Tetsuji Shinohara

Oita University, Ōita, Ōita, Japan

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Publications (79)297.48 Total impact

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    ABSTRACT: Cardiac resynchronization therapy (CRT) has been established as a treatment for patients with chronic heart failure (HF). We tested the hypothesis that assessment of peripheral endothelial function are associated with the long-term outcome of CRT and its linkage to coronary flow reserve (CFR) was also investigated. From 2010, a total of 34 consecutive patients implanted with CRT for the treatment of advanced HF were evaluated at baseline (Immediately before CRT) and 6-8 months after CRT. Endothelial function was evaluated by measurement of reactive hyperemia peripheral arterial tonometry (RH-PAT). In 24 out of 34 patients, CFR was determined by transthoracic echocardiography. Based on the ROC curves, depressed RH-PAT index (RHI) was defined as ≤1.5. Accurate follow-up information during the mean of 343±120 days was obtained in 20 preserved RHI group (mean age 66±1.8 years) and 14 depressed RHI group (71±2.2 years). Kaplan-Meier survival analysis demonstrated that depressed RHI group had higher prevalence of new hospitalization due to HF progression (log-rank 5.40). Cox proportional hazards regression analysis revealed that the baseline log BNP (hazard ratio 5.95) and the baseline RHI value (hazard ratio 0.066) were independently associated with the incidence of new hospitalization due to HF progression. The baseline RHI values were positively correlated with the 6-8 month change of CFR (R = 0.434, p = 0.0343). Our results suggest that the baseline peripheral endothelial function could predict the long-term outcome of CRT. The results also suggest that improvement of coronary microcirculation might be associated with the better baseline endothelial function. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Jul 2015 · Pacing and Clinical Electrophysiology
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    ABSTRACT: The spleen is important for cardiac remodeling induced by myocardial infarction. However, the role of the spleen in inflammatory atrial fibrosis induced by pressure overload is unknown. This study investigated whether splenectomy (SPX) attenuates or exacerbates pressure overload-induced atrial inflammatory fibrosis and vulnerability to atrial fibrillation (AF) in rats. Male Sprague Dawley rats (6 weeks old) were divided into Sham+Sham, Sham+SPX, abdominal aortic constriction (AAC)+Sham, and AAC+SPX groups, and were evaluated for inflammation, fibrosis, and AF on days 2, 4, 14, and 28. On day 4, an AAC-induced rise in IL-10 level was observed in the spleen, serum, and left atrium (LA), with SPX showing inhibitory effects in the latter two instances. In addition, AAC-induced M2 macrophage recruitment into the LA was decreased by SPX, as determined by immunofluorescence labeling (P<0.05). On day 28, AAC-induced heterogeneous interstitial fibrosis of the LA was enhanced by SPX (P<0.05). Electrophysiological recordings revealed that the duration of AF and prolongation of interatrial conduction time induced by AAC were increased by SPX (P<0.01 and P<0.05, respectively). Furthermore, in the AAC+SPX group, the number of macrophages infiltrating into the LA on day 2 was marginal, but increased on day 28 relative to the AAC+Sham group. IL-10 administration attenuated the AAC-induced atrial remodeling that was aggravated by SPX. These results suggest that SPX exacerbates AAC-induced inflammatory atrial fibrosis and increases vulnerability to AF after 4 weeks, likely due to the depletion of spleen-derived IL-10. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Jul 2015 · Heart rhythm: the official journal of the Heart Rhythm Society
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    Preview · Article · Jan 2015

  • No preview · Article · Oct 2014 · Journal of Cardiac Failure
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    ABSTRACT: Background Resting plasma norepinephrine (NE) level was reportedly related to high mortality in patients with heart failure. The current study investigated whether resting NE could predict long-term major adverse cerebral and cardiovascular events (MACCEs) in Japanese type 2 diabetic patients without heart disease. Methods and subjects We evaluated resting NE in 95 patients with type 2 diabetes who did not have severe complications. Based on the ROC curves, high NE was defined as ≥333 pg/ml. Accurate follow-up information during a mean of 3.6 ± 1.9 years was obtained in 27 high NE patients (13 female, mean age 64 ± 12 years) and 68 low NE patients (29 female, 60 ± 12 years). Essential results The Kaplan–Meier curves revealed that MACCE-free ratio was significantly lower in the high NE patients than in the low NE patients (log-rank 10.3, p = 0.0013). Cox proportional hazards regression analysis revealed that female gender (hazard ratio 7.75), low baroreflex sensitivity (hazard ratio 6.66), and high NE (hazard ratio 5.40) were independently associated with the incidence of MACCE. Principal conclusions Our results suggest that resting NE is comparably useful to identify the high-risk patients for MACCE to baroreflex sensitivity in type 2 diabetic patients. The results also suggest that pathogenic sympathetic activation leading to MACCE may be identified by the assessment of resting NE, more easily and less expensively compared to cardiac iodine 123 metaiodobenzylguanidine scintigraphy in this population.
