担当区分：最終著者   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/j.hrthm.2022.05.018

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Modification of the low-voltage zone in the left atrium (LA-LVZ) in addition to pulmonary vein isolation (PVI) has not shown sufficient improvement in arrhythmia-free survival in patients with persistent atrial fibrillation (PerAF). Further, the effect of electrical posterior wall isolation (PWI) is controversial. We investigated the impact of existence of LA-LVZ on the outcome of patients undergoing additional PWI for PerAF. METHODS: A total of 347 patients with PerAF who underwent primary catheter ablation with LA-LVZ based strategy were retrospectively analyzed. Voltage mapping in the left atrium (LA) was performed during sinus rhythm. Additional LVZ ablation was performed in patients with LA-LVZ. The operators decided whether additional PWIs were to be performed. RESULTS: Of 347 patients, 108 had LA-LVZ. In the LVZ group, patients with additional PWI (N = 70) had higher rates of freedom from tachyarrhythmia recurrence than those without (77.1% vs. 42.1%, p < 0.001). Furthermore, even when patients were limited to those with LA-LVZ in areas other than the posterior wall (N = 85), PWI had higher success rates (80.9% vs. 42.1%, p < 0.001). In contrast, in patients without LVZ (N = 239), there was no significant difference in the rate of successful outcome between those with and without PWI (81.3% vs. 88.1%, p = 0.112). On the other hand, the patients with PWI had greater atrial tachycardia (AT) recurrence rate than those without PWI (10.0% vs. 2.5%, p = 0.003). CONCLUSIONS: PWI, in addition to PVI and LVZ modification, may improve single procedural outcomes in patients with PerAF who have LVZ, regardless of the distribution in the LA. A combination of voltage-guided ablation and PWI may be a simple, tailored, and effective ablation strategy.

DOI： 10.1007/s00380-022-02069-0

PubMed

researchmap

掲載種別：研究論文（学術雑誌）   出版者・発行元：Japanese Circulation Society  

DOI： 10.1253/circrep.cr-21-0154

researchmap

記述言語：英語  

Fasciculo-ventricular and nodo-ventricular pathways (FVP and NVP) are rare preexcitation variants. Normally, NVP is electrophysiologically different from FVP. We describe a unique type of NVP emerging from the distal part of the slow pathway, designated as "distal type" NVP. The distal type NVP resembled FVP but was proven by unexpected elimination of the NVP during the slow pathway ablation. Also, NVP was distinguishable from FVP by a careful comparison of the HV intervals during conduction over the fast and slow pathways. Demonstration of this novel type NVP provides insights into how the insertion site of NVP affects its electrophysiologic behaviors.

DOI： 10.1111/pace.14468

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：(一社)日本循環器学会  

BACKGROUND: Development of heart failure is associated with fluid balance, including that of extracellular water (ECW) and intracellular water (ICW). This study determined whether sodium-glucose cotransporter 2 (SGLT2) inhibitors affect fluid balance and improve heart failure in patients after acute myocardial infarction (AMI). METHODS: EMBODY was a prospective, randomized, double-blinded, placebo-controlled trial of Japanese patients with AMI and type 2 diabetes. Overall, 55 patients who underwent bioelectrical impedance analysis (BIA) were randomized to receive once daily 10 mg empagliflozin or placebo 2 weeks after AMI onset. We investigated the time course of body fluid balance measured using the BIA device, "InBody®." Primary endpoints were changes in body fluid balance from weeks 0 to 24. RESULTS: Changes between baseline and week 24 in the empagliflozin and placebo groups were -0.21 L (p=0.127) and +0.40 L (p=0.001) in ECW [p=0.001], and -0.23 L (p=0.264) and +0.74 L (p<0.001) in ICW [p<0.001], respectively. In a stratified analysis, the rise in ECW and ICW was significantly attenuated in the empagliflozin group in contrast to the placebo group in participants with body mass index ≥25 but not in those with <25 kg/m2. CONCLUSIONS: Early SGLT2 inhibitor administration may attenuate changes in ECW and ICW.

DOI： 10.1016/j.cardfail.2021.07.022

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

INTRODUCTION: Plasma volume status (PVS), a parameter of the discrepancy between actual plasma volume (PV) and ideal PV, has been recently evaluated as a prognostic marker in patients with heart failure. This subgroup analysis of the EMBODY trial was designed to determine whether a sodium-glucose cotransporter 2 (SGLT2) inhibitor affects the alleviation of heart failure and improvement of PVS in patients after acute myocardial infarction (AMI) with congestive heart failure (CHF). METHODS: The EMBODY trial was a prospective, multicenter, randomized, double-blind, placebo-controlled trial to identify the effect of an SGLT2 inhibitor on cardiac sympathetic hyperactivity in patients with AMI and type 2 diabetes mellitus (T2DM) in Japan. In total, 105 patients were randomized (1:1) to receive 10 mg empagliflozin or a placebo (once daily), 2 weeks after the onset of AMI. In this subanalysis, we investigated the time-course of PVS at baseline and weeks 4, 12, and 24. RESULTS: Overall, 96 patients were included in the subgroup analysis set (age 64.3 ± 10.9 years, 80.2% men; 46 in the empagliflozin group and 50 in the placebo group). Body weight and PVS decreased in the empagliflozin group compared with the placebo group at 24 weeks (- 2.2 vs. + 0.1 kg, P < 0.001, and - 5.1 vs. - 0.3%, P < 0.001, respectively). Decreased PVS, defined as a change in PVS of < - 4.5%, was associated with the administration of empagliflozin (odds ratio 2.61, 95% confidence interval 1.11-6.15, P = 0.028). N-terminal pro b-type natriuretic peptide levels decreased in both the empagliflozin and placebo groups (1028.7-370.3 pg/mL, P < 0.001, and 1270.6-673.7 pg/mL, P < 0.01, respectively). CONCLUSION: Empagliflozin reduced the body weight and PVS. Early SGLT2 inhibitor administration in patients with AMI, CHF, and T2DM can therefore be effective in reducing the body weight and PVS. TRIAL REGISTRATION: UMIN 000030158.

DOI： 10.1007/s13300-021-01103-0

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

AIMS: Although the reno-protective effects of sodium-glucose cotransporter 2 inhibitors are known in patients with heart failure or type 2 diabetes mellitus (T2DM), this effect has not been confirmed in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: The prospective, multicentre, randomized, double-blind, placebo-controlled EMBODY trial investigated patients with AMI and T2DM in Japan. The eligible patients included adults aged 20 years or older, diagnosed with AMI and T2DM, and who could be discharged within 2-12 weeks after the onset of AMI. One hundred and five patients were randomized (1:1) to receive once daily 10 mg empagliflozin or placebo within 2 weeks of AMI onset. In this sub-analysis, we investigated the time course of renal functional parameters such as serum creatinine levels and estimated glomerular filtration rate (eGFR) from baseline to Weeks 4, 12, and 24. Ninety-six patients (64 ± 11 years, 78 male) were included in the full analysis (n = 46 and 50 in the empagliflozin and placebo groups, respectively). We used serum creatinine and eGFR as indicators of renal function. In the placebo group, eGFR decreased from 66.14 mL/min/1.73 m2 at baseline to 62.77 mL/min/1.73 m2 by Week 24 (P = 0.023) but remained unchanged in the empagliflozin group (from 64.60 to 64.36 mL/min/1.73 m2 , P = 0.843). In the latter group, uric acid improved from 5.8 mg/dL at baseline to 4.9 mg/dL at Week 24 (P < 0.001). In the earlier analysis of 56 patients with eGFR ≥ 60 mL/min/1.73 m2 , the eGFR decreased and the serum creatinine increased from baseline to 24 weeks in the placebo group, significantly different to the empagliflozin group (-6.61 vs. +0.22 mL/min/1.73 m2 , P = 0.008 and +0.063 vs. -0.001 mg/dL, P = 0.030, respectively). The changes in serum creatinine and eGFR from baseline to Week 24 were significantly correlated with those in uric acid in the placebo group (r = 0.664, P < 0.001 and r = -0.675, P < 0.001, respectively) but not in the empagliflozin group. CONCLUSIONS: Empagliflozin prevented the kidney functional decline in patients with AMI and T2DM, especially those with baseline eGFR ≥ 60 mL/min/1.73 m2 . Early administration of sodium-glucose cotransporter 2 inhibitors in these patients is considered desirable for renal protection.

DOI： 10.1002/ehf2.13509

PubMed

researchmap

記述言語：英語   出版者・発行元：(一社)日本循環器学会  

researchmap

掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/j.hrthm.2020.06.036

researchmap

掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/j.jacep.2020.07.007

researchmap

掲載種別：研究論文（学術雑誌）  

© 2020 The Author(s). Background: Protection from lethal ventricular arrhythmias leading to sudden cardiac death (SCD) is a crucial challenge after acute myocardial infarction (AMI). Cardiac sympathetic and parasympathetic activity can be noninvasively assessed using heart rate variability (HRV) and heart rate turbulence (HRT). The EMBODY trial was designed to determine whether the Sodium-glucose cotransporter 2 (SGLT2) inhibitor improves cardiac nerve activity. Methods: This prospective, multicenter, randomized, double-blind, placebo-controlled trial included patients with AMI and type 2 diabetes mellitus (T2DM) in Japan; 105 patients were randomized (1:1) to receive once-daily 10-mg empagliflozin or placebo. The primary endpoints were changes in HRV, e.g., the standard deviation of all 5-min mean normal RR intervals (SDANN) and the low-frequency-to-high-frequency (LF/HF) ratio from baseline to 24 weeks. Secondary endpoints were changes in other sudden cardiac death (SCD) surrogate markers such as HRT. Results: Overall, 96 patients were included (46, empagliflozin group; 50, placebo group). The changes in SDANN were + 11.6 and + 9.1 ms in the empagliflozin (P = 0.02) and placebo groups (P = 0.06), respectively. Change in LF/HF ratio was - 0.57 and - 0.17 in the empagliflozin (P = 0.01) and placebo groups (P = 0.43), respectively. Significant improvement was noted in HRT only in the empagliflozin group (P = 0.01). Whereas intergroup comparison on HRV and HRT showed no significant difference between the empagliflozin and placebo groups. Compared with the placebo group, the empagliflozin group showed significant decreases in body weight, systolic blood pressure, and uric acid. In the empagliflozin group, no adverse events were observed. Conclusions: This is the first randomized clinical data to evaluate the effect of empagliflozin on cardiac sympathetic and parasympathetic activity in patients with T2DM and AMI. Early SGLT2 inhibitor administration in AMI patients with T2DM might be effective in improving cardiac nerve activity without any adverse events. Trial Registration: The EMBODY trial was registered by the UMIN in November 2017 (ID: 000030158). UMIN000030158; https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000034442.

DOI： 10.1186/s12933-020-01127-z

Scopus

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Wiley  

INTRODUCTION: Early recurrence (ER) of atrial fibrillation (AF) is defined as the recurrence of atrial tachyarrhythmias within 3 months after AF ablation, however, this definition is based on data from the era of radiofrequency catheter ablation (RFCA), without contact force (CF) technology. We investigated the significance of ER as a risk factor for late recurrence (LR) in paroxysmal AF (PAF) patients treated with CF and non-CF-guided ablation. METHODS AND RESULTS: We studied 395 patients with PAF who underwent RFCA. Of these, 97 patients underwent RFCA without-CF technology (non-CF group) and 298 underwent with CF technology (CF group). Over a 2-year postablation follow-up period, LR occurred in 54 (55.7%) patients in the non-CF group, and in 105 (35.2%) patients in the CF group. ER had a more significant relationship with LR in the CF group, and all patients in the CF group with ER in the third month developed LR. CONCLUSION: PAF patients with ER who have undergone CF-guided ablation have a greater risk of LR than those who have undergone non-CF-guided ablation. ER in the third month after CF-guided ablation may indicate an absolute risk of LR. Blanking period could be defined as 2 months in the CF era.

DOI： 10.1111/jce.14643

PubMed

researchmap

その他リンク： https://onlinelibrary.wiley.com/doi/full-xml/10.1111/jce.14643

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1152/ajpheart.00486.2018

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Blackwell Publishing Inc.  

