite LA high UV (HUV, ≥4 areas of >2.7 mV) or multisite LA wall thickening (≥5 areas of >1.6 mm), defined as LA hypertrophy (LAH), was related to higher ATA recurrence. Among 92 LAH patients, 66 had HUV (LAH-HUV) and the remaining 26 had low UV (LAH-LUV), characterized by history of non-paroxysmal AF and heart failure, reduced LV ejection fraction, or enlarged LA. In addition, LAH-LUV showed the worst ablation outcome, followed by LAH-HUV and No LAH (log-rank P < 0.001). CONCLUSION: Combining UV and LAWT enables us to stratify recurrence risk and suggest a tailored ablation strategy according to LA tissue properties.
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Journal of arrhythmia 36(5) 874-882 2020年10月BACKGROUND: To investigate the clinical implication of the temporal difference in atrial fibrillation (AF)-onset in acute decompensated heart failure (ADHF) and its impact on post-discharge prognosis. METHODS: 336 new-onset ADHF patients without any history of AF before admission were enrolled (201 males, 63 ± 16 year-old) and classified into two groups based on their history of AF: the Control group (No AF was detected during hospitalization, n = 278), and the In-hos-AF group (AF occurred during hospitalization, n = 58). Post discharge prognosis including rehospitalization due to worsening HF, cardiac death, all-cause death and cerebrovascular event were compared. RESULTS: Kaplan-Meier analysis demonstrated that the incidence of rehospitalization due to HF, cardiac death, all-cause death and cerebrovascular event in the In-hos-AF group was not significantly different from that in the Control group (P > 0.05 respectively). However, when AF recurred in the In-hos-AF group patients (n = 24, 41%) after discharge, the incidence of rehospitalization due to HF and cardiac deaths were higher than those without AF recurrence (P = 0.018 and P = 0.027 respectively). Cox proportional analysis revealed that AF developing after discharge was proven to be an independent risk factor for rehospitalization due to HF (HR 1.845, P = 0.043), cardiac death (HR 3.562, P = 0.013) and all-cause deaths (HR 2.138, P = 0.020). CONCLUSION: Clinical outcomes of new-onset in-hospital AF patients were as good as those without AF history until AF recurrence. However, AF recurrence led to worse prognosis. Therefore, treatment for new-onset in-hospital AF in ADHF patients might be postponed until AF recurrence.
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Circulation. Arrhythmia and electrophysiology 13(10) e008602 2020年10月BACKGROUND: The mechanism of esophageal thermal injury (ETI; esophageal mucosal injury and periesophageal nerve injury leading to gastric hypomotility) remains unknown when using a high-power short-duration (HP-SD) setting. This study sought to evaluate the characteristics of esophageal injuries in atrial fibrillation ablation using a HP-SD setting. METHODS: After exclusion of 5 patients with their esophagus at the right portion of left atrium and 21 patients with additional ablations such as box isolation and low voltage area ablation in left atrium posterior wall, 271 consecutive patients (62±10 years, 56 women) who underwent pulmonary vein isolation by radiofrequency catheter ablation were analyzed. In the 101 patients, a HP-SD setting at 45 to 50 W with an Ablation Index module was used (HP-SD group). In the remaining 170 patients before introduction of the HP-SD setting, a conventional power setting of 20 to 30 W with contact force monitoring was used (conventional group). We performed esophagogastroduodenoscopy after pulmonary vein isolation in all patients and investigated the incidence and characteristics of ETI. RESULTS: Although the incidence of ETI was significantly higher in the HP-SD group compared with the conventional group (37% versus 22%, P=0.011), the prevalence of esophageal lesions did not differ between the groups (7% versus 8%). Multivariate logistic regression analysis revealed that the use of the HP-SD setting (odds ratio, 6.09, P<0.001), and the parameters that suggest anatomic proximity surrounding the esophagus, were independent predictors of ETI. However, the majority of ETI in the HP-SD group was gastric hypomotility, and the thermal injury was limited to the shallow layer of the periesophageal wall using the HP-SD setting. CONCLUSIONS: Although the use of the HP-SD setting was a strong predictor of ETI, it could avoid deeper thermal injuries that reach the esophageal mucosal layer.
