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Evaluation of longitudinal strain (LS) from two-dimensional echocardiography is useful for global and regional left ventricular (LV) dysfunction assessment. We determined whether the LS reflects contraction process in patients with asynchronous LV activation. We studied 144 patients with an ejection fraction ≤ 35%, who had left bundle branch block (LBBB, n = 42), right ventricular apical (RVA) pacing (n = 34), LV basal- or mid-lateral pacing (n = 23), and no conduction block (Narrow-QRS, n = 45). LS distribution maps were constructed using 3 standard apical views. The times from the QRS onset-to-early systolic positive peak (Q-EPpeak) and late systolic negative peak (Q-LNpeak) were measured to determine the beginning and end of contractions in each segment. Negative strain in LBBB initially appeared in the septum and basal-lateral contracted late. In RVA and LV pacing, the contracted area enlarged centrifugally from the pacing site. Narrow-QRS showed few regional differences in strain during the systolic period. The Q-EPpeak and Q-LNpeak exhibited similar sequences characterized by septum to basal-lateral via the apical regions in LBBB, apical to basal regions in RVA pacing, and lateral to a relatively large delayed contracted area between the apical- and basal-septum in LV pacing. Differences in Q-LNpeaks between the apical and basal segments in delayed contracted wall were 107 ± 30 ms in LBBB, 133 ± 46 ms in RVA pacing, and 37 ± 20 ms in LV pacing (p

Atrial fibrillation (AF) is associated with an increased risk of heart failure (HF), stroke, and death. Although fibrillation cycle length (FCL) is used as a surrogate for atrial refractoriness, its impact on outcomes remains unclear. This study aimed to identify predictors of cardiovascular events, including FCL, in patients with long-standing persistent AF. The study included 190 consecutive patients with long-standing persistent AF (mean age 74 years, 74% male). Patients with valvular AF or hemodialysis-dependent end-stage renal disease and those on anti-arrhythmic drugs were excluded. The primary composite outcome was occurrence of cardiovascular events (myocardial infarction, HF), cerebrovascular events (stroke, transient ischemic attack), and all-cause death. FCL was calculated by fast Fourier transformation analysis of fibrillation waves in the surface electrocardiogram. Over a median follow-up of 2.6 years, the primary outcome occurred in 31 patients (cardiovascular events, n = 18; cerebrovascular events, n = 8; all-cause death, n = 5). In multivariate analysis, longer FCL and history of HF were independent predictors of these outcomes. In a Cox proportional hazards model adjusted for age, sex, and history of HF, patients with an FCL > 160 ms (cut-off determined by receiver-operating characteristic curve analysis) were at increased risk of the outcome (hazard ratio 12.9; 95% confidence interval 4.99–44.10; p

Each direct oral anticoagulant (DOAC) has different dose reduction criteria. Here, we evaluated the differences in the doses of three anti-Xa DOACs and clinical events based on the dose reduction criteria in patients with atrial fibrillation (AF).Consecutive AF patients prescribed with anti-Xa DOACs [rivaroxaban (Riva), apixaban (Apix), and edoxaban (Edox)] between April 2011 and May 2016 were retrospectively evaluated. The incidences of thromboembolic and bleeding events were evaluated by the end of December 2020, focusing on the dose proportion.A total of 786 patients (72 ± 10 years old, 66.9% male) were enrolled in this study [Riva (The patients with a standard dose of Apix had a higher incidence of minor bleeding events than the other dosages. A reduced dose of apixaban was not prone to being chosen because of the dose reduction criteria, which may have been associated with a higher minor bleeding rate in patients with Apix.

Background Recent clinical trials have demonstrated the possible pleiotropic effects of SGLT2 (sodium–glucose cotransporter 2) inhibitors in clinical cardiovascular diseases. Atrial electrical and structural remodeling is important as an atrial fibrillation (AF) substrate. Methods and Results The present study assessed the effect of canagliflozin (CAN), an SGLT2 inhibitor, on atrial remodeling in a canine AF model. The study included 12 beagle dogs, with 10 receiving continuous rapid atrial pacing and 2 acting as the nonpacing group. The 10 dogs that received continuous rapid atrial pacing for 3 weeks were subdivided as follows: pacing control group (n=5) and pacing+CAN (3 mg/kg per day) group (n=5). The atrial effective refractory period, conduction velocity, and AF inducibility were evaluated weekly through atrial epicardial wires. After the protocol, atrial tissues were sampled for histological examination. The degree of reactive oxygen species expression was evaluated by dihydroethidium staining. The atrial effective refractory period reduction was smaller ( P =0.06) and the degree of conduction velocity decrease was smaller in the pacing+CAN group compared with the pacing control group ( P =0.009). The AF inducibility gradually increased in the pacing control group, but such an increase was suppressed in the pacing+CAN group ( P =0.011). The pacing control group exhibited interstitial fibrosis and enhanced oxidative stress, which were suppressed in the pacing+CAN group. Conclusions CAN and possibly other SGLT2 inhibitors might be useful for preventing AF and suppressing the promotion of atrial remodeling as an AF substrate.