DOI： 10.1111/jce.13423

Scopus

PubMed

researchmap

記述言語：英語  

DOI： 10.1016/j.hrcr.2017.10.012

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.jacep.2017.05.014

Scopus

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：WILEY-BLACKWELL  

BackgroundLeft ventricular (LV) diastolic dysfunction depends on an impaired relaxation and stiffness. Abnormal LV relaxation contributes to the development of atrial fibrillation (AF), but the role of LV stiffness in AF remains unclear.
HypothesisDiastolic wall strain (DWS), a load-independent, noninvasive direct measure of LV stiffness, correlates with prevalent AF.
MethodsThis study included 328 consecutive subjects with structurally normal hearts: 164 paroxysmal AF patients and 164 age- and sex-matched (1:1) controls. We calculated the DWS from the M-mode echocardiographic measurements of the LV posterior wall thickness at end-systole and end-diastole during sinus rhythm.
ResultsThe DWS was lower in the AF patients (0.350.07) than in the controls (0.41 +/- 0.06; P &lt; 0.001). After adjusting for the risk factors of AF using a conditional logistic regression analysis, a history of hypertension, plasma brain-type natriuretic peptide level, and DWS were independently associated with AF prevalence, whereas body mass index, LV mass index, left atrial volume, and any conventional indices of the diastolic function were not. A low DWS (&lt;0.380) was the strongest indicator of AF (odds ratio: 6.22, 95% confidence interval: 3.08-14.2, P &lt; 0.001).
ConclusionsIncreased LV stiffness estimated by DWS was a strong determinant of the prevalence of AF. LV stiffness may play a role in the pathogenesis of paroxysmal AF in structurally normal hearts.

DOI： 10.1002/clc.22595

Web of Science

PubMed

researchmap

記述言語：英語   出版者・発行元：ELSEVIER SCIENCE INC  

DOI： 10.1016/j.hrthm.2016.03.052

Web of Science

PubMed

researchmap

記述言語：英語   出版者・発行元：WILEY-BLACKWELL  

DOI： 10.1111/jce.12896

Web of Science

PubMed

researchmap

記述言語：英語   出版者・発行元：(一社)日本循環器学会  

researchmap

記述言語：英語   出版者・発行元：WILEY-BLACKWELL  

DOI： 10.1111/jce.12778

Web of Science

PubMed

researchmap

記述言語：英語   出版者・発行元：WILEY-BLACKWELL  

DOI： 10.1111/jce.12747

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：JAPANESE CIRCULATION SOC  

Background: Few reports are available on the characteristics of electrical storms of ventricular tachycardia (VT storm) refractory to intravenous (IV) amiodarone.
Methods and Results: IV-amiodarone was administered to 60 patients with ventricular tachyarrhythmia between 2007 and 2012. VT storms, defined as 3 or more episodes of VT within 24 h, occurred in 30 patients (68 +/- 12 years, 7 female), with 12 having ischemic and 18 non-ischemic heart disease. We compared the clinical and electrocardiographic characteristics of the patients with VT storms suppressed by IV-amiodarone (Effective group) to those of patients not affected by the treatment (Refractory group). IV-amiodarone could not control recurrence of VT in 9 patients (30%). The Refractory group comprised 5 patients with acute myocardial infarctions. Although there was no difference in the VT cycle length, the QRS duration of both the VT and premature ventricular contractions (PVCs) followed by VT was narrower in the Refractory group than in the Effective group (140 +/- 30 vs. 178 +/- 25 ms, P&lt;0.01; 121 +/- 14 vs. 179 +/- 22 ms, P&lt;0.01). In the Refractory group, additional administration of IV-mexiletine and/or Purkinje potential-guided catheter ablation was effective.
Conclusions: IV-amiodarone-refractory VT exhibited a relatively narrow QRS tachycardia. The narrow triggering PVCs, suggesting a Purkinje fiber origin, may be treated by additional IV-mexiletine and endocardial catheter ablation.

DOI： 10.1253/circj.CJ-15-0213

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier  

Background It is unclear whether false tendons (FTs) are a substantial part of the reentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT). This study aimed to prove the association between FTs and the slow conduction zone by evaluating the electro-anatomical relationship between the so-called diastolic Purkinje (Pd) potentials and FTs using an electro-anatomical mapping (EAM) system (CARTO). Methods The 1st protocol evaluated the spatial distribution of Pd and presystolic Purkinje (Pp) potentials in 6 IVLT patients using a conventional CARTO system. In the remaining 2 patients (2nd protocol), the electro-anatomical relationship between the Pd-Pp fusion potential and the septal connection of the FT was evaluated using an EAM system incorporating an intra-cardiac echo (CARTO-Sound). Results Pd potentials were observed in the posterior-posteroseptal region of the LV and had a slow conduction property, whereas Pp potentials were widely distributed in the interventricular (IV) septum. At the intersection of the 2 regions, which was located in the mid-posteroseptal area, both Pd and Pp potentials were closely spaced and often had a fused configuration. In the latter 2 patients (2nd protocol), it was confirmed that the intra-cardiac points at which the Pd-Pp fusion potential was recorded were located in the vicinity of the attachment site of the FT to the IV septum. In all patients, ILVTs were successfully eliminated by the application of radiofrequency at those points. Conclusion FTs may at least partly contribute to the formation of the Pd potential, and thus form a critical part of the reentry circuit of ILVT.

DOI： 10.1016/j.joa.2015.01.003

Scopus

PubMed

researchmap

記述言語：日本語   出版者・発行元：公益財団法人 日本心臓財団  

&lt;p&gt; 症例は68歳, 男性. 再発性のnarrow QRS頻拍を認め, アデノシン三リン酸投与にてP波を伴わずに頻拍は停止した. 右室刺激時には房室結節を介する室房伝導が間欠的に見られるのみだったが, 心房刺激により高位右房を最早期興奮部位とする非持続性の頻拍が誘発された. イソプロテレノール投与後, 右室刺激時1 : 1室房伝導となったが, 心房興奮はHis束領域が早く, 心室の刺激部位を変更しても頻拍時の奇異的な心房興奮順序は再現できなかった. 傍His束ペーシングの結果, 逆伝導は房室結節パターンであった. 以上より心房頻拍を疑い, 心房興奮パターンより右房起源と考え, 頻拍中に右房をmappingすると, 最早期興奮部位は心房中隔であった. 同部位を通電したものの, 頻拍に影響を与えなかった. イソプロテレノール投与下で頻拍は持続性となったため, 頻拍中の心室オーバードライブペーシングを行うと頻拍は毎回停止しエントレインはできなかったが, QRS波がfusionしている段階で心房波を捕捉

researchmap

記述言語：英語   掲載種別：論文集(書籍)内論文   出版者・発行元：Springer-Verlag London Ltd  

Electrophysiologic testing refers to a catheter procedure that involves the recording of intracardiac electrical signals and programmed electrical stimulation. Electrophysiologic testing provides clinically valuable information in the management of patients with known or suspected cardiac arrhythmias and is useful to determine the mechanisms and physiological characteristics of the cardiac arrhythmia or the future risks of cardiac adverse events. Electrophysiologic testing either may be performed for diagnostic purposes only or may be part of a combined diagnostic and therapeutic (e.g., catheter ablation) procedure. In this chapter, clinical indications, practical diagnostic procedures for various types of cardiac arrhythmia, and an overview of cardiac mapping are reviewed.

DOI： 10.1007/978-1-4471-5316-0_14

Scopus

researchmap

記述言語：英語   掲載種別：論文集(書籍)内論文   出版者・発行元：Springer-Verlag London Ltd  

Electrical storm is a life-threatening syndrome that is defined by three or more sustained episodes of ventricular tachycardia or ventricular fibrillation within a relatively short period of time. Electrical storm typically leads to a poor outcome and its management is challenging. Electrical storm can occur in various conditions, and the effective management of electrical storm requires an understanding of the mechanisms underlying the recurrent arrhythmia. Here, we present a review of recent advances in the approach and management of electrical storm including pharmacological and non-pharmacological therapies.

DOI： 10.1007/978-1-4471-5316-0_22

Scopus

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

DOI： 10.1016/j.hrthm.2014.03.051

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Background Measuring postpacing intervals (PPIs) is the standard maneuver for localizing reentrant tachycardia circuits. However, changes or termination of the tachycardia during entrainment pacing, or difficulties in defining the correct local activity, limit the use of PPIs.
Methods and Results We hypothesized that the number of pacing stimuli needed to entrain (NNE) was useful for mapping intra-atrial reentrant tachycardias. First, 10 patients with typical atrial flutter were studied to characterize the NNE. Next, 317 entrainment attempts in 30 patients with 76 intra-atrial reentrant tachycardias were analyzed to determine the efficacy of the NNE. The NNE was small at sites within the reentrant circuit (median 2) and large at remote sites during typical atrial flutter. The NNE depended on the pacing cycle length and coupling interval of the initial paced beat, where the NNE became smaller at shorter pacing cycle lengths and coupling intervals. The NNE highly correlated with the difference between the PPI and tachycardia cycle length (r = 0.906; P&lt;0.001). When the pacing cycle length and coupling interval were 16 to 30 ms below the tachycardia cycle length, a NNE 2 and &gt;3 predicted a PPI-tachycardia cycle length 20 and &gt;20 ms, respectively, with 100% accuracy. Thirty-six (11%) entrainment attempts changed or terminated intra-atrial reentrant tachycardia. Importantly, the NNE remained valid in those cases. Furthermore, the NNE provided additional information in cases with some difficulties with PPI measurements.
Conclusions The NNE is a simple and reliable criterion, which facilitates mapping intra-atrial reentrant tachycardia.
Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT001747.

DOI： 10.1161/CIRCEP.113.001416

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：SPRINGER  

The membrane voltage clock and calcium (Ca2+) clock jointly regulate sinoatrial node (SAN) automaticity. VK-II-36 is a novel carvedilol analog that suppresses sarcoplasmic reticulum (SR) Ca2+ release but does not block the beta-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 Ca2+ clock. We simultaneously mapped intracellular Ca2+ 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 Ca2+ 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 &lt; 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 mu mol/l) abolished both the ISO-induced shift of the pacemaking site and augmentation of LDCAE (P &lt; 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 Ca2+ clock via SR Ca2+ release during beta-adrenergic stimulation.

DOI： 10.1007/s00380-013-0378-2

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

BACKGROUND Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear.
OBJECTIVE The purpose of this study was to test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by I-KATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia.
METHODS Intracellular calcium (Ca-i) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts.
RESULTS Repeated episodes of electrically induced ventricular fibrillation (VF) at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K+](0), 4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmoL/L [K+](o), 9 of 10 hearts (90%) in 1.5 mmol/L [K+](o), and 7 of 7 hearts (100%) in 1.0 mmol/L [K+](o) (P &lt; .001). Optical mapping showed that isoproterenol and hypokalemia enhanced Ca-i transient duration (CaiTD) and heterogeneously shortened action potential duration (APD) after defibrillation, leading to late phase 3 EAD and SVF. I-KATP blacker (glibenclamide, 5 mu mol/L) reversed the post-defibrillation APD shortening and suppressed recurrent SVF in all hearts studied despite no evidence of ischemia. Nifedipine reliably prevented recurrent VF when given before, but not after, the development of VF. I-Kr, blacker (E-4031) and small-conductance calcium-activated potassium channel blacker (apamin) failed to prevent recurrent SVF.
CONCLUSION Beta-adrenergic stimulation and concomitant hypokalemia could cause nonischemic activation of I-KATP, heterogeneous APD shortening, and prolongation of CaiTD to provoke late phase 3 EAD, triggered activity, and recurrent SVF. I-KATP inhibition may be useful in managing ES during resistant hypokalemia.