    No preview · Article · Sep 2014 · Journal of Cardiology
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    ABSTRACT: Background: Vasovagal syncope (VVS) is the result of an autonomic reflex that has a final effect of reducing sympathetic drive and increasing vagal activity. However, whether syncopal symptoms are associated with pathological cardiac autonomic modulation is not fully known. We tested the hypothesis that cardiac autonomic function is impaired in patients with VVS. Methods: Eighty-four consecutive patients (59 males; 48.8 ± 20.9 years) with recurrent unexplained syncope were enrolled. The head-up tilt test (HUTT) was positive in 38 patients and negative in 46 patients. Cardiac autonomic function was assessed by baroreflex sensitivity (BRS), heart rate variability, plasma concentrations of norepinephrine, and (123) I-metaiodobenzylguanidine (MIBG) scintigraphy. Results: BRS indices were significantly lower in the HUTT-positive group than in the HUTT-negative group (6.1 ± 5.5 mm Hg/s vs 9.8 ± 7.6 mm Hg/s, P = 0.02). With regard to cardiac (123) I-MIBG scintigraphy, the mean heart-to-mediastinum ratio at the delayed phase tended to be lower in HUTT-positive than in HUTT-negative individuals, but this difference was not significant (2.75 ± 0.55 vs 3.02 ± 0.49, P = 0.08).The percent washout rate of (123) I-MIBG was significantly higher in the positive group compared with the negative group (40.7 ± 13.1% vs 31.5 ± 13.3%, P = 0.02). Multivariate logistic analysis revealed that the appearance of HUTT-induced VVS was predicted independently by a high percent washout rate of (123) I-MIBG (odds ratio, 0.954; 95% confidence interval, 0.903-0.998; P = 0.048). Conclusions: Our results suggest that pathological autonomic cardiac modulation may play a role in the appearance of syncope in VVS patients.
    No preview · Article · Aug 2014 · Pacing and Clinical Electrophysiology
  • Hidekazu Kondo · Tetsuji Shinohara · Naohiko Takahashi
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    ABSTRACT: This case report describes a 19-year-old man with early repolarization (ER) in the inferolateral leads and a normal QT interval who survived a cardiac arrest that was likely related to polymorphic ventricular tachycardia (VT). Electrocardiograms (ECGs) also showed unifocal premature ventricular beats (PVBs) with a relatively narrow QRS duration. A Holter ECG documented occasional short-coupled PVBs following non-sustained VTs. Pharmacological stress testing was also performed to assess the effects of anti-arrhythmic drugs on ER (the J wave) and PVBs. We performed successful radiofrequency catheter ablation to prevent the recurrence of ventricular fibrillation after cardioverter-defibrillator implantation.