Dipeptidyl peptidase 4 (DPP-4) inhibitors have recently been reported to exhibit additional cardioprotective effects; however, their effect in atrial remodeling, such as in atrial fibrillation (AF), remains unclear. In this study, the effect of linagliptin on atrial electrical and structural remodeling was evaluated in a canine AF model. Sixteen beagle dogs with 3-week atrial rapid stimulation were divided into the linagliptin group (9 mg/kg/day, n = 8) and pacing control group (n = 8). Three additional dogs without rapid pacing were assigned into non-pacing group, which was used as sham in this study. In the dogs with rapid pacing, the atrial effective refractory period (AERP), conduction velocity (CV), and AF inducibility were evaluated and blood was sampled every week. After the entire protocol, atrial tissue was sampled for histological examinations using HE, Azan, and dihydroethidium (DHE) staining to evaluate any tissue damage or oxidative stress. The pacing control group exhibited a gradual AERP shortening and CV decrease along the time course as previously reported. In the linagliptin group, the AERP shortening was not affected, but the CV decrease was suppressed in comparison to the control group (p

It is known that the efficacy of catheter ablation for atrial fibrillation (AF) is high, but cardiac tamponade may occur in 1–2% cases. Even in such cases, fatal condition can be avoided by appropriate drainage, but reversal of anticoagulation therapy might also be necessary. Here, we report a case of use of idarucizumab for cardiac tamponade during AF ablation. Although the drainage with pericardial centesis should be selected, we could not perform because echo free space was too thin at least at the precordial or apical side of the ventricle. Fortunately, dabigatran reversal by idarucizumab suppressed cardiac tamponade progress and the patient recovered without undergoing any invasive procedures. The pericardial drainage must be the principal therapy for cardiac tamponade, but reversal of anticoagulant might be helpful for patients’ recovery. It might be thought that dabigatran, the only direct oral anticoagulant with a specific reversal agent, should be the safest choice in case of risk for bleeding complications such as AF ablation.

Background: Cardiac troponin T (cTnT) has been reported to be associated with cardiac mortality. In the present study, we evaluated the role of routine assessment of cTnT as a predictor of future cardiac death in patients with left ventricular (LV) dysfunction. Methods: Patients who were eligible for prophylactic implantable cardioverter defibrillator (ICD) were included from cardiac catheterization database. Inclusion criteria were patients with LV ejection fraction of ≤ 35% and with New York Heart Association (NYHA) ≥class II. Exclusion criteria were patients with acute coronary syndrome, ICD for secondary prevention, NYHA class IV, and lack of data. The final study patients were divided into the following three groups in accordance with two quartile points of serum cTnT levels: low cTnT, intermediate cTnT, and high cTnT groups. The primary endpoint of this study was cardiac death. Results: A total of 70 patients were included (mean age, 62±13 years; male individuals, 56; ischemic, 36; and non-ischemic, 34). During the observation period of 2.2 years, cardiac death was observed in 17 patients (fatal arrhythmic event, 9; heart failure, 7; myocardial infarction, 1). In the Kaplan–Meier analysis, the high cTnT group showed the highest risk among all the groups (p

A seventy year-old male was referred to our hospital to undergo radiofrequency catheter ablation (RFCA) for drug-refractory paroxysmal atrial fibrillation (AF). Pre-operative three-dimensional computed tomography revealed a unique left atrial (LA) roof vein. Electrophysiological findings showed expansion of the myocardial sleeve and local firing in the LA roof vein. We performed isolation of this arrhythmogenic abnormal vein concomitant with general pulmonary vein isolation in this case, and AF did not recur after the procedure.