DOI： 10.1016/j.hrthm.2013.12.032

Web of Science

PubMed

researchmap

DOI： 10.1111/jce.12176

PubMed

researchmap

記述言語：英語   出版者・発行元：ELSEVIER SCIENCE INC  

DOI： 10.1016/j.hrthm.2012.06.001

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：論文集(書籍)内論文   出版者・発行元：Springer-Verlag London Ltd  

Zoll et al. first reported the successful termination of ventricular fibrillation (VF) by externally applied electrical countershocks. In the same seminal report, the authors also discovered that recurrent VF may occur shortly after successful ventricular defibrillation. Due to the general availability of the implantable cardioverter-defibrillator (ICD), patients may survive the initial VF episodes but suffer from multiple recurrent VF and defibrillation shocks within a short period of time. The clustering of recurrent VF episodes (electrical storm) after initial successful defibrillation suggests that the first episode of VF begets subsequent episodes of VF. The mechanisms by which VF begets VF remains poorly understood. In this chapter we will discuss the mechanisms of neural remodeling after myocardial infarction (MI). We propose that nerve sprouting and sympathetic hyperinnervation occur after MI. The increased sympathetic nerve densities in the heart is highly heterogeneous, with portions of the heart showing increased nerve densities while the remaining portions of the heart showing denervation. During sympathetic nerve activation, there is increased heart rate and augmented intracellular calcium (Ca&lt
inf&gt
i&lt
/inf&gt
) concentration. In addition, we found that the action potential duration (APD) is abbreviated after a fibrillation-defibrillation episode in failing ventricles. The shortened APD and the elevated Ca&lt
inf&gt
i&lt
/inf&gt
promotes late phase 3 early afterdepolarization (EAD) and Ca&lt
sup&gt
2+&lt
/sup&gt
-transient triggered firing (CTTF), leading to recurrent cardiac fibrillation. We also propose that the mechanisms of APD shortening after fibrillation-defibrillation episodes in the failing (but not in the normal) ventricles are due to the upregulation of small conductance Ca&lt
sup&gt
2+&lt
/sup&gt
activated potassium (SK) currents. We hope that these discussions will help the readers better understand the relevance of cardiac neural remodeling and electrical remodeling in the mechanisms of arrhythmogenesis.

DOI： 10.1007/978-1-4471-4881-4_13

Scopus

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

Background: Carvedilol and its analogues suppress delayed afterdepolarizations (DADs) and catecholaminergic polymorphic ventricular tachycardias by direct action on the cardiac ryanodine receptor type 2 (RyR2). Objective: To test a hypothesis that carvedilol analogue may also prevent triggered activities (TAs) through the suppression of early afterdepolarizations (EADs). Methods: Intracellular Ca2+ and membrane voltage were simultaneously recorded by using optical mapping technique in Langendorff-perfused mouse and rabbit hearts to study the effect of carvedilol analogue VK-II-36, which does not have significant beta-blocking effects. Results: Spontaneous intracellular Ca2+ elevations (SCaEs) during diastole were induced by rapid ventricular pacing and isoproterenol infusion in intact rabbit ventricles. Systolic and diastolic SCaEs were simultaneously noted in Langendorff-perfused RyR2 R4496+/- mouse hearts after creating atrioventricular block. VK-II-36 effectively suppressed SCaEs and eliminated TAs observed in both mouse and rabbit ventricles. We tested the effect of VK-II-36 on EADs by using a rabbit model of acquired long QT syndrome, in which phase 2 and phase 3 EADs were observed in association with systolic SCaEs. VK-II-36 abolished the systolic SCaEs and phase 2 EADs, and greatly decreased the dispersion of repolarization and the amplitude of phase 3 EADs. VK-II-36 completely prevented EAD-mediated TAs in all ventricles studied. Conclusions: A carvedilol analogue, VK-II-36, inhibits ventricular tachyarrhythmias in intact mouse and rabbit ventricles by the suppression of SCaEs, independent of beta-blocking activity. The RyR2 may be a potential target for treating focal ventricular arrhythmias triggered by either EADs or DADs. © 2013 Heart Rhythm Society.

DOI： 10.1016/j.hrthm.2012.09.006

Scopus

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

The heart failure guideline in Japan has stated the necessity of investigating the role of oral inotropic agents in patients with chronic heart failure (CHF), which are clinically available only in Japan. A total of 1,846 consecutive patients with heart failure (mean: 69.5 years old, 1,279 males) treated at our institute from November 2009 to August 2010 were investigated retrospectively. Thirty-one patients (1.84%) who had taken oral inotropic agents (pimobendan 27, docarpamine 6, and denopamine 4) were extracted for this study, and the efficacy and limitations of the treatments were analyzed. Following the oral inotropic treatment, the NYHA functional class (P = 0.017), cardiothoracic ratio (P = 0.002) and B-type natriuretic peptide levels (P = 0.011) were significantly improved, and the number of emergency room (ER) visits (P &lt
0.001) and hospitalizations (P &lt
0.001) were significantly reduced. The nonsurviving patients (n = 7/31, 22.6%) were significantly older (P = 0.02) and tended to have a larger cardiothoracic ratio (P = 0.084) compared with the survivors. An absence of concomitant beta-blocker therapy was significantly associated with a worse prognosis (oneyear mortality 2/21 versus 5/10, log rank, P = 0.011). Oral inotropic agents brought about improvements in the clinical parameters of CHF and a reduction in ER visits and hospitalizations. However, concomitant beta-blocker therapy should be considered for patients receiving oral inotropic treatment.

DOI： 10.1536/ihj.54.75

Scopus

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：JAPAN SOC INTERNAL MEDICINE  

A 17-year-old girl with multiple areas of skin hemangiomas that had been present since birth was referred to our institution complaining of sudden onset of dyspnea. Enhanced CT demonstrated a pulmonary thromboembolism and transthoracic echocardiogram showed a thrombus-like echo in the right ventricle. CT further revealed thrombi in the inferior vena cava (IVC) and peripheral vein. The thrombi, especially those in the RV, were highly life-threatening; therefore, immediate thrombectomy was performed and an IVC filter was placed. Because no major complications occurred, the patient was discharged 34 days after admission. In such young women, carefully using anticoagulation therapy and planning pregnancy are recommended.

DOI： 10.2169/internalmedicine.52.9149

Web of Science

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：SPRINGER  

Protein complex of the cardiac junctional sarcoplasmic reticulum (SR) membrane formed by type 2 ryanodine receptor, junction, triadin, and calsequestrin is responsible for controlling SR calcium (Ca) release. Increased intracellular calcium (Ca-i) activates the electrogenic sodium-Ca exchanger current, which is known to be important in afterdepolarization and triggered activities (TAs). Using optical-mapping techniques, it is possible to simultaneously map membrane potential (V (m)) and Ca-i transient in Langendorff-perfused rabbit ventricles to better define the mechanisms by which V (m) and Ca-i interactions cause early afterdepolarizations (EADs). Phase 3 EAD is dependent on heterogeneously prolonged action potential duration (APD). Electrotonic currents that flow between a persistently depolarized region and its recovered neighbors underlies the mechanisms of phase 3 EADs and TAs. In contrast, "late phase-3 EAD" is induced by APD shortening, not APD prolongation. In failing ventricles, upregulation of apamin-sensitive Ca-activated potassium (K) channels (I (KAS)) causes APD shortening after fibrillation-defibrillation episodes. Shortened APD in the presence of large Ca-i transients generates late-phase 3 EADs and recurrent spontaneous ventricular fibrillation. The latter findings suggest that I (KAS) may be a novel antiarrhythmic targets in patients with heart failure and electrical storms.

DOI： 10.1007/s00246-012-0236-5

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：SPRINGER  

Specifically, FK506-binding proteins 12 (FKBP12) and 12.6 (FKBP12.6) are cis-trans peptidyl prolyl isomerases that are expressed in the heart. Both FKBP12 and FKBP12.6 were previously known to interact with ryanodine receptors in striated muscles. Although FKBP12 is abundantly present in the heart, its function in the heart is largely uncertain. Recently, by generating FKBP12 transgenic overexpression and cardiac-restricted knockout mice, we showed that FKBP12 is critically important in regulating trans-sarcolemmal ionic currents, predominately the voltage-gated Na+ current, I (Na), but it appears to be less important for regulating cardiac ryanodine receptor function. Similar genetic approaches also confirm the role of FKBP12.6 in regulating cardiac ryanodine receptors. The current study demonstrated that FKBP12 and FKBP12.6 have very different physiologic functions in the heart.

DOI： 10.1007/s00246-012-0298-4

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

BACKGROUND Na channel blockers are effective in suppressing delayed afterdepolarizations (DADs) in isolated Purkinje fibers. However, in isolated mouse ventricular myocytes lacking calsequestrin, only those Na channel blockers that also inhibit type 2 ryanodine receptor channels were effective against spontaneous Ca elevation (SCaE) and DADs.
OBJECTIVE To test the hypothesis that combined Na channel and type 2 ryanodine receptor channel blocker ((R)-propafenone) is more effective than a Na channel blocker (lidocaine) in suppressing SCaE and DADs in the intact rabbit ventricles.
METHODS We compared (R)-propafenone (3 mu mol/L) with lidocaine (50 mu mol/L) on SCaE and DADs by using epicardial optical mapping of intracellular calcium (Ca-i) and membrane voltage in Langendorff-perfused rabbit hearts. SCaE and DADs were induced by rapid pacing trains and isoproterenol (0.3 mu mol/L) infusion. One arbitrary unit is equivalent to the Ca transient amplitude of paced beats.
RESULTS SCaEs were observed at the cessation of rapid pacing in all hearts at baseline. (R)-Propafenone nearly completely inhibited DADs and SCaE (0.04 arbitrary units [95% confidence interval 0.02-0.06] vs 0.23 arbitrary units [95% confidence interval 0.18-0.28] at baseline; n = 6 hearts; P &lt; .001). Lidocaine also significantly reduced the SCaE but was significantly (P &lt; .05) less effective than (R)-propafenone. Both drugs increased the rise time of action potential upstroke and reduced conduction velocity to a similar extent, suggesting a significant inhibition of I-Na.
CONCLUSIONS Both Na channel blockers significantly reduced tachycardia-induced SCaEs in the rabbit ventricles, but (R)-propafenone was significantly more effective than lidocaine. These data suggest that type 2 ryanodine receptor inhibition potentiates the activity of Na channel blockers against SCaE and DADs in the intact hearts.

DOI： 10.1016/j.hrthm.2012.02.031

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1253/circj.CJ-11-1301

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Background-We hypothesize that inferior vena cava-inferior atrial ganglionated plexus nerve activity (IVC-IAGPNA) is responsible for ventricular rate (VR) control during atrial fibrillation (AF) in ambulatory dogs.
Methods and Results-We recorded bilateral cervical vagal nerve activity (VNA) and IVC-IAGPNA during baseline sinus rhythm and during pacing-induced sustained AF in 6 ambulatory dogs. Integrated nerve activities and average VR were measured every 10 seconds over 24 hours. Left VNA was associated with VR reduction during AF in 5 dogs (from 211 bpm [95% CI, 186-233] to 178 bpm [95% CI, 145-210]; P&lt;0.001) and right VNA in 1 dog (from 208 bpm [95% CI, 197-223] to 181 bpm [95% CI, 163-200]; P&lt;0.01). There were good correlations between IVC-IAGPNA and left VNA in the former 5 dogs and between IVC-IAGPNA and right VNA in the last dog. IVC-IAGPNA was associated with VR reduction in all dogs studied. Right VNA was associated with baseline sinus rate reduction from 105 bpm (95% CI, 95-116) to 77 bpm (95% CI, 64-91; P&lt;0.01) in 4 dogs, whereas left VNA was associated with sinus rate reduction from 111 bpm (95% CI, 90-1250) to 81 bpm (95% CI, 67-103; P&lt;0.01) in 2 dogs.
Conclusions-IVC-IAGPNA is invariably associated with VR reduction during AF. In comparison, right or left VNA was associated with VR reduction only when it coactivates with the IVC-IAGPNA. The vagal nerve that controls VR during AF may be different from that which controls sinus rhythm. (Circ Arrhythm Electrophysiol. 2012;5:571-580.)