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Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc 25(4) e12749 2020年7月BACKGROUND: Cardiac amyloidosis (CA) is characterized by left ventricular hypertrophy (LVH) and autonomic nervous imbalance due to amyloid infiltration. However, autonomic dysfunction is often seen in heart failure (HF) with LVH from other etiologies. We aimed to characterize autonomic dysfunction in CA from other etiologies of LVH. METHODS: Fifty-five HF patients with LVH (35 males, mean age 65 ± 16 years) were enrolled. LVH was defined as left ventricular mass index measured by echocardiography >95 g/m2 in women and 115 g/m2 in men. The etiology was as follows: amyloid light chain (AL)-CA, n = 14; hypertrophic cardiomyopathy, n = 21; and aortic stenosis (AS), n = 20. With the patient in a clinically stable condition, heart rate variability (HRV) and heart rate turbulence (HRT), which reflect autonomic dysfunction, were measured using Holter monitoring and compared among the three groups. RESULTS: Brain natriuretic peptide levels, LVH severity, left ventricular ejection fraction, and tissue Doppler index E/e' did not differ among the three groups. However, severe abnormalities of HRV and HRT were obtained in AL-CA. In the ROC analysis to identify AL-CA in HF with LVH, the best cutoff value for standard deviation of all R-R intervals, standard deviation of the 5-min mean R-R intervals, turbulence onset, and turbulence slope were 68.5 ms (AUC: 0.865), 58.5 ms (AUC: 0.834), 0.25% (AUC: 0.813), and 1.00 ms/RR (AUC 0.736), respectively. CONCLUSION: Autonomic dysfunction is a hallmark of AL-CA, and its noninvasive assessment by Holter monitoring may be a useful tool for differential diagnosis of HF with LVH.
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Journal of Interventional Cardiac Electrophysiology 54(2) 101-108 2019年3月 査読有り
MISC
57-
JOURNAL OF CELLULAR PHYSIOLOGY 220(3) 706-715 2009年9月This study was conducted to examine the role of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in monocyte adhesion-induced redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in endothelial cells (ECs). LOX-1 was blocked by an antibody-neutralizing LOX-1 TS92 or small interfering RNA. In cultured human aortic ECs, monocyte adhesion activated Rac1 and p47(phox), and increased NADPH oxidase activity and reactive oxygen species (ROS) generation within 30 min and NF-kappa B phosphorylation within I h, resulting in redox-sensitive gene expression. Akt and eNOS phosphorylation was induced 15 min after adding monocytes and returned to control level after 30 min, whereas NO production was not altered by monocyte adhesion. Blockade of LOX-1 blunted the monocyte adhesion-triggered redox-sensitive signaling pathway and Akt/eNOS phosphorylation in ECs. Both endothelial intracellular Ca2+ mobilization and Ca2+ influx caused by monocyte attachment were markedly attenuated by pretreatment of ECs with TS92. This suggests that LOX-1 is involved in redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in monocyte adhesion to ECs independent of oxidized low-density lipoprotein (ox-LDL). Furthermore, blockade of Ca2+ inhibited monocyte adhesion-triggered Rac1 and p47(phox) activation and ROS generation in ECs, whereas Ca2+ signaling was suppressed by blockade of NADPH oxidase and ROS generation. Finally, TS92 blocked the monocyte adhesion to ECs stimulated with or without tumor necrosis factor-alpha or ox-LDL. We provide evidence that LOX-1 plays a role in redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in monocyte adhesion to ECs independent of the ox-LDL-LOX-1 axis. J. Cell. Physiol. 220: 706-715, 2009. (C) 2009 Wiley-Liss, Inc.
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CORONARY ARTERY DISEASE 20(6) 400-408 2009年9月The role of endothelial dysfunction in coronary vasospasm is controversial. We hypothesized that reactive oxygen species (ROS) and endothelin-1 (ET-1) are plausible candidates as the mediator of vasospasm is linked to endothelial dysfunction. In a pig model with repetitive endothelial injury in coronary arteries, intracoronary administration of serotonin induced a vasospasm at the endothelial injury site. The level of endothelin-converting enzyme was upregulated at that site where, upon exposure to serotonin, there were also increases in p47(phox), ROS, and ET-1 fluorescence intensities, and myosin light chain phosphorylation and RhoA activation were detected. The nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin, had the effect of extinguishing not only ROS but also the appearance of ET-1. The chronic blockade of endothelin type-A receptor prevented a serotonin-triggered vasospasm along with the inhibition of ROS generation and myosin light chain phosphorylation. Under the coronary artery endothelial dysfunction, ET-1 is essential for an ROS-dependent coronary vasospasm. Our findings suggest that endothelial dysfunction plays a critical role in clinically defined human Prinzmetal angina. Coron Artery Dis 20:400-408 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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JOURNAL OF CELLULAR PHYSIOLOGY 220(3) 706-715 2009年9月This study was conducted to examine the role of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in monocyte adhesion-induced redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in endothelial cells (ECs). LOX-1 was blocked by an antibody-neutralizing LOX-1 TS92 or small interfering RNA. In cultured human aortic ECs, monocyte adhesion activated Rac1 and p47(phox), and increased NADPH oxidase activity and reactive oxygen species (ROS) generation within 30 min and NF-kappa B phosphorylation within I h, resulting in redox-sensitive gene expression. Akt and eNOS phosphorylation was induced 15 min after adding monocytes and returned to control level after 30 min, whereas NO production was not altered by monocyte adhesion. Blockade of LOX-1 blunted the monocyte adhesion-triggered redox-sensitive signaling pathway and Akt/eNOS phosphorylation in ECs. Both endothelial intracellular Ca2+ mobilization and Ca2+ influx caused by monocyte attachment were markedly attenuated by pretreatment of ECs with TS92. This suggests that LOX-1 is involved in redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in monocyte adhesion to ECs independent of oxidized low-density lipoprotein (ox-LDL). Furthermore, blockade of Ca2+ inhibited monocyte adhesion-triggered Rac1 and p47(phox) activation and ROS generation in ECs, whereas Ca2+ signaling was suppressed by blockade of NADPH oxidase and ROS generation. Finally, TS92 blocked the monocyte adhesion to ECs stimulated with or without tumor necrosis factor-alpha or ox-LDL. We provide evidence that LOX-1 plays a role in redox-sensitive, Akt/eNOS and Ca2+ signaling pathways in monocyte adhesion to ECs independent of the ox-LDL-LOX-1 axis. J. Cell. Physiol. 220: 706-715, 2009. (C) 2009 Wiley-Liss, Inc.