Background Distinction of paroxysmal atrial fibrillation (PAF) from non-PAF is important in clinical practice, but this is often difficult at the time of first documented AF. Given that fibrillation cycle length (FCL) is longer in PAF than in non-PAF, the aim of this study was to compare various clinical parameters including FCL to establish a scoring system to distinguish PAF and non-PAF.Methods and Results:The subjects consisted of 382 consecutive patients with AF on digital ECG at the present institute between 2008 and 2011. They were divided into PAF and non-PAF groups according to the following clinical course. Propensity score matching yielded 88 matched patient pairs with similar mean age and gender between the 2 groups. FCL was evaluated using customized fibrillation wave analyzer with fast Fourier transform analysis. On multivariate analysis, higher HR, longer FCL, and smaller LAD were independent predictors of PAF. For the scoring, cut-offs for each parameter were determined according to highest sensitivity and specificity on the ROC curves, and 1 point assigned for each parameter. Using this scoring system, 2 points detected PAF with 64% sensitivity and 84% specificity. Conclusions We propose a scoring system including FCL to distinguish PAF from non-PAF. Further studies are needed to validate the results.

The effect of DPP-4 inhibitor on the electrical and structural remodeling in myocardial injury has not been evaluated. We hypothesized that linagliptin, DPP-4 inhibitor, suppresses myocardial remodeling in the isoproterenol (ISP)-induced myocardial injury model.Sprague-Dawley rats were assigned to 3 groups: 1) sham group, 2) ISP group (subcutaneous ISP injection of 70 mg/kg), and 3) ISP + linagliptin (ISP + Lin) (5 mg/kg/day, p.o.) group. Serum was sampled on day 1 (acute phase) and day 7 (sub-acute phase) to evaluate derivatives of reactive oxidative metabolites (d-ROMs). The electrophysiological study was performed in sub-acute phase for the evaluation of the ventricular effective refractory period (VERP) and monophasic action potential duration (MAPD). The VERP and MAPD were markedly prolonged in the ISP group in comparison with the sham (MAPD20: 14 ± 6 versus 11 ± 3 ms, MAPD90: 57 ± 8 versus 44 ± 7 ms, VERP: 74 ± 22 versus 38 ± 10 ms, P < 0.05). In contrast in the ISP + Lin group, such prolongations were suppressed, and the parameters were shorter than the ISP group (MAPD20: 9 ± 2 ms, MAPD90: 35 ± 6 ms, VERP: 52 ± 13 ms, P < 0.05). ISP treatment induced myocardial injury. The injured area was reduced in the ISP + Lin group in comparison with the ISP group (P < 0.05). Serum d-ROMs level in acute phase was higher in ISP group than the other 2 groups (sham: 214 ± 55 versus ISP: 404 ± 45 versus ISP + Lin: 337 ± 20 U.CARR, P < 0.05).Linagliptin suppressed structural and electrical changes, possibly through the antioxidative effect, in this myocardial injury model.

Ventricular capture management is an automatic pacing threshold adjustment algorithm that automatically measures pacing threshold through detection of the evoked response after a pacing stimulus. Although it is principally designed to save device battery under the maintenance of the patient׳s safety, we experienced a rare case with serious pacing failure due to a weakness of this algorithm. This pacing failure might be explained by a large variation in the ventricular pacing threshold depending on the atrioventricular interval and daily variation of pacing threshold and concomitant steroid use in this patient. Keywords: Automatic pacing threshold adjustment algorithm, Pacing failure

Discrimination between paroxysmal and persistent atrial fibrillation (PAF and persistent AF) is important for determining the therapeutic strategy in patients with new-onset AF. We evaluated various clinical factors and P wave morphology to discriminate PAF and persistent AF patients in patients with new-onset AF.The study population consisted of 79 patients with new-onset AF (70.3 ± 10.8 years, female:male 33:46) who were retrospectively selected from 8,632 AF patients in the Kitasato University Hospital ECG storing system. PAF (n = 38) and persistent AF (n = 41) patients were diagnosed by whether the initial PAF episode continued for 1 week. The P wave morphologies were analyzed using the most recent 12 lead-ECG recording of sinus rhythm. P wave dispersion was defined as the difference between the maximum and minimum durations of all leads. Along with these data, various clinical factors were evaluated and compared between PAF and persistent AF patients.Multivariate analysis identified P wave dispersion (56.6 ± 14.8 versus 66.5 ± 12.8 msec, P = 0.002) and left atrial dimension (LAD: 40.2 ± 7.0 versus 47.7 ± 8.2 mm, P < 0.001) as independent factors for discrimination between PAF and persistent AF patients. Combining these two parameters achieved a specificity of 88.9%, a positive predictive value of 81.8%, a sensitivity of 95.3%, and a negative predictive value of 88.9%.In patients with new-onset AF, P wave dispersion and LAD were independent factors for discrimination between PAF and persistent AF.