DOI： 10.1161/CIRCEP.111.967737

Web of Science

PubMed

researchmap

記述言語：英語   出版者・発行元：ELSEVIER SCIENCE INC  

DOI： 10.1016/j.hrthm.2010.12.021

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：WILEY-BLACKWELL  

Reduced Vagal Control in Heart Failure. Objective: We tested the hypothesis that heart failure (HF) results in right atrial ganglionated plexus (RAGP) denervation that contributes to sinoatrial node dysfunction. Background: HFis associated with sinoatrial node dysfunction. However, the detailed mechanisms remain unclear. Methods: We recorded nerve activity (NA) from the RAGP, right stellate ganglion (SG), and right vagal nerve in 7 ambulatory dogs at baseline and after pacing-induced HF. We also determined the effects of RAGP stimulation in isolated normal and HF canine RA. Results: NAs in both the SG and vagal were significantly higher in HF than at baseline. The relationship between 1-minute integrated NAs of vagal and RAGP showed either a positive linear correlation (Group 1, n = 4) or an L-shaped correlation (Group 2, n = 3). In all dogs, a reduced heart rate was observed when vagal-NA was associated with simultaneously increased RAGP-NA. On the other hand, when vagal-NA was not associated with increased RAGP-NA, the heart rate was not reduced. The induction of HF significantly decreased RAGP-NA in all dogs (P &lt; 0.05). Stimulating the superior RAGP in isolated RA significantly reduced the sinus rate in normal but not the HF hearts. Immunohistochemical staining revealed lower densities of tyrosine hydroxylase-and choline acetyltransferase-positive nerve tissues in HF RAGP than normal (P &lt; 0.001 and P = 0.001, respectively). Conclusions: The RAGP-NA is essential for the vagal nerve to counterbalance the SG in sinus rate control. In HF, RAGP denervation and decreased RAGP-NA contribute to the sinus node dysfunction. (J Cardiovasc Electrophysiol, Vol. 23, pp. 404-412, April 2012)

DOI： 10.1111/j.1540-8167.2011.02204.x

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

Objectives The purpose of this study was to evaluate the changes of left stellate ganglionic nerve activity (SGNA) and left thoracic vagal nerve activity (VNA) after acute myocardial infarction (MI).
Background Whether MI results in remodeling of extracardiac nerve activity remains unclear.
Methods We implanted radiotransmitters to record the SGNA, VNA, and electrocardiogram in 9 ambulatory dogs. After baseline monitoring, MI was created by 1-h balloon occlusion of the coronary arteries. The dogs were then continuously monitored for 2 months. Both stellate ganglia were stained for growth-associated protein 43 and synaptophysin. The stellate ganglia from 5 normal dogs were used as control.
Results MI increased 24-h integrated SGNA from 7.44 +/- 7.19 Ln(Vs)/day at baseline to 8.09 +/- 7.75 Ln(Vs)/day after the MI (p &lt; 0.05). The 24-h integrated VNA before and after the MI was 5.29 +/- 5.04 Ln(Vs)/day and 5.58 +/- 5.15 Ln(Vs)/day, respectively (p &lt; 0.05). A significant 24-h circadian variation was noted for the SGNA (p &lt; 0.05) but not the VNA. The SGNA/VNA ratio also showed significant circadian variation. The nerve densities from the left SG were 63,218 +/- 34,719 mu m(2)/mm(2) and 20,623 +/- 4,926 mu m(2)/mm(2) for growth-associated protein 43 (p &lt; 0.05) and were 32,116 +/- 8,190 mu m(2)/mm(2)and 16,326 +/- 4,679 mu m(2)/mm(2) for synaptophysin (p &lt; 0.05) in MI and control groups, respectively. The right SG also showed increased nerve density after MI (p &lt; 0.05).
Conclusions MI results in persistent increase in the synaptic density of bilateral stellate ganglia and is associated with increased SGNA and VNA. There is a circadian variation of the SGNA/VNA ratio. These data indicate significant remodeling of the extracardiac autonomic nerve activity and structures after MI. (J Am Coll Cardiol 2012;59:954-61) (C) 2012 by the American College of Cardiology Foundation

DOI： 10.1016/j.jacc.2011.11.030

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：JAPANESE CIRCULATION SOC  

Background: Studies using isolated sinoatrial node (SAN) cells indicate that rhythmic spontaneous sarcoplasmic reticulum calcium release (Ca clock) plays an important role in SAN automaticity. In the intact SAN, cross-contamination of optical signals from the SAN and the right atrium (RA) prevent the definitive testing of Ca clock hypothesis. The aim of this study was to use a novel approach to selectively mapping the intact SAN to examine the Ca clock mechanism.
Methods and Results: We simultaneously mapped intracellular Ca (Cai) and membrane potential (V-m) in 10 isolated, Langendorff-perfused normal canine RAs. The excitability of the RA was suppressed with high-potassium Tyrode's solution, allowing selective optical mapping of V-m and Cai of the SAN. Isoproterenol (ISO, 0.03 mu mol/L) decreased the cycle length of the sinus beats, and shifted the leading pacemaker site from the middle or inferior SAN to the superior SAN in all RAs. The Cai upstroke preceded the V-m in the leading pacemaker site by up to 18 +/- 2 ms. ISO-induced changes to SAN were inhibited by ryanodine (3 mu mol/L), but not ZD7288 (3 mu mol/L), a selective l(1) blocker.
Conclusions: We conclude that, in the isolated canine RA, a high extracellular potassium concentration can suppress atrial excitability thus leading to SAN-RA conduction block, allowing selective optical mapping of the intact SAN. Acceleration of Ca cycling in the superior SAN underlies the mechanism of sinus tachycardia during sympathetic stimulation. (Circ J 2012; 76: 309-316)

DOI： 10.1253/circj.CJ-11-0734

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：OXFORD UNIV PRESS  

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inheritable myocardial disorder associated with fibrofatty replacement of myocardium and ventricular arrhythmia. A subset of ARVC is categorized as Naxos disease, which is characterized by ARVC and a cutaneous disorder. A homozygous loss-of-function mutation of the Plakoglobin (Jup) gene, which encodes a major component of the desmosome and the adherens junction, had been identified in Naxos patients, although the underlying mechanism remained elusive. We generated Jup mutant mice by ablating Jup in cardiomyocytes. Jup mutant mice largely recapitulated the clinical manifestation of human ARVC: ventricular dilation and aneurysm, cardiac fibrosis, cardiac dysfunction and spontaneous ventricular arrhythmias. Ultra-structural analyses revealed that desmosomes were absent in Jup mutant myocardia, whereas adherens junctions and gap junctions were preserved. We found that ventricular arrhythmias were associated with progressive cardiomyopathy and fibrosis in Jup mutant hearts. Massive cell death contributed to the cardiomyocyte dropout in Jup mutant hearts. Despite the increase of beta-catenin at adherens junctions in Jup mutant cardiomyoicytes, the Wnt/beta-catenin-mediated signaling was not altered. Transforming growth factor-beta-mediated signaling was found significantly elevated in Jup mutant cardiomyocytes at the early stage of cardiomyopathy, suggesting an important pathogenic pathway for Jup-related ARVC. These findings have provided further insights for the pathogenesis of ARVC and potential therapeutic interventions.

DOI： 10.1093/hmg/ddr392

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Background-We hypothesize that left-sided low-level vagus nerve stimulation (LL-VNS) can suppress sympathetic outflow and reduce atrial tachyarrhythmias in ambulatory dogs.
Methods and Results-We implanted a neurostimulator in 12 dogs to stimulate the left cervical vagus nerve and a radiotransmitter for continuous recording of left stellate ganglion nerve activity, vagal nerve activities, and ECGs. Group 1 dogs (N=6) underwent 1 week of continuous LL-VNS. Group 2 dogs (N=6) underwent intermittent rapid atrial pacing followed by active or sham LL-VNS on alternate weeks. Integrated stellate ganglion nerve activity was significantly reduced during LL-VNS (7.8 mV/s; 95% confidence interval [CI] 6.94 to 8.66 versus 9.4 mV/s [95% CI, 8.5 to 10.3] at baseline; P=0.033) in group 1. The reduction was most apparent at 8 AM, along with a significantly reduced heart rate (P=0.008). Left-sided low-level vagus nerve stimulation did not change vagal nerve activity. The density of tyrosine hydroxylase-positive nerves in the left stellate ganglion 1 week after cessation of LL-VNS were 99 684 mu m(2)/mm(2) (95% CI, 28 850 to 170 517) in LL-VNS dogs and 186 561 mu m(2)/mm(2) (95% CI, 154 956 to 218 166; P=0.008) in normal dogs. In group 2, the frequencies of paroxysmal atrial fibrillation and tachycardia during active LL-VNS were 1.4/d (95% CI, 0.5 to 5.1) and 8.0/d (95% CI, 5.3 to 12.0), respectively, significantly lower than during sham stimulation (9.2/d [95% CI, 5.3 to 13.1]; P=0.001 and 22.0/d [95% CI, 19.1 to 25.5], P&lt;0.001, respectively).
Conclusions-Left-sided low-level vagus nerve stimulation suppresses stellate ganglion nerve activities and reduces the incidences of paroxysmal atrial tachyarrhythmias in ambulatory dogs. Significant neural remodeling of the left stellate ganglion is evident 1 week after cessation of continuous LL-VNS. (Circulation. 2011; 123: 2204-2212.)

DOI： 10.1161/CIRCULATIONAHA.111.018028

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Rationale: FK506 binding protein (FKBP) 12 is a known cis-trans peptidyl prolyl isomerase and highly expressed in the heart. Its role in regulating postnatal cardiac function remains largely unknown.
Methods and Results: We generated FKBP12 overexpressing transgenic (alpha MyHC-FKBP12) mice and cardiomyocyte-restricted FKBP12 conditional knockout (FKBP12(f/f)/alpha MyHC-Cre) mice and analyzed their cardiac electrophysiology in vivo and in vitro. A high incidence (38%) of sudden death was found in alpha MyHC-FKBP12 mice. Surface and ambulatory ECGs documented cardiac conduction defects, which were further confirmed by electric measurements and optical mapping in Langendorff-perfused hearts. alpha MyHC-FKBP12 hearts had slower action potential upstrokes and longer action potential durations. Whole-cell patch-clamp analyses demonstrated an approximate to 80% reduction in peak density of the tetrodotoxin-resistant, voltage-gated sodium current I(Na) in alpha MyHC-FKBP12 ventricular cardiomyocytes, a slower recovery of I(Na) from inactivation, shifts of steady-state activation and inactivation curves of I(Na) to more depolarized potentials, and augmentation of late I(Na), suggesting that the arrhythmogenic phenotype of alpha MyHC-FKBP12 mice is attributable to abnormal I(Na). Ventricular cardiomyocytes isolated from FKBP12(f/f)/alpha MyHC-Cre hearts showed faster action potential upstrokes and a more than 2-fold increase in peak I(Na) density. Dialysis of exogenous recombinant FKBP12 protein into FKBP12-deficient cardiomyocytes promptly recapitulated alterations in I(Na) seen in alpha MyHC-FKBP12 myocytes.
Conclusions: FKBP12 is a critical regulator of I(Na) and is important for cardiac arrhythmogenic physiology. FKPB12-mediated dysregulation of I(Na) may underlie clinical arrhythmias associated with FK506 administration. (Circ Res. 2011;108:1042-1052.)

DOI： 10.1161/CIRCRESAHA.110.237867

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：WILEY-BLACKWELL  

Methods and Results: We simultaneously mapped Ca-i and membrane potential in 31 isolated Langendorff-perfused canine right atriums (RA). Isoproterenol increased heart rate and late diastolic Ca-i elevation (LDCAE) of the superior SAN, leading to consistent SAN automaticity in all 31 RAs. However, DAD-like diastolic depolarizations (DD) were transiently observed in 4 RAs during isoproterenol infusion. These DAD-like DDs were preceded by LDCAE, but did not trigger a full action potential. The LDCAE preceding DAD-like DDs had smaller amplitude (0.41 +/- 0.08 AU vs 0.48 +/- 0.07 AU, P = 0.001) and less steep slopes (3.7 +/- 1.3 AU/s vs 4.8 +/- 1.4 AU/s, P = 0.001) than that of sinus beats. The coupling interval of DAD-like DDs was longer than that of the preceding normal beats (407 +/- 48 ms vs 371 +/- 44 ms, P = 0.002).
Conclusion: The isoproterenol-induced LDCAE of superior SAN induced a full action potential in most cases. However, if the LDCAE was too small to trigger an action potential, then it induces only DAD-like DD. The failure of DAD-like DD to consistently trigger a sinus beat is a novel mechanism of atrial arrhythmogenesis. (J Cardiovasc Electrophysiol, Vol. 22, pp. 448-454).