    No preview · Article · Aug 2014 · Journal of Arrhythmia
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    ABSTRACT: Brugada syndrome and idiopathic ventricular fibrillation (VF) associated with infero-lateral early repolarization patterns are termed "J-wave syndromes". In such patients, an implantable cardioverter-defibrillator (ICD) is first-line therapy for prevention of sudden cardiac death. However, frequent ICD shocks due to recurrent VF remain serious problems. We wished to ascertain if combination therapy of cilostazol and bepridil could suppress recurrent VF. We enrolled 7 patients with J-wave syndromes who experienced ICD shocks due to recurrent VF after ICD implantation. At first, cilostazol was instituted. In all subjects, palpitations due to sinus tachycardia caused by cilostazol were symptomatic. Addition of bepridil attenuated cilostazol-induced palpitations and maintained the suppressive effect of cilostazol against VF (87±12 to 66±7 bpm, P<0.01). Six patients remained free of VF. Three patients underwent replacement of the ICD generator 4-5 years after ICD implantation. Cilostazol was discontinued 2 days before replacement because of its anti-platelet effects. In all 3 patients, temporary discontinuation of cilostazol led to the reappearance of J waves, culminating in VF and an appropriate ICD shock in one of them. J waves disappeared upon re-institution of cilostazol. These data suggest that combination therapy of cilostazol and bepridil may be effective and safe in suppressing VF recurrence in some cases of J-wave syndromes.
    No preview · Article · May 2014 · Heart rhythm: the official journal of the Heart Rhythm Society
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    ABSTRACT: Recent studies showed that J-waves are associated with vulnerability to ventricular fibrillation. Recently we reported the association between false tendons (FTs) and J-waves in a retrospective study. We prospectively studied 50 young healthy men (mean age 24.6±2.7years). FTs were detected echocardiographically and classified based on their points of attachment as type 1 (longitudinal type), type 2 (diagonal type), and type 3 (transverse type). J-waves were defined as terminal QRS notching or slurring with ≥0.1mV. The filtered QRS duration (fQRSd), RMS40, and LAS40 were measured on signal-averaged ECGs. FTs were detected in 37 of the 50 subjects (74%). The incidence of J-waves was significantly higher in subjects with type 1 or type 2 FTs than those with no- or type 3 FTs (61% vs. 26%, p<0.05). The leads with J-waves were closely associated with the location of the FT. While no late potential was recorded in any study subjects, fQRSd and LAS40 were significantly longer in subjects with type 1 or type 2 FTs (p<0.05). Univariate and multivariate logistic regression analysis revealed that only the existence of FTs (type 1 or 2) was an independent predictor of the presence of J-waves. Our results suggest that FTs were related to the genesis of J-waves with conduction delay.
    No preview · Article · Jan 2014 · International journal of cardiology
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    ABSTRACT: Brugada syndrome (BrS) is an inherited disease characterized by right precordial ST-segment elevation on electrocardiograms (ECG) that predisposes patients to sudden cardiac death as a result of polymorphic ventricular tachyarrhythmia or ventricular fibrillation (VF). In BrS patients, except for SCN5A, mutations in other responsible genes are poorly elucidated. We identified four KCNH2 mutations, T152I, R164C, W927G, and R1135H, in 236 consecutive probands with BrS or Brugada-like ECG. Three of these mutation carriers showed QTc intervals shorter than 360 ms(1/2) and one experienced VF. We performed patch-clamp analyses on IKr reconstituted with the KCNH2 mutations in Chinese hamster ovary (CHO) cells and compared the phenotypes of the patients with different genotypes. Three mutations, R164C, W927G, and R1135H, increased IKr densities. Three mutations, T152I, R164C, and W927G, caused a negative shift in voltage-dependent activation curves. Only the R1135H mutant channel prolonged the deactivation time constants. We also identified 20 SCN5A and five CACNA1C mutation carriers in our cohort. Comparison of probands' phenotypes with three different genotypes revealed that KCNH2 mutation carriers showed shorter QTc intervals and SCN5A mutation carriers had longer QRS durations. All KCNH2 mutations that we identified in probands with BrS exerted gain-of-function effects on IKr channels, which may partially explain the ECG findings in our patients. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2014 · Journal of Cardiovascular Electrophysiology
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    Preview · Article · Jan 2014
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    Naohiko Takahashi · Tetsuji Shinohara · Mikiko Nakagawa · Masahide Hara · Tetsunori Saikawa

    Preview · Article · Jan 2014
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    ABSTRACT: Background Brugada syndrome and idiopathic ventricular fibrillation (VF) associated with infero-lateral early repolarization patterns are termed “J-wave syndromes”. In such patients, an implantable cardioverter-defibrillator (ICD) is first-line therapy for prevention of sudden cardiac death. However, frequent ICD shocks due to recurrent VF remain serious problems. Objective We wished to ascertain if combination therapy of cilostazol and bepridil could suppress recurrent VF. Methods We enrolled 7 patients with J-wave syndromes who experienced ICD shocks due to recurrent VF after ICD implantation. At first, cilostazol was instituted. In all subjects, palpitations due to sinus tachycardia caused by cilostazol were symptomatic. Addition of bepridil attenuated cilostazol-induced palpitations and maintained the suppressive effect of cilostazol against VF (87±12 to 66±7 bpm, P<0.01). Results Six patients remained free of VF. Three patients underwent replacement of the ICD generator 4–5 years after ICD implantation. Cilostazol was discontinued 2 days before replacement because of its anti-platelet effects. In all 3 patients, temporary discontinuation of cilostazol led to the reappearance of J waves, culminating in VF and an appropriate ICD shock in one of them. J waves disappeared upon re-institution of cilostazol. Conclusions These data suggest that combination therapy of cilostazol and bepridil may be effective and safe in suppressing VF recurrence in some cases of J-wave syndromes.