We have shown that a dipeptidyl peptidase 4 (DPP-4) inhibitor suppresses atrial remodeling in a canine atrial fibrillation (AF) model. Glucagon-like peptide-1 (GLP-1) is increased by DPP-4 inhibitors. However, it is not clear whether GLP-1 is involved in the suppression of atrial remodeling. In this study, we evaluated the effect of liraglutide (a GLP-1 analog) on atrial electrophysiological changes using the same canine AF model. We established a canine AF model using continuous 3-week rapid atrial stimulation in seven beagle dogs divided into two groups: a liraglutide group with four dogs (3-week atrial pacing with liraglutide (150 µg/kg/day) administration) and a pacing control group with three dogs (3-week pacing without any medicine). We evaluated the atrial effective refractory period (AERP), conduction velocity (CV), and AF inducibility every week during the protocol using implanted epicardial wires against the surfaces of both atria. In the pacing control group, the AERP was gradually shortened and the CV was decreased along the time course. In the liraglutide group, the AERP was similarly shortened as in the pacing control group (94 ± 4% versus 85 ± 2%, respectively; p = 0.5926), but the CV became significantly higher than that in the pacing control group after 2 and 3 weeks (95 ± 4 versus 83 ± 5%, respectively; p = 0.0339). The AF inducibility was gradually increased in the pacing control group, but it was suppressed in the liraglutide group (5 ± 9% versus 73 ± 5%; p = 0.0262). Liraglutide suppressed electrophysiological changes such as AF inducibility and CV decrease in our canine AF model.

The wearable cardioverter-defibrillator (WCD) represents an alternative clinical approach to prevent sudden cardiac death as a bridge to therapy when making a final decision regarding the need for an implantable cardioverter defibrillator (ICD), especially in patients who are in the so-called gray zone according to ICD guidelines. Although the WCD system was introduced in Japan in April 2014, data regarding its usage and experience are limited. We report the first case of appropriate shock therapy using the WCD in an outpatient setting in Japan. We describe the case of a 22-year-old-woman who received the first case of successful appropriate WCD shock therapy in an outpatient setting in Japan.

The avoidance of inappropriate shock therapy is an important clinical issue in implantable cardioverter-defibrillator (ICD) patients. We retrospectively analyzed therapeutic events in ICD patients, and the effect of tachycardia detection interval (TDI) and tachycardia cycle length (TCL) guided reprograming on the reduction of inappropriate ICD therapy. The clinical determinants of after reprogramming were also evaluated.A total of 254 consecutive ICD patients were included in the study, and the incidence of antitachycardia therapy was evaluated during the follow-up period of 27.3 ± 18.7 months. When inappropriate antitachycardia therapy appeared, TDI was reprogrammed not to exceed the detected TCL and the patients continued to be followed-up. Various clinical parameters were compared between patients with and without inappropriate ICD therapy. During the initial follow-up period of 18.6 ± 15.6 months, ICD therapy occurred in 127/254 patients (50%) including inappropriate antitachycardia pacing (ATP) (12.9%) and shock (44.35%). Determinants of initial inappropriate therapy were dilated cardiomyopathy (DCM), history of therapeutic hypothermia, and QRS duration. Of the 61 patients with inappropriate therapy, 24 received TCL guided reprogramming. During the additional observation period of 17.0 ± 16.8 months, inappropriate therapy recurred in 5/24 patients (2 ATP, 3 shocks). The determinant of these inappropriate therapy events after reprogramming was the presence of supraventricular tachycardia.By applying simple TCL and TDI guided reprogramming, inappropriate therapy was reduced by 79%. The determinant of inappropriate therapy after reprogramming was the presence of supraventricular tachycardia.

Background Dabigatran etexilate (DE), an effective direct oral anticoagulant for patients with atrial fibrillation (AF), should be carefully used in patients with renal insufficiency. Data on the safety of DE in Japanese “real world” patients with mildly impaired renal function are limited. We hypothesized that low-dose DE (110 mg, twice daily) could be safely used in Japanese AF patients with mildly impaired renal function compared to those with preserved renal function. Methods and results One hundred ninety-six consecutive AF patients taking low-dose DE were retrospectively enrolled in this study, and were divided into two groups: preserved creatinine clearance (CCr ≥50 ml/min; n = 127) and reduced CCr (30–49 ml/min; n = 69). Baseline characteristics including CHADS2, CHA2DS2-VASc, and HAS-BLED scores were evaluated. Activated partial thromboplastin time (aPTT) was measured as a surrogate marker of the anticoagulant activity of DE, which was evaluated at 661 time points in total and the data were divided into five time windows after the last DE intake. The incidence of bleeding complications was compared between the two groups of reduced and preserved CCr. Reduced CCr group showed higher age (76.9 ± 6.3 years vs. 67.6 ± 6.7 years), higher CHADS2 (2.6 ± 1.4 vs. 1.8 ± 1.2), higher CHA2DS2-VASc (4.3 ± 1.6 vs. 3.2 ± 1.6), and higher HAS-BLED (2.3 ± 1.0 vs. 2.0 ± 1.0) scores in comparison with preserved CCr group (p Conclusion Low-dose DE was safe in AF patients with mildly reduced CCr.