DOI： 10.1111/j.1540-8167.2010.01905.x

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

BACKGROUND Whether autonomic nerve activity is important in the development of pacing-induced sustained atrial fibrillation (AF) is unclear.
OBJECTIVE The purpose of this study was to test the hypothesis that patterns of baseline autonomic nerve activity are important in the development of pacing-induced sustained AF.
METHODS Radiotransmitters were implanted in 12 ambulatory dogs to record left stellate ganglion nerve activity (SGNA) and vagal nerve activity (VNA). Sustained (&gt; 48 hours) AF was induced with intermittent rapid atrial pacing.
RESULTS At baseline (before pacing), 1-minute integrated nerve activity between SGNA and VNA demonstrated either a single linear relationship with excellent correlation (group 1, N = 3, r = 0.816 +/- 0.105) or nonlinear relationships with poor correlation (group 2, N = 9, r = 0.316 +/- 0.162, P &lt; .05 vs group 1). Group 1 dogs had higher VNA (97.0 +/- 11.5 mV-s) compared to group 2 (33.4 +/- 21.7 mV-s, P &lt; .001). Group 1 dogs had more frequent sympathovagal co-activation episodes than did group 2 (50 +/- 19 per day vs 15 +/- 6 per day, P &lt; .05) and more paroxysmal atrial tachycardia (PAT; 5 +/- 1 per day vs 2 +/- 1 per day, P &lt; .05) at baseline. Sustained AF occurred after 16 +/- 4 days (range 13-20 days) of pacing in group 1 and after 46 +/- 18 days (range 23-72 days) of pacing in group 2 (P &lt; .05). In the week before development of sustained AF, VNA of group 2 dogs was significantly increased compared to baseline (P &lt; .05).
CONCLUSION Ambulatory dogs with good linear sympathovagal correlation and higher vagal tone at baseline have more PAT episodes at baseline and faster induction of sustained AF by rapid pacing. Rapid atrial pacing increased the VNA of the remaining dogs before induction of sustained AF.

DOI： 10.1016/j.hrthm.2010.11.040

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：JAPANESE CIRCULATION SOC  

Background: Anodal stimulation hyPerpolarizes the cell membrane and increases the intracellular Ca(2+) (Ca) transient. This study tested the hypothesis that the maximum slope of the Cai decline (-(dCai/dt)(max)) corresponds to the timing of anodal dip on the strength-interval curve and the initiation of repetitive responses and ventricular fibrillation (VF) after a premature stimulus (S2).
Methods and Results: We simultaneously mapped the membrane potential (Vn) and Cai in 23 rabbit ventricles. A dip in the anodal strength interval curve was observed. During the anodal dip, ventricles Were captured by anodal break excitation directly under the S2 electrode. The Cai following anodal stimuli is larger than that following cathodal stimuli. The S1-S2 intervals of the anodal dip (203 +/- 10ms) coincided with the -(dCai/dt)(max) (199 +/- 10ms, P=NS). BAPTA-AM (n=3). inhibition of the electrogenic Na(+)-Ca(2+) exchanger current (/(Ncx)) by low extracellular Na(+) (n=3), and combined ryanodine and thapsigargin infusion (n=2) eliminated the anodal supernormality. Strong S2 during the relative refractory period (n=5) induced 29 repetitive responses and 10 VF episodes. The interval between S2 and the first non-driven beat was coincidental with the time of -(dCai/dt)(max).
Conclusions: Larger Cai transient and /(NCX) activation induced by anodal stimulation produces anodal supernormality. The time of maximum /(NCX) activation is coincidental to the induction of non-driven beats from the Cai sinkhole after a strong premature stimulation. (Circ J 2011: 75: 834-843)

DOI： 10.1253/circj.CJ-10-1014

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Rationale: Fibrillation/defibrillation episodes in failing ventricles may be followed by action potential duration (APD) shortening and recurrent spontaneous ventricular fibrillation (SVF).
Objective: We hypothesized that activation of apamin-sensitive small-conductance Ca2+-activated K+ (SK) channels is responsible for the postshock APD shortening in failing ventricles.
Methods and Results: A rabbit model of tachycardia-induced heart failure was used. Simultaneous optical mapping of intracellular Ca2+ and membrane potential (V-m) was performed in failing and nonfailing ventricles. Three failing ventricles developed SVF (SVF group); 9 did not (no-SVF group). None of the 10 nonfailing ventricles developed SVF. Increased pacing rate and duration augmented the magnitude of APD shortening. Apamin (1 mu mol/L) eliminated recurrent SVF and increased postshock APD(80) in the SVF group from 126 +/- 5 to 153 +/- 4 ms (P&lt;0.05) and from 147 +/- 2 to 162 +/- 3 ms (P&lt;0.05) in the no-SVF group but did not change APD(80) in nonfailing group. Whole cell patch-clamp studies at 36 degrees C showed that the apamin-sensitive K+ current (I-KAS) density was significantly larger in the failing than in the normal ventricular epicardial myocytes, and epicardial I-KAS density was significantly higher than midmyocardial and endocardial myocytes. Steady-state Ca2+ response of I-KAS was leftward-shifted in the failing cells compared with the normal control cells, indicating increased Ca2+ sensitivity of I-KAS in failing ventricles. The K-d was 232 +/- 5 nmol/L for failing myocytes and 553 +/- 78 nmol/L for normal myocytes (P = 0.002).
Conclusions: Heart failure heterogeneously increases the sensitivity of I-KAS to intracellular Ca2+, leading to upregulation of I-KAS, postshock APD shortening, and recurrent SVF. (Circ Res. 2011;108:971-979.)

DOI： 10.1161/CIRCRESAHA.110.238386

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Background-Both phase 2 and phase 3 early afterdepolarizations (EADs) occur in long-QT syndromes, but their respective roles in generating arrhythmias in intact cardiac tissue are incompletely understood.
Methods and Results-Intracellular Ca (Cai) and membrane voltage (V(m)) were optically mapped in a quasi 2-dimensional model of cryoablated Langendorff-perfused rabbit ventricles (n=16). E-4031 (an I(Kr) blocker) combined with reduced extracellular K ([K(+)](o)) and Mg ([Mg(2+)](o)) prolonged action potential duration heterogeneously and induced phase 2 and phase 3 EADs. Whereas phase 2 EADs were Cai-dependent, phase 3 EADs were not. The origins of 47 triggered activity episodes were attributed to phase 2 EADs in 12 episodes (26%) and phase 3 EADs in 35 episodes (74%). When phase 2 EADs accompanied phase 3 EADs, they accentuated action potential duration heterogeneity, creating a large Vm gradient across the boundary between long and short action potential duration regions from which triggered activity emerged. The amplitude of phase 3 EADs correlated with the V(m) gradient (r=0.898, P &lt; 0.001). Computer simulation studies showed that coupling of cells with heterogeneous repolarization could extrinsically generate phase 3 EADs via electrotonic current flow. Alternatively, reduced I(K1) caused by low [K(+)](o) could generate intrinsic phase 3 EADs capable of inducing triggered activity at the boundary zone.
Conclusions-Phase 3 EADs can be extrinsic as the result of electrotonic current across steep repolarization gradients or intrinsic as the result of low I(K1) and do not require spontaneous sarcoplasmic reticulum Ca release. Reduction of I(K1) by low [K(+)](o) strongly promotes ventricular arrhythmias mediated by phase 3 EADs in acquired long-QT syndrome caused by I(Kr) blockade. (Circ Arrhythm Electrophysiol. 2011;4:103-111.)

DOI： 10.1161/CIRCEP.110.959064

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

Objective: Ventricular tachycardia/fibrillation (VT/VF) can recur repeatedly after defibrillation (i.e. electrical storm). We tested the hypothesis that intracellular Ca2+ (Cai overload during VF and sensitivity of membrane voltage (Vm) to Cai (Cai-Vm coupling gain) is important for post-shock arrhythmias. Methods and Results: We simultaneously mapped Cai and Vm on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Cai elevation (SCaE) was noted after defibrillation in 32% of VT/VF at baseline, 83% during isoproterenol infusion. SCaE was reproducibly induced by rapid ventricular pacing and inhibited by ryanodine. We found triggered activities (TAs) originating from 6 of 14 endocardial surfaces but none from epicardial surfaces, despite similar SCaEs between epicardial and endocardial surfaces. This was because delayed afterdepolarizations induced by SCaEs were larger on endocardial surfaces due to higher Cai-Vm coupling gain. Purkinje-like potentials preceded the TAs. /K1 suppression with CsCl or BaCl2 enhanced Cai-Vm coupling gain and enabled epicardium to also generate TAs. Further enhancement of Cai overload and Cai-Vm coupling gain by low [K+]o induced post-shock VTs and spontaneous VF recurrences leading to electrical storm. Conclusions: Cai-Vm coupling gain is important for the genesis of post-shock VT/VF and electrical storm. Purkinje fibers serve as arrhythmogenic substrate because of its higher Cai-Vm coupling gain. /K1 is a major determinant for Cai-Vm coupling gain. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.OP16_5

Scopus

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：AMER PHYSIOLOGICAL SOC  

Shinohara T, Park HW, Han S, Shen MJ, Maruyama M, Kim D, Chen PS, Lin SF. Ca2+ clock malfunction in a canine model of pacing-induced heart failure. Am J Physiol Heart Circ Physiol 299: H1805-H1811, 2010. First published October 1, 2010; doi:10.1152/ajpheart.00723.2010.-The mechanisms of sinoatrial node (SAN) dysfunction in heart failure (HF) remain unclear. We hypothesized that impaired rhythmic spontaneous sarcoplasmic reticulum Ca2+ release (Ca2+ clock) plays an important role in SAN dysfunction in HF. HF was induced in canine hearts by rapid ventricular pacing. The location of pacemaking sites was determined in vivo using computerized electrical mapping in acute open-chest preparations (normal, n = 3; and HF, n = 4). Isoproterenol (Iso, 0.2 mu g . kg(-1) . min(-1)) infusion increased heart rate and shifted the pacemaking site to the superior SAN in all normal hearts. However, in failing hearts, Iso did not induce superior shift of the pacemaking site despite heart rate acceleration. Simultaneous optical recording of intracellular Ca2+ and membrane potential was performed in Langendorff- perfused isolated right atrium (RA) preparations from normal (n = 7) and failing hearts (n = 6). Iso increased sinus rate, enhanced late diastolic Ca2+ elevation (LDCAE), and shifted the pacemaking sites to the superior SAN in all normal but in none of the HF RAs. Caffeine (2 ml, 20 mmol/l) caused LDCAE and increased heart rate in four normal RAs but in none of the three HF RAs. Iso induced ectopic beats from lower crista terminalis in five of six HF RAs. These ectopic beats were suppressed by ZD-7288, a specific pacemaker current (I-f) blocker. We conclude that HF results in the suppression of Ca2+ clock, resulting in the unresponsiveness of superior SAN to Iso and caffeine. HF also increases the ectopic pacemaking activity by activating the I-f at the latent pacemaking sites in lower crista terminalis.

DOI： 10.1152/ajpheart.00723.2010

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

Objectives
The purpose of this study was to test the hypothesis that rhythmic spontaneous sarcoplasmic reticulum calcium (Ca) release (the "Ca clock") plays an important role in atrioventricular junction (AVJ) automaticity.
Background
The AVJ is a primary backup pacemaker to the sinoatrial node. The mechanisms of acceleration of AVJ intrinsic rate during sympathetic stimulation are unclear. Methods We simultaneously mapped transmembrane potential and intracellular Ca in Langendorff-perfused canine AVJ preparations that did not contain sinoatrial node (n = 10).
Results
Baseline AVJ rate was 37.5 +/- 4.0 beats./min. The wavefront from leading pacemaker site propagated first through the slow pathway, then the fast pathway and atria. There was no late diastolic Ca elevation (LDCAE) at baseline. Isoproterenol up to 3 mu mol./l increased heart rate to 100 +/- 6.8 beats./min, concomitant with the appearance of LDCAE that preceded the phase 0 of action potential by 97.3 +/- 35.2 ms and preceded the onset of late diastolic depolarization by 23.5 +/- 3.5 ms. Caffeine also produced LDCAE and AVJ acceleration. The maximal slope of LDCAE and diastolic depolarization always colocalized with the leading pacemaker sites. Ryanodine markedly slowed the rate of spontaneous AVJ rhythm. Isoproterenol did not induce LDCAE in the presence of ryanodine. The If blocker ZD 7288 did not prevent LDCAE or AVJ acceleration induced by isoproterenol (n = 2).
Conclusions Isoproterenol and caffeine induced LDCAE and accelerated intrinsic AVJ rhythm. Consistent colocalization of the maximum LDCAE and the leading pacemaker sites indicates that the Ca clock is important to the intrinsic AVJ rate acceleration during sympathetic stimulation. (J Am Coll Cardiol 2010; 56: 805-12) (C) 2010 by the American College of Cardiology Foundation

DOI： 10.1016/j.jacc.2010.03.070

Web of Science

PubMed

researchmap

記述言語：英語   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

DOI： 10.1161/CIRCEP.110.936385

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Rationale: Recurrent ventricular arrhythmias after initial successful defibrillation are associated with poor clinical outcome.
Objective: We tested the hypothesis that postshock arrhythmias occur because of spontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) from tissues with high sensitivity of resting membrane voltage (V(m)) to elevated intracellular calcium (Ca(i)) (high diastolic Ca(i)-voltage coupling gains).
Methods and Results: We simultaneously mapped Ca(i) and V(m) on epicardial (n = 14) or endocardial (n = 14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Ca(i) elevation (SCaE) was noted after defibrillation in 32% of ventricular tachycardia/ventricular fibrillation at baseline and in 81% during isoproterenol infusion (0.01 to 1 mu mol/L). SCaE was reproducibly induced by rapid ventricular pacing and inhibited by 3 mu mol/L of ryanodine. The SCaE amplitude and slope increased with increasing pacing rate, duration, and dose of isoproterenol. We found TAs originating from 6 of 14 endocardial surfaces but none from epicardial surfaces, despite similar amplitudes and slopes of SCaEs between epicardial and endocardial surfaces. This was because DADs were larger on endocardial surfaces as a result of higher diastolic Ca(i)-voltage coupling gain, compared to those of epicardial surfaces. Purkinje-like potentials preceded TAs in all hearts studied (n = 7). I(K1) suppression with CsCl (5 mmol/L, n = 3), BaCl(2) (3 mu mol/L, n = 3), and low extracellular potassium (1 mmol/L, n = 2) enhanced diastolic Ca(i)-voltage coupling gain and enabled epicardium to also generate TAs.
Conclusions: Higher diastolic Ca(i)-voltage coupling gain is essential for genesis of TAs and may underlie postshock arrhythmias arising from Purkinje fibers. I(K1) is a major factor that determines the diastolic Ca(i)-voltage coupling gain. (Circ Res. 2010; 106: 399-408.)