    No preview · Article · Jan 2014
  • Tetsuji Shinohara · Naohiko Takahashi

    No preview · Article · Oct 2013 · Circulation Journal
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    ABSTRACT: Purpose: Glucose instability in diabetes mellitus has been attracting much attention due to increasing cardiovascular complications more than stable hyperglycemia. Diabetes is one of the major risk factors of atrial fibrillation (AF). Recent studies revealed that atrial fibrosis is common feature of structural remodeling in clinical AF. In the present study, we investigated whether glucose fluctuations aggravate cardiac fibrosis and increase the occurrence of AF in diabetic rats. Methods: Adult male Sprague-Dawley rats were divided into 3 groups: the control group (CNT), diabetes group (DM), and DM with glucose fluctuations group (DF). Diabetes was induced by single intravenous injection of streptozotocin (60 mg/kg). Glucose fluctuations were induced by 24h-fasting and additional insulin injection (0.5 IU/kg) three times a week for consecutive 3 weeks. After glucose fluctuations period, to test the inducibility of AF, we applied programmed electrical stimulation under Langendorff perfusion. Left atrial and ventricular tissues were collected differently to evaluate interstitial fibrosis by Masson trichrome staining. The protein expression relating to profibrotic signals were also estimated by Western blot analysis. Results: Cardiac fibrosis evaluated in atrium and ventricle by histological examination and the expressions of collagen type I and alpha-smooth muscle actin were accelerated in DM more than CNT, which was more pronounced in DF. Consistently, left ventricular diastolic function was more deteriorated in DF compared with DM and CNT. The inducibility of AF by double extrastimuli was significantly increased in DM compared to CNT, which was more exaggerated in DF. To explore the mechanism of cardiac fibrosis, we investigated the level of reactive oxygen species (ROS) and apoptosis. The expression of malondialdehyde, an indicator of ROS level, was significantly up-regulated in DF more than CNT and DF concomitant with increased expression of thioredoxin interacting protein (Txnip). Further, expression of caspase-3 and the number of TUNEL-positive cells were significantly increased in DF group. These results indicate that up-regulation of Txnip and resulting oxidative stress may facilitate apoptosis and cardiac fibrosis. Conclusions: Glucose fluctuations increased the inducibility of AF. Atrial fibrosis and left ventricular diastolic dysfunction are possible mechanisms of increased susceptibility to AF.
    Preview · Article · Aug 2013 · European Heart Journal
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    ABSTRACT: The membrane voltage clock and calcium (Ca(2+)) clock jointly regulate sinoatrial node (SAN) automaticity. VK-II-36 is a novel carvedilol analog that suppresses sarcoplasmic reticulum (SR) Ca(2+) release but does not block the β-receptor. The effect of VK-II-36 on SAN function remains unclear. The purpose of this study was to evaluate whether VK-II-36 can influence SAN automaticity by inhibiting the Ca(2+) clock. We simultaneously mapped intracellular Ca(2+) and membrane potential in 24 isolated canine right atriums using previously described criteria of the timing of late diastolic intracellular Ca elevation (LDCAE) relative to the action potential upstroke to detect the Ca(2+) clock. Pharmacological interventions with isoproterenol (ISO), ryanodine, caffeine, and VK-II-36 were performed after baseline recordings. VK-II-36 caused sinus rate downregulation and reduced LDCAE in the pacemaking site under basal conditions (P < 0.01). ISO induced an upward shift of the pacemaking site in SAN and augmented LDCAE in the pacemaking site. ISO also significantly and dose-dependently increased the sinus rate. The treatment of VK-II-36 (30 μmol/l) abolished both the ISO-induced shift of the pacemaking site and augmentation of LDCAE (P < 0.01), and it suppressed the ISO-induced increase in sinus rate (P = 0.02). Our results suggest that the sinus rate may be partly controlled by the Ca(2+) clock via SR Ca(2+) release during β-adrenergic stimulation.