Purpose Recent reports have documented the appearance of Brugada-type ST elevation in cases of overdose of antiepileptic drugs (AEDs). However, little is known about changes on electrocardiographs (ECGs) during AED use at therapeutic doses. AEDs may cause Brugada-type ST elevation or J -wave-like intraventricular conduction delays through an ion channel-blocking effect. In the present study, we sought to elucidate ECG abnormalities in patients on AED therapy. Methods The study population consisted of 120 consecutive patients with epilepsy who continued to take AEDs and had ECGs recorded during these therapies. Their clinical background and ECGs were retrospectively analyzed. Brugada-type ST elevation was classified according to the consensus report on Brugada syndrome. A J-wave-like ECG abnormality was defined as the appearance of notching or slurring of the QRS complex (>0.1mV) in the inferior/lateral leads. Results Of the 120 patients, 15 (12.5%) exhibited Brugada-type ST elevation and 35 (29.2%) showed a J -wave-like ECG abnormality. Polytherapy with sodium channel-blocking AEDs (e.g., carbamazepine, phenytoin, lamotrigine) was more frequently observed in patients with Brugada-type ST elevation ( p =0.048). However, the serum concentrations of these medicines did not differ between patients with and without ECG abnormalities (carbamazepine: 7.9±4.1 vs. 7.2±5.9μg/dL; phenytoin: 12.7±4.1 vs. 15.5±9.5μg/dL, NS). Conclusion ST-T abnormalities were frequently seen in patients using AEDs. The presence of Brugada-type ST elevation was associated with polytherapy with sodium channel-blocking AEDs.

Background: Although implantable cardioverter-defibrillator (ICD) prevents sudden death of patients with life-threatening arrhythmia, prediction of upcoming ICD therapy, if possible, would be an important issue in device management. In the present study, the relationship between ICD therapeutic episodes and preceding routine device data was evaluated to clarify the predictors for ICD actuation in near future. Methods: The study population consisted of 100 consecutive ICD patients. All patients were followed up in the device clinic in every 4-month period, and their total follow-up periods of 22.8±4.1 months were divided into 734 4-month observation windows. The common data in device clinic including 12-lead ECG, chest X-ray, and interrogated device data were compared between patients with and without ICD therapeutic episodes during upcoming 4-month windows. To avoid inappropriate weighting on data of specific cases, such as unusual data in cases with frequent shock therapy, sampling number was limited 4-8 times in one case, and all data were evaluated as change during preceding 4 months, e.g., QTc calculated by subtracting 4 month preceding QTc from the recent QTc. Results: During 3.2±1.3 month follow-up, among 734 observation windows, appropriate and inappropriate ICD therapies appeared in 54 (ATP: 29, shock: 25) and 20 (ATP: 11, shock: 9) windows. When the patients were divided into spontaneous rhythm and paced-rhythm groups (n=558 and 170), spontaneous rhythm group did not show any significant difference in parameters between the windows with and without therapeutic episodes. In contrast in paced-rhythm group, RV lead impedance was significantly lower in the windows with therapeutic episodes in comparison with those without (-19.8±43.5Ω vs. 7.4±44.7Ω, p=0.047). Conclusions: Upcoming ICD therapy in near future might be able to be predicted by change in RV lead impedance at least in cases with paced-rhythm in ICD patients. It might reflect the electrical instability in cases with ICD therapeutic episodes.

It is unknown whether 12-lead ECG can predict new-onset AF. In the present study, we identified patients with new onset AF from our digitally stored ECG database, and the P wave morphologies were analyzed in their preceding sinus rhythm recordings as the precursor state for AF. The P wave was analyzed in the most recent ECG recording of sinus rhythm preceding new onset AF within 12 months. The duration and amplitude of P waves were analyzed in 12 leads and compared between the 2 groups with the other clinical parameters. The study population consisted of 68 patients with new-onset AF and 68 age and sex-matched controls. Multivariate analysis revealed that the P wave amplitude in leads II and V1 (0.157 ± 0.056 versus 0.115 ± 0.057 mV, P = 0.032, and 0.146 ± 0.089 versus 0.095 ± 0.