DOI： 10.1161/CIRCRESAHA.109.211292

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

BACKGROUND Recent evidence indicates that spontaneous sarcoplasmic reticulum (SR) calcium (Ca) release underlies the mechanism of sinoatrial node (SAN) acceleration during beta-stimulation, indicating the importance of the Ca clock in SAN automaticity. Whether or not the same mechanism applies to atrial ectopic pacemakers (AEPs) remains unclear.
OBJECTIVE The purpose of this study was to assess the mechanism of AEP.
METHODS We simultaneously mapped intracellular calcium(Ca(i)) and membrane potential in 12 isolated canine right atria. The late diastolic Ca(i) elevation (LDCAE) was used to detect the Ca clock activity. Pharmacological interventions with isoproterenol (ISO), ryanodine, and ZD7288, a blocker of the I(f) membrane current, were performed.
RESULTS Ryanodine, which inhibits SR Ca release, reduced LDCAE in SAN, resulting in an inferior shift of the pacemaking site. Cycle length increased significantly in a dose-dependent way. In the presence of 3 to 10 mu mol/l of ryanodine, ISO infusion consistently induces AEPs from the lower crista terminalis. All ectopic beats continuing over 30 seconds were located at the lower crista terminalis. These AEPs were resistant to ryanodine treatment even at high doses. Subsequent blockade of I(f) inhibited the AEP and resulted in profound bradycardia.
CONCLUSION Spontaneous SR Ca release underlies ISO-induced increase of superior SAN activity. As compared with SAN, the AEP is less dependent on the Ca clock and more dependent on the membrane clock for its automaticity. AEPs outside the SAN can effectively serve as backup pacemakers when the Ca clock functionality is reduced.

DOI： 10.1016/j.hrthm.2009.09.068

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

BACKGROUND The mechanism of sinoatrial node (SAN) dysfunction in atrial fibrillation (AF) is unclear.
OBJECTIVE The purpose of this study was to test the hypothesis that defective spontaneous sarcoplasmic reticulum (SR) Ca(2+) release (Ca(2+) clock) is in part responsible for SAN dysfunction in AF.
METHODS Arrhythmic events and SAN function were evaluated in pacing-induced AF dogs (n = 7) and in normal dogs (n = 19) with simultaneous intracellular calcium (Cai) and membrane potential recording.
RESULTS AF dogs had frequent sinus pauses during Holter monitoring. Isolated right atrium (RA) from AF dogs showed slower heart rate (P = .001), longer SAN recovery time (P = .001), and longer sinoatrial conduction time (P = .003) than normal. In normal RAs, isoproterenol 0.3 and 1 mu mol/L increased heart rate by 96% and 105%, respectively. In contrast, in RAs from AF dogs, isoproterenol increased heart rate by only 60% and 72%, respectively. Isoproterenol induced late diastolic Cai elevation (LDCAE) at superior SAN in all 19 normal RAs but in only 3 of 7 AF RAs (P = .002). In AF RAs without LDCAE (n = 4), heart rate increased by the acceleration of ectopic foci. Caffeine (20 mmol/L) injection increased heart rate with LDCAE in all 6 normal RAs but did not result in LDCAE in any of the 5 AF RAs (P = .002). Type 2 ryanodine receptor (RyR2) in the superior SAN of AF dogs was decreased to 33% of normal (P = .02).
CONCLUSION SAN dysfunction in AF is associated with Ca(2+) clock malfunction, characterized by unresponsiveness to isoproterenol and caffeine and down-regulation of RyR2 in SAN.

DOI： 10.1016/j.hrthm.2009.09.018

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Background-Recent evidence indicates that membrane voltage and Ca(2+) clocks jointly regulate sinoatrial node (SAN) automaticity. Here we test the hypothesis that sinus rate acceleration by beta-adrenergic stimulation involves synergistic interactions between these clock mechanisms.
Methods and Results-We simultaneously mapped intracellular calcium (Ca(i)) and membrane potential in 25 isolated canine right atrium, using previously described criteria of the timing of late diastolic Ca(i) elevation (LDCAE) relative to the action potential upstroke to detect the Ca(2+) clock. Before isoproterenol, the earliest pacemaking site occurred in the inferior SAN, and LDCAE was observed in only 4 of 25 preparations. Isoproterenol infusion (1 mu mol/L) increased sinus rate and shifted pacemaking site to superior SAN, concomitant with the appearance of LDCAE preceding the action potential upstroke by 98 +/- 31 ms. Caffeine had similar effects, whereas sarcoplasmic reticulum Ca(2+) depletion with ryanodine and thapsigargin prevented isoproterenol-induced LDCAE and blunted sinus rate acceleration. Ca(i) transient relaxation time during isoproterenol was shorter in superior SAN (124 +/- 34 ms) than inferior SAN (138 +/- 24 ms; P=0.01) or right atrium (164 +/- 33 ms; P=0.001) and was associated with a lower sarcoplasmic reticulum Ca(2+) ATPase pump to phospholamban protein ratio in SAN than in right atrium. Hyperpolarization-activated pacemaker current (I(f)) blockade with ZD 7288 modestly blunted but did not prevent LDCAE or sinus rate acceleration by isoproterenol.
Conclusions-Acceleration of the Ca(2+) clock in the superior SAN plays an important role in sinus acceleration during beta-adrenergic stimulation, interacting synergistically with the voltage clock to increase sinus rate. (Circulation. 2009;119:788-796.)

DOI： 10.1161/CIRCULATIONAHA.108.817379

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：BLACKWELL PUBLISHING  

Introduction: Despite recent advances in clinical electrophysiology, diagnosis of atrial tachycardia (AT) originating near Koch's triangle remains challenging. We sought a novel technique for rapid and accurate diagnosis of AT in the electrophysiologic laboratory.
Methods: Sixty-two supraventricular tachycardias including 18 ATs (10 ATs arising from near Koch's triangle), 32 atrioventricular nodal reentrant tachycardias (AVNRTs), and 12 orthodromic reciprocating tachycardias (ORTs) were studied. Overdrive pacing during the tachycardia from different atrial sites was performed, and the maximal difference in the postpacing VA intervals (last captured ventricular electrogram to the earliest atrial electrogram of the initial beat after pacing) among the different pacing sites was calculated (delta-VA interval).
Results: The delta-VA intervals were &gt; 14 ms in all AT patients and &lt; 14 ms in all AVNRT/ORT patients, and thus, the delta-VA interval was diagnostic for AT with the sensitivity, specificity, and positive and negative predictive values all being 100%. When the diagnostic value of the delta-VA interval and conventional maneuvers were compared for differentiating AT from atypical AVNRT, both a delta-VA interval &gt; 14 ms and "atrial-atrial-ventricular" response after overdrive ventricular pacing during the tachycardia were diagnostic. However, the "atrial-atrial-ventricular" response criterion was available in only 52% of the patients because of poor ventriculoatrial conduction.
Conclusions: The delta-VA interval was useful for diagnosing AT irrespective of patient conditions such as ventriculoatrial conduction.

DOI： 10.1111/j.1540-8167.2007.00928.x

Web of Science

PubMed

researchmap

記述言語：日本語   出版者・発行元：(一社)日本循環器学会  

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

BACKGROUND Because the anatomic features of the cavotricuspid isthmus (CTI) are complex, radiofrequency (RF) energy requirements for CTI ablation may vary at each point within the CTI. Conventionally, multiple-site mapping has been required for determining CTI conduction block.
OBJECTIVES The purpose of this study was to develop a more efficacious method for ablation of isthmus-dependent atrial flutter.
METHODS Forty consecutive patients underwent CTI ablation using a CTI mapping-guided approach (20 patients) or a conventional approach (20 patients). In the CTI mapping-guided approach, an octapolar catheter was positioned on the CTI parallel to, and downstream from, the intended ablation tine in order to map and ablate the breakthrough point.
RESULTS Complete CTI block was achieved in all study patients. CTI mapping of incomplete ablation tines revealed that the site with the shortest interval between double potentials did not always coincide with the conduction gap. Disappearance of a breakthrough pattern on the CTI electrograms corresponded to creation of complete CTI block. During ablation, CTI mapping exhibited pseudo-CTI block in 8% of patients in the clockwise direction and 63% of patients in the counterclockwise direction. The number and total time of RF applications were significantly tower with the CTI mapping-guided approach than with the conventional approach (7.7 +/- 3.9 applications vs 13.8 +/- 8.9 applications and 8.9 +/- 4.4 minutes vs 16.3 +/- 11.9 minutes, respectively, P &lt; .05). In the CTI mapping-guided approach, RF applications were not required along the entire CTI in 7 patients (35%).
CONCLUSION This simplified technique was feasible for creating and determining complete CTI block, with fewer RF applications required.

DOI： 10.1016/j.hrthm.2006.02.008

Web of Science

PubMed

researchmap

記述言語：日本語   出版者・発行元：The Medical Association of Nippon Medical School  

Cholesterol crystal embolism (CCE) is a systemic disorder caused by microshowers of cholesterol crystals. It brings about decreased microcirculation and is manifested in various organs including the kidneys, skin, brain and extremities. Cholesterol microshowers are thought to occur in about 50% of invasive vascular procedures, but most cases are clinically silent. CCE has a high mortality rate, but there are as yet no established methods for managing it. We report two cases (63-year-old and 73-year-old males) of progressive renal insufficiency with eosinophilia and peripheral ischemic symptoms such as livedo reticularis and foot pain following percutaneous coronary intervention (PCI) for acute myocardial infarction. In the first case, we made a diagnosis of CCE based on clinical findings, which included deteriorating renal failure after PCI, peripheral eosinophilia, livedo reticularis, smoking history, uncontrollable hypertension, and severe atherosclerotic plaque of the aorta demonstrated by transesophageal echocardiography. In the second case, skin biopsy specimens confirmed a diagnosis of CCE. In both cases, treatment with prostaglandins and statins was unsatisfactory. However, additional treatment with LDL apheresis (LDL-A) and corticosteroids improved the eosinophillia, livedo reticularis, foot pain and renal function, suggesting that this combined treatment may have a beneficial effect on CCE.<br>

DOI： 10.1272/manms.2.115

CiNii Books

researchmap

その他リンク： https://jlc.jst.go.jp/DN/JALC/00277693950?from=CiNii

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

Background Atrial tachycardia (AT) can originate from the proximal coronary sinus (CS). However, detailed electrophysiologic characteristics of the tachycardia are not available.
Objectives We describe the electrophysiologic characteristics, response to adenosine 5'-triphosphate, and results of radiofrequency ablation of AT with the earliest activation in the proximal CS.
Methods In 7 of 54 patients (age 57 +/- 18 years) with nonmacroreentrant "focal" AT undergoing electrophysiologic study and radiofrequency ablation, the earliest atrial activation site was located in the proximal CS.
Results The earliest activation site was inside the CS 13 +/- 3 mm from the ostium. The AT could be induced and terminated by atrial extrastimuli or burst pacing. In all patients, the AT was also terminated by a very small dose of adenosine 5'-triphosphate (4.2 +/- 1.1 mg). Rapid ventricular pacing during the tachycardia produced ventriculoatrial dissociation. Radiofrequency ablation directed at the earliest atrial activation site was effective in only three patients (group A). In the remaining four patients (group 13), after the radiofrequency energy deliveries, the earliest activation site shifted to an adjacent site with a small increase in the cycle length. Three group B patients underwent successful ablation in the slow pathway region. No recurrence was observed over a follow-up period of 22 +/- 5 months.
Conclusion AT with earliest activation in the proximal CS is sensitive to a small dose of adenosine 5'-triphosphate. In some patients, radiofrequency applications in the slow pathway region are effective even if the local activation is not early.

DOI： 10.1016/j.hrthm.2005.08.030

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

To test the hypothesis that the reverse mode of the Na+/Ca2+ exchange augmented by a rapid heart rate has an antiarrhythmic effect by shortening the action potential duration, we examined the effects of KB-R7943 (2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl] isothiourea methanesulfonate), a selective inhibitor of the reverse mode of the Na+/Ca2+ exchange, to attenuate this effect. We recorded the electrocardiogram, monophasic action potential (MAP), and left ventricular pressure in canine beating hearts. In comparison to the control, KB-R7943 significantly increased the QTc value and MAP duration. MAP alternans and left ventricular pressure alternans were observed after changing the cycle length to 300 milliseconds in the control studies. KB-R7943 magnified both types or alternans and produced spatially discordant alternans between tight and left ventricles. Early after-depolarizations and nonsustained ventricular tachycardia occurred in the presence or KB-R7943. Our data suggest that the reverse mode of the Na+/Ca2+ exchange may contribute to suppression of arrhythmias by abbreviating action potential duration under pathophysiological conditions. This conclusion is based on further confirmation by future studies of the specificity of KB-R7943 for block of the reverse mode of the Na+/Ca2+ exchange. (c) 2005 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2004.12.001

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：JAPANESE CIRCULATION SOCIETY  

Background Atrial fibrillation, is a progressive disease, which in the paroxysmal form (PAF) becomes more frequent and finally becomes chronic (CAF). A retrospective analysis of patients with PAF was conducted to examine the hypothesis that angiotensin-converting enzyme inhibitors (ACEI) will prevent the progression to CAF.
Methods and Results On the basis of their treatment, 95 patients with PAF were divided into 2 groups: 42 patients treated with ACEI for hypertension throughout the period of treatment and follow-up (ACEI group) and 53 patients not given ACEI (non-ACEI group). Cardiac rhythms were assessed either from the medical records or the electrocardiograms recorded every 2-4 weeks at follow-up visits. The mean follow-up time was 8.3 +/- 3.5 years. There was no significant difference in the use of antiarrhythmic drugs, left atrial diameter or left ventricular ejection fraction between the 2 groups. The Kaplan-Meier curve for the time to occurrence of CAF showed a lower incidence of CAF in the ACEI group and demonstrated that the 5-year probability for persistence of PAF without progression to CAF was 88.3%, but 47.5% in the non-ACEI group.
Conclusions These results indicate that ACEI will prevent progression from PAF to CAF.

DOI： 10.1253/circj.69.671

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

Introduction: Due to the difficulty in performing detailed mapping around the tricuspid annulus and the high occurrence of mechanical trauma during the procedure, the outcome of right-sided accessory pathway (AP) ablation still has a relatively high primary failure and recurrence rate. Methods and Results: Six patients with right free-wall APs underwent electroanatomical mapping. The AP had retrograde unidirectional conduction in 3 patients, anterograde unidirectional conduction in 1 patient, and bidirectional conduction in 2 patients. The right atrial (RA) activation map was constructed during right ventricular (RV) pacing (n = 5), and the RV activation map was constructed during RA pacing (n = 3). During mapping, the AP conduction was interrupted by catheter mechanical trauma in 3 patients. The first RF application successfully eliminated the AP conduction within 2 seconds in 3 patients with concealed pathways. In the remaining 3 patients, rescue RF energy was delivered at the tagged bump site on the map. The mean procedure time was 214 ± 77 minutes, and mean fluoroscopy time 63 ± 23 minutes. No recurrence occurred during 12 ± 3.2 months of follow-up in any of the patients. Conclusions: With the guidance of an electroanatomical mapping system, right-sided accessory pathways can be satisfactorily eliminated without later recurrence. © 2005, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.21.459

Scopus

researchmap

記述言語：日本語   出版者・発行元：日本医科大学医学会  

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）  

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：BLACKWELL FUTURA PUBLISHING, INC  

Unusual manifestations of the mode of termination were observed in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). After administration of verapamil during AVNRT isorhythmic atrioventricular dissociation occurred without termination of the tachycardia. The sinus rate was slightly faster than that of the AVNRT, leading to the P wave preceding the QRS complex with a normal PR interval (e.g., pseudotermination). This phenomenon emphasizes the importance of continuous monitoring during an attempt to terminate AVNRT.

DOI： 10.1111/j.1540-8159.2003.00374.x

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

We investigated the role of the sarcoplasmic reticulum's (SR) Ca2+ pump function of the in the mechanism of alternans. We recorded the surface ECG, monophasic action potential (MAP) and left ventricular pressure (LVP) in the canine beating heart. Alternans was induced with an abrupt shortening of the cycle length from 1000 to 350 ms. After the control studies, we administered propranolol or isoproterenol. In the presence of propranolol, we administered milrinone or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In the presence of isoproterenol, we administered thapsigargin. Isoproterenol and milrinone attenuated both the electrical and mechanical alternans. Thapsigargin, a specific SR Ca2+ pump inhibitor, and propranolol magnified both types of alternans. DIDS, a Ca2+-activated Cl- current (I-Cl(Ca)) inhibitor, attenuated the MAP alternans without an affect on the LVP alternans. Thus, the delayed intracellular Ca2+ cycling caused by the impaired SR Ca2+ pump function might produce electrical and mechanical alternans. beta-adrenergic stimulation eliminated these alternans. The I-Cl(Ca) contributed to the appearance of the electrical alternans.

DOI： 10.1054/jelc.2003.50021

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

We sought to characterize the electrical activity within the persistent left superior vena cava (LSVC), which normally becomes the ligament of Marshall (LOM) that is known to be related to the genesis of atrial tachyarrhythmias. A 20-pole electrode catheter was used to record the entire activation sequence in the LSVC in a patient with Wolff-Parkinson-White syndrome. Electrical activity representing the musculature of the LSVC could be recorded up to a level as high as the pulmonary artery. Multiple electrical connections between the LSVC and left atrium were shown, and one of the connections exhibited unidirectional conduction block. It might be important to take into account the presence of multiple electrical connections when we consider the LOM as a target for radiofrequency catheter ablation or its role in clinical arrhythmias.

DOI： 10.1054/jelc.2003.50004

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：FUTURA PUBL CO  

A 52-year-old man with a history of vasospastic angina experienced a severe ischemic episode accompanied by a non-Q wave myocardial infarction. Two episodes of ventricular fibrillation (VF) occurred during the acute phase of the event. Osborn waves were observed on the ECG preceding each episode of VF. In the second episode, the gradual development of Osborn waves until VF occurred was confirmed on ECG. The Osborn waves appeared to be related to the occurrence of VF. This case may provide clinical evidence that a prominent It. participates in the development of VF during myocardial ischemia.

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：FUTURA PUBL CO  

The exact reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) remains unclear. This case report demonstrates the reentrant circuit of ILVT. A 20-pole electrode catheter was placed along the left posterior fascicle during electrophysiologic study. ILVT was reproducibly induced by programmed ventricular stimulation. During the tachycardia, sequential diastolic potentials bridging the entire diastolic period were observed in the recordings from the electrodes positioned from left ventricular mid-septum to inferoapical septum. The slow conduction zone appeared to be composed of a false tendon in this patient. Entrainment of the ILVT from the right ventricular outflow tract at a different pacing cycle length revealed that a dominant conduction delay occurred at the proximal site of the slow conduction zone. Entrainment studies from several sites on the left ventricular septum confirmed that these sites where sequential electrical activity was recorded were included within the reentrant circuit. However, the left posterior fascicle itself seemed to be a bystander. This report provides the direct evidence of macroreentry as the underlying mechanism of this ILVT, adjacent to the left posterior fascicle.

Web of Science

PubMed

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Web of Science

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Web of Science

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Web of Science

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Web of Science

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Web of Science

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Web of Science

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS  

Web of Science

researchmap

記述言語：日本語   出版者・発行元：臨床心臓電気生理研究会  

症例は23歳、男性。動悸発作の精査加療目的にEPSを施行。洞調律時、V1で±、III・aVFで陽性のデルタ波を認めた。心房刺激周期短縮とともにQRS幅の増大とAV間隔の延長を認め、減衰伝導特性を有する副伝導路と診断。副伝導路を順行、房室結節を逆行する右脚ブロック型の房室回帰性頻拍(AVRT)が誘発された。CARTO systemを用いCSペーシング中に左室をマッピング。心室波の最早期部位は僧帽弁輪から約15mmの中中隔、His束電位記録部位から10mm下方に位置していた。後中隔弁輪部から心室波の最早期部位にかけて15mmにわたりMahaim束電位(MP)が記録され、MP記録部位心尖部端は左脚後枝電位記録部位と15mm離れていた。弁輪部のMP記録部位での通電で焼灼に成功した。走行を詳細にマッピングしえた左側atrio-ventricular Mahaim束の1例を経験したので報告する。(著者抄録)

J-GLOBAL

researchmap

記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：ELSEVIER SCIENCE INC  

Web of Science

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

症例は合併奇形のない修正大血管転位の36歳、女性。動悸発作のため電気生理学的検査を施行。解剖学的左室刺激で減衰伝導特性を有し冠状静脈洞(CS)入口部が最早期の室房伝導を認めた。順行伝導は2重伝導特性を認めなかった。イソプロテレノール投与下、右室2連期外刺激で周期340msecのlong R-P&#039;頻拍が誘発。頻拍中の心房興奮順序は心室ペーシング時と変化なくヒス束不応期中の心室早期刺激によりリセットされないことより非通常型房室結節リエントリー性頻拍と診断。解剖学的左室刺激中の心房最早期興奮部位であるCS入口部付近の通電で心房興奮順序が変化し頻拍は誘発されなくなった。残存した弱い逆行伝導は右心耳の入口部付近が最早期興奮部位であった。修正大血管転位では前房室結節伝導路(anterior node)と後房室結節伝導路(posterior node)があり通常後者は機能しない。本症例の房室結節リエントリー性頻拍はposterior nodeが関与し、anterior nodeを介する逆行伝導が残存したと考えられる。非通常型房室結節リエントリー性頻拍を合併した修正大血管転位の報告例はなく、考察を加え報告する。(著者抄録)

DOI： 10.11281/shinzo1969.40.Supplement4_5

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本循環器学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：臨床心臓電気生理研究会  

症例は71歳、男性。心筋梗塞(後下壁)に対するCABG後、多形性VTとVFを繰り返したためCARTOシステムを用いて左室マッピングを施行。下・後壁〜中隔低の広範囲でQRSに先行するPurkinje電位(PP)が記録され、VT・VFのトリガーとなる3種類のVPCはすべてPurkinje起源であった。PPを選択的に捕捉する2〜3連期外刺激を行うとVTは容易に誘発された。周期270msecのPP捕捉3連刺激中のQRS波形は、1拍目がVPC#3,2拍目がVPC#1に類似し、3拍目はVPC#2波形となりVTが誘発された。また、VPC連発でもVTは開始され、連発中PPはQRSに先行、QRS波形が変化しながらVTに移行した。一方、PP非記録部位の刺激ではVT誘発は困難であった。PP記録部位を広範囲に焼灼したところVPCは消失し、VT誘発性も低下した。VPC連発や連続刺激中のPurkinje網内での伝導時間・伝導方向の変化がVT開始機序として重要であることが示唆された。(著者抄録)

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

DOI： 10.11281/shinzo1969.40.Supplement1_4

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

症例は38歳、男性。2005年末より労作時呼吸困難を自覚、2006年2月脳梗塞にて近医入院し、同時に高度徐脈(心拍数30bpm台)を認めたため当院転院。12誘導心電図ではP波を同定し得ず、心エコードプラ法で左房収縮は検出されなかった(EFは62%と正常)。心内電位上、冠静脈洞で50bpmの自発興奮が記録されたが心房内でブロックのため心室は37bpmの接合部調律であった。CARTOシステムを用いたマッピングにおいて右房は中隔の一部を除き広範なscarを示し部分的心房静止と診断。至適ペーシング部位は右房になく、かろうじて左房後壁からのペーシングが可能だった。ペースメーカー植え込み時には開胸下に左房後壁に心房リードを留置し心房-心室順次ペーシングを行った。術後の経胸壁心臓ドプラ法では心房波を認めるようになった。切除した右心耳の組織検査では正常心筋組織は認められず広範な線維化を認めた。CARTOシステムを用いたマッピングの所見を参考に生理的ペースメーカー植え込みが可能であった部分的心房静止の1例を経験したので報告する。(著者抄録)

DOI： 10.11281/shinzo1969.39.Supplement4_22

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

症例は32歳、男性。特記すべき既往や家族歴はない。3年前より冷水を嚥下中に眩暈を伴う動悸を自覚することがあった。誘因なく動悸が頻回に出現するようになり精査のため前医に入院した。心電図では発作性心房細動のほか、自然停止する多形性心室頻拍(polymorphic ventricular tachycardia;PVT)が頻発し、リドカイン静注でPVTは消失した。その後精査加療のため本院に転院した。12誘導心電図では下壁誘導にJ波を伴うST上昇を認めた。心エコー、冠動脈造影、心筋SPECTでは異常なく、運動負荷試験で立位時にV2,V3誘導のSTが上昇し1肋間上げたV2誘導でcoved型ST上昇を認めた。ST上昇は運動時に軽減、運動後に増強しBrugada症候群と診断した。本例では前胸部誘導でも潜在的なST上昇が認められ、また、前医でみられた多形性心室頻拍は初期数拍から最大15拍目まで同一パターンを示していた。この症例に特異的な再分極の空間的不均一性が存在することが示唆され、稀な症例であると考えられたため報告する。(著者抄録)

DOI： 10.11281/shinzo1969.39.11_992

researchmap

その他リンク： http://search.jamas.or.jp/link/ui/2008074087

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：臨床心臓電気生理研究会  

症例は60歳、男性。心筋梗塞に合併した心室頻拍(VT)に対して40歳時に心内膜切除術を施行した。今回、右脚ブロック上方軸偏位型のVT(370msec)が頻発し心臓電気生理検査を施行。VT中の左室マッピングでは、瘤下壁端と健常心筋との境界を最早期とする巣状興奮パターンを示し、最早期部位(s-QRS:330msec)から瘤前壁(s-QRS:100msec)にかけてpost pacing間隔が頻拍周期に一致したconcealed entrainmentを認めるisolated potentialを追えた。最早期部位と瘤前壁との間では、最早期から順行する興奮と最遅延部位から最早期に向かう電位のdouble potentialが記録された。後者は刺激で捕捉されず心外膜側の興奮を反映、最早期部位は心外膜から心内膜側へのbreakthroughと考えられた。瘤前壁のisolated potential記録部位での高周波通電でVTは根治できた。【総括】心外膜側残存心筋と瘤瘢痕内残存心筋を含むマクロリエントリーであった心内膜切除術後心室頻拍の1例を報告した。(著者抄録)

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本循環器学会  

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本循環器学会  

J-GLOBAL

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：(株)ライフ・サイエンス  

症例1は88歳女で、持続性VTに対してアミオダロンを150mg/日で開始するとともにICD植え込み術を施行した。アミオダロン開始後8ヵ月時に頻回のICD作動を認めたため、同薬を200mg/日に増量した。その約1年後、全身倦怠感が出現し、入院となった。GOT高値(800IU/L)を認めたためアミオダロンを150mg/日まで減量したところGOT値は低下し、150mg/日を継続しながら退院となった。退院1ヵ月後に腹囲の増大傾向を認め、その2ヵ月後には意識障害が出現し、再入院となった。諸検査によりアミオダロンが原因の肝機能障害と診断した。腹部CT検査では大量の腹水とともに肝萎縮が認められ、肝不全の状態を呈していた。各種治療に反応せず、入院後約1ヵ月で死亡した。症例2は61歳女で、拡張型心筋症に伴う持続性VTに対してICD植え込み術を施行し、2年後、VTが頻発するようになったためアミオダロン200mg/日の投与を開始した。その5年後、GOT高値(300IU/L)を認め、入院となった。諸検査によりアミオダロンが原因の肝機能障害と診断した。肝不全を示唆する所見は認めず、アミオダロンを中止したところ肝機能は正常化した。

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

症例は74歳、女性。難治性の閉塞性肥大型心筋症に対し経皮的中隔心筋焼灼術を施行。術後一過性に完全房室ブロックとなったが、その後もPR時間延長を伴う右脚ブロックが見られたため電気生理学検査を行った。検査時、洞周期は一定だったが、著明なHV時間の一心拍ごとの交互変化が見られた(90⇔190msec)。心房頻回刺激では刺激周期の短縮に伴いHV時間が正常化し、刺激周期350msecでAHブロックが起きるまで1対1房室伝導を示した。洞調律中に心房期外刺激を加えるとH1H2 900msec以上ではH1H2延長に伴いH2V2が延長し、H1H2 550〜900msecではH2V2は54msecで一定だったが、H1H2 540msec以下ではH1H2短縮に伴いH2V2は再び進行性に延長した。Overdrive suppressionにより一過性に洞周期を延長させるとHVブロックが出現した。propranolol 2mgを静注したところHV時間は正常化し、またH1H2時間に伴う変化も抑制された。本症例の所見から、ヒトの病的刺激伝導系における第4相ブロックの機序につき考察した。(著者抄録)

DOI： 10.11281/shinzo1969.38.Supplement4_95

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(NPO)日本小児循環器学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(株)ライフ・サイエンス  

拡張型心筋症22例をアミオダロン投与群(7例)と非投与群に分け,単球のケモカイン(MPC-1,IL-8)産生量を比較した.投与群でのみMPC-1,IL-8が有意に減少し,心機能が有意に改善された.さらに投与群では心不全の一指標とされるTNF-αの有意な減少が認められた

researchmap

記述言語：日本語   出版者・発行元：臨床心臓電気生理研究会  

症例は68歳,男性.陳旧性下壁梗塞による心不全で入院し,QRS幅140msecの右脚ブロック+上方軸偏位型の単形性心室性期外収縮(VPC)をトリガーとする単形性心室頻拍(VT)を繰り返した.Electroanatomical mapping(EAM)を用いたVPC中の左室マッピングでは,下壁・後壁から中隔にかけて広範囲に低電位領域を認め,その約1/2の領域でQRSより先行するPurkinje potential(PP)が記録された.VPCのactivationは下壁中部のPP最早期部位から低電位領域内のPP記録部位を心尖部・後壁および中隔方向に速やかに伝播し,最後に下壁基部のPP非記録部位が興奮するパターンを示した.左室のほとんどの領域でQRS波のonsetから50msec以内に心室波の興奮を認めた.PP異常興奮の連発によりPP-V間隔の延長と軸偏位を伴いVTが開始し,連発によるPurkinje network内での伝導遅延や一方向性ブロックの発生がVT開始の機序であることが示唆された(著者抄録)

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

J-GLOBAL

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

DOI： 10.11281/shinzo1969.38.supplement1_10

CiNii Research

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

74歳女.70歳時に僧帽弁置換術と慢性心房細動に対するradial手術を施行されたが,術後2ヵ月より周期220msの心房頻拍(AT)が持続したため心臓電気生理学的検査(EPS)目的で入院となった.EPSではAT中,冠静脈洞(CS)の興奮順序は遠位から近位であり,CS内広範囲でpost-pacing interval(PPI)が頻拍周期とほぼ一致するconcealed entrainment(CE)を認めたことから僧帽弁輪を回旋するATと考えられた.左房後壁切開線に接合する僧帽弁輪部直下のCS内部に波高の高い電位が記録され,PPIが頻拍周期に一致するCEを認め,同部位への高周波通電開始4秒後に頻拍は停止し以後誘発不能となった.本症例ではradial手術において凍結凝固が完全に行われなかったCS筋層を介する伝導が頻拍発生の原因になったと考えられた

DOI： 10.11281/shinzo1969.37.Supplement4_115

researchmap

その他リンク： http://search.jamas.or.jp/link/ui/2006092299

記述言語：日本語   出版者・発行元：(株)ライフ・サイエンス  

アミオダロンを投与した拡張型心筋症7例(男6例・女1例,平均63歳:A群)と非投与の15例(男12例・女3例,平均65歳:B群)を対象に,末梢血より単核球を抽出し,ELISA法により上清液中の炎症性サイトカイン濃度を測定した.その結果,A群では投与開始4週間後のBNP値が投与前に比較して有意に低下していた.単球が産生するTNF-α,IL-6についても,アミオダロン投与前後で有意な減少を認めた.B群ではこれらの有意な変化は認めなかった.また,左室駆出率はA群では有意な改善を認めたが,B群では認めなかった

researchmap

記述言語：日本語   出版者・発行元：臨床心臓電気生理研究会  

64歳男.動悸発作の出現を契機に心電図にてlong RP型頻拍を認め,ATP投与で頻拍は停止した.心房期外刺激で誘発される頻拍であり,最早期興奮はHis束領域であった.また,洞調律時に心室期外刺激により特定の連結期に過剰伝導を認め,逆行性fast pathway伝導も認めた.His束近傍に分裂電位を認め,同部位の通電で頻拍は停止した

researchmap

記述言語：日本語   出版者・発行元：臨床心臓電気生理研究会  

26歳男.動悸発作を契機に先行周期およびQRS波形が微妙に異なる2種類の右脚ブロック・右軸偏位型のQRS波形が交互に出現する頻拍を認めた.VerapamilでQRS波形の変化なしに頻拍周期の差が増大し頻拍が停止した.2つの不整脈は右室頻回刺激で誘発された.電気生理学的に左室前壁に異常放電部位の存在が確認され,同部に通電を行ったところ,頻拍は停止し,以後は誘発されなくなった

researchmap

記述言語：日本語   出版者・発行元：(NPO)日本不整脈学会  

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：(NPO)日本不整脈学会  

researchmap

記述言語：日本語   出版者・発行元：(NPO)日本不整脈学会  

J-GLOBAL

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

researchmap

記述言語：日本語   出版者・発行元：(公財)日本心臓財団  

66歳女.心電図上II,III,aVfで陰性P波を示すlong RP頻拍を認め心臓電気生理学的検査を施行した.洞調律中の右心室連続刺激および早期刺激でも房室伝導を認めず,冠状静脈洞(Cs)内,開口部から18mmの部位に最早期心房興奮部位を有する周期410msの頻拍が,右心房刺激で容易に誘発された.頻拍中の右心室連続刺激で房室解離を認めたことから,心房頻拍と診断した.この頻拍はATPの5mg急速静注によりAV間隔不変のまま房室ブロックになる前に停止し,最早期興奮部位における高周波通電を施行した.その結果,頻拍は停止するもののその後も誘発され,その度ごとに最早期興奮部位が隣接する位置に移動し,頻拍周期が徐々に延長した.Cs内部および僧帽弁輪下壁側で計18回の通電後には最早期興奮部位はヒス束電位記録部位に至った.最早期の通電を避け,slow pathway領域における高周波通電としたところ通電開始1.5秒で頻拍は停止,接合部調律が出現して,以後誘発不能となった

researchmap

記述言語：日本語   出版者・発行元：日本臨床生理学会  

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

researchmap

記述言語：日本語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：(NPO)日本不整脈学会  

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：(一社)日本不整脈心電学会  

researchmap

記述言語：日本語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：英語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

J-GLOBAL

researchmap

J-GLOBAL

researchmap

記述言語：日本語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：(株)総合医学社  

56歳男,ショック状態にある急性心筋梗塞に伴う難治性心室性不整脈に対し,MS-551の持続静注を試み,発作の停止,抑制共に著効を示した.同薬剤の投与は循環動態を悪化させることはなかった.MS-551は本症例のように,高度に心機能低下した,他剤無効の重症心室性不整脈に対しても有効かつ安全に使用できる薬剤として期待される

researchmap

記述言語：日本語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap

記述言語：日本語   出版者・発行元：社団法人日本循環器学会  

CiNii Books

researchmap