    No preview · Article · Jul 2013 · Heart and Vessels
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    ABSTRACT: Background: We examined the hypothesis that leptin signaling contributes to the atrial fibrosis and atrial fibrillation (AF) evoked by angiotensin II (AngII). Methods and results: Eight-week-old male CL57/B6 (CNT) and leptin-deficient ob/ob mice (Ob) were subcutaneously infused with AngII (2.0 mg/kg per day). Two weeks later, transesophageal burst pacing and an electrophysiological study using isolated perfused hearts were performed. Left-atrial tissues were collected to determine interstitial fibrosis by Masson trichrome staining, and the expressions of mRNAs related to inflammatory profibrotic signals were assessed. Left-atrial fibroblasts were isolated from adult Sprague-Dawley and Zucker rats. The effects of leptin (100 ng/mL) or AngII (100 nmol/L) treatment were evaluated. In CNT-AngII mice, leptin expression in the left atrium was upregulated (P<0.01). Transesophageal burst pacing induced atrial fibrillation in 88% (7/8) of CNT-AngII mice, but not in Ob-AngII mice (0/8; P<0.01). In isolated perfused hearts, atrial fibrillation was induced only in CNT-AngII mice (4/6; 67%). Interatrial conduction time was prolonged in CNT-AngII mice (P<0.01), but not in Ob-AngII mice. The upregulation of collagen 1, collagen 3, transforming growth factor-β1, α-smooth muscle actin, MCP-1, F4/80, and RANTES mRNA, which was seen in CNT-AngII mice, was attenuated in Ob-AngII mice. In cultured Sprague-Dawley rat atrial fibroblasts, AngII treatment increased leptin expression (P<0.01). Addition of leptin increased transforming growth factor-β1, α-smooth muscle actin, MCP-1, and RANTES expressions in Sprague-Dawley rat atrial fibroblasts, but not in Zucker rat atrial fibroblasts. Conclusions: Our results demonstrate for the first time that leptin signaling is essential for the development of atrial fibrosis and atrial fibrillation evoked by AngII.
    Preview · Article · Feb 2013 · Circulation Arrhythmia and Electrophysiology
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    ABSTRACT: Background: Although J-waves are seen in both patients with idiopathic ventricular fibrillation (IVF) and the general population, their genesis remains unclear. To assess the relationship between J-waves and autonomic tone we investigated the circadian variation of J-waves in individuals with and without IVF. Methods and results: In study 1, we obtained resting 12-lead ECG and Holter ECG recordings in 258 individuals undergoing screening for heart disease. In 60 of these subjects (23.3%), we detected J-waves on Holter ECGs; 40 of them (66.7%) had shown no J-waves on 12-lead ECGs. In study 2, we measured the J-wave amplitude, heart rate (HR), and HR variability [high frequency (HF) and the ratio of low- to high-frequency (LF/HF)] on Holter ECGs recorded in 5 patients with IVF and 20 control subjects who had manifested J-waves. The J-wave amplitude increased at night and decreased during the day in both groups; it was significantly higher in the IVF patients (P<0.0001). In both groups, the J-wave amplitude showed a significant negative correlation with HR and LF/HF and a significant positive correlation with HF. The slope of the J/HR and J/(LF/HF) relationship was significantly steeper in the IVF patients. Conclusions: The J-wave amplitude was more significantly influenced by the autonomic balance in IVF patients than in the controls. Autonomic J-wave modulation may yield important information on the genesis of J-waves.