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CORONARY ARTERY DISEASE 20(6) 400-408 2009年9月The role of endothelial dysfunction in coronary vasospasm is controversial. We hypothesized that reactive oxygen species (ROS) and endothelin-1 (ET-1) are plausible candidates as the mediator of vasospasm is linked to endothelial dysfunction. In a pig model with repetitive endothelial injury in coronary arteries, intracoronary administration of serotonin induced a vasospasm at the endothelial injury site. The level of endothelin-converting enzyme was upregulated at that site where, upon exposure to serotonin, there were also increases in p47(phox), ROS, and ET-1 fluorescence intensities, and myosin light chain phosphorylation and RhoA activation were detected. The nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin, had the effect of extinguishing not only ROS but also the appearance of ET-1. The chronic blockade of endothelin type-A receptor prevented a serotonin-triggered vasospasm along with the inhibition of ROS generation and myosin light chain phosphorylation. Under the coronary artery endothelial dysfunction, ET-1 is essential for an ROS-dependent coronary vasospasm. Our findings suggest that endothelial dysfunction plays a critical role in clinically defined human Prinzmetal angina. Coron Artery Dis 20:400-408 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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ATHEROSCLEROSIS 193(1) 44-54 2007年7月We investigated the role of RhoA activation and its mechanism in plasminogen activator inhibitor-1 (PAI-1) gene expression induced in endothelial cells by monocyte adhesion. Isolated human peripheral blood monocytes were added to cultured human coronary endothelial cells. Monocyte adhesion to endothelial cells increased PAI- 1 expression at the transcriptional level and activated RhoA which was accompanied by an increase in the activity of geranylgeranyl transferase I (GGTase 1), an enzyme responsible for geranylgeranylation, and actin stress fiber formation. Inhibition of RhoA by C3 exoenzyme or by adenovirus-mediated expression of N19RhoA, as well as by pravastatin, prevented the upregulation of PAI-1 induced by monocyte adhesion. GGTI-286, an inhibitor of GGTase 1, prevented the monocyte-induced RhoA activation and PAI- 1 expression in endothelial cells. Monocyte attachment induced an increase in intracellular Ca2+ concentration ([Ca (2+)],) in endothelial cells and Ca2+ chelation prevented the increased promoter activity and expression of PAI- 1 induced by monocyte adhesion. 0 exoenzyme and GGTI-286 also suppressed endothelial intracellular Ca2+ mobilization and Ca2+ entry induced by monocytes. The present study shows that GGTase I plays a role in the RhoA activation in endothelial cells induced by monocyte adhesion and that GGTase I-mediated Ca2+ signaling may contribute to RhoA-dependent PAI- 1 gene expression. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
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ATHEROSCLEROSIS 193(1) 44-54 2007年7月We investigated the role of RhoA activation and its mechanism in plasminogen activator inhibitor-1 (PAI-1) gene expression induced in endothelial cells by monocyte adhesion. Isolated human peripheral blood monocytes were added to cultured human coronary endothelial cells. Monocyte adhesion to endothelial cells increased PAI- 1 expression at the transcriptional level and activated RhoA which was accompanied by an increase in the activity of geranylgeranyl transferase I (GGTase 1), an enzyme responsible for geranylgeranylation, and actin stress fiber formation. Inhibition of RhoA by C3 exoenzyme or by adenovirus-mediated expression of N19RhoA, as well as by pravastatin, prevented the upregulation of PAI-1 induced by monocyte adhesion. GGTI-286, an inhibitor of GGTase 1, prevented the monocyte-induced RhoA activation and PAI- 1 expression in endothelial cells. Monocyte attachment induced an increase in intracellular Ca2+ concentration ([Ca (2+)],) in endothelial cells and Ca2+ chelation prevented the increased promoter activity and expression of PAI- 1 induced by monocyte adhesion. 0 exoenzyme and GGTI-286 also suppressed endothelial intracellular Ca2+ mobilization and Ca2+ entry induced by monocytes. The present study shows that GGTase I plays a role in the RhoA activation in endothelial cells induced by monocyte adhesion and that GGTase I-mediated Ca2+ signaling may contribute to RhoA-dependent PAI- 1 gene expression. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
講演・口頭発表等
150Works(作品等)
1共同研究・競争的資金等の研究課題
1-
日本学術振興会 科学研究費助成事業 2012年4月 - 2013年3月