    No preview · Article · Oct 2012 · Circulation Journal
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    ABSTRACT: Background: We previously reported that baroreflex sensitivity (BRS) or cardiac iodine 123 metaiodobenzylguanidine ((123)I-MIBG) scintigraphic findings can predict cardiovascular prognosis in type 2 diabetic patients. We therefore tested the hypothesis that the combination of BRS and (123)I-MIBG scintigraphic findings could strengthen the predictive power for major adverse cerebral and cardiovascular events (MACCE). Methods and results: From 1998, we have evaluated both BRS and (123)I-MIBG scintigraphy in 165 type 2 diabetic patients (77 females, 88 males, mean age 59 ± 12 years). Based on the ROC curves, depressed BRS was defined as <5.63 mmHg/s, and enhanced washout ratio (WR) was defined as ≥ 41.4%. Each patient was divided into 3 groups based on the "BRS-MIBG combination score" as follows: 0, patients having both preserved BRS and preserved WR; 1, patients having either depressed BRS or enhanced WR; 2, patients having both depressed BRS and enhanced WR. During the mean of 4.7 ± 2.7 years of follow-up, 19 patients developed MACCE. The MACCE-free ratio was significantly higher in the lower BRS-MIBG combination score group (log-rank 16.41, P=0.0003). Cox proportional hazards regression analysis revealed that BRS-MIBG combination score was independently associated with the incidence of MACCE (hazard ratio 4.06, P=0.0237). Conclusions: Our results suggest that combined assessment of the BRS and (123)I-MIBG scintigraphic findings is more useful for identifying the type 2 diabetic patients at high risk for MACCE.
    No preview · Article · Sep 2012 · Circulation Journal
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    ABSTRACT: BACKGROUND: An animal model of atrial fibrillation (AF) associated with chronic kidney disease (CKD) has not been available. OBJECTIVE: The purpose of this study was to test the validity of 5/6 nephrectomy (5.6Nx) as an appropriate model of AF associated with CKD and to investigate the role of oxidative stress. METHODS: Male Sprague-Dawley rats were subjected to 5.6Nx. A novel derivative of lipoic acid, sodium zinc dihydrolipoylhistidinate (DHLHZn), was subcutaneously infused. Four weeks later, hearts were isolated. RESULTS: We observed 5 main findings. (1) 5.6Nx induced renal dysfunction with elevation of systolic blood pressure and impaired glucose tolerance. (2) In the left atrium (LA), expressions of α-smooth muscle action and collagen type I, the compositional proteins of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and malondialdehyde were increased by 5.6Nx, which was reversed by DHLHZn treatment. (3) In the LA, the tissue content of angiotensin II was elevated by 5.6Nx, which was also reversed by DHLHZn. (4) Masson trichrome staining revealed that heterogeneous LA interstitial fibrosis was induced by 5.6Nx, which was attenuated by DHLHZn. (5) In isolated perfused heart experiments, 5.6Nx caused slowing of interatrial conduction. In the hearts of rats of the 5.6Nxgroup, right atrial extrastimuli invariably induced AF (8/8 [100%]), which were suppressed by DHLHZn (3/8 [38%], P <.05). CONCLUSION: We successfully established an appropriate model of AF associated with CKD in rats. Because the amount of NADPH oxidase was increased and the potent antioxidant agent DHLHZn was effective, oxidative stress may be involved in the pathogenesis of LA fibrosis and enhanced AF vulnerability in our model.
    No preview · Article · Aug 2012 · Heart rhythm: the official journal of the Heart Rhythm Society

Publication Stats

940 Citations
297.48 Total Impact Points

Institutions

  • 2003-2015
    • Oita University
      • • Faculty of Medicine
      • • Department of Laboratory Medicine
      Ōita, Ōita, Japan
  • 2009-2012
    • Indiana University-Purdue University School of Medicine
      • Department of Medicine
      Indianapolis, Indiana, United States
  • 2010-2011
    • Indiana University-Purdue University Indianapolis
      Indianapolis, Indiana, United States
    • Beth Israel Deaconess Medical Center
      • Department of Medicine
      Boston, Massachusetts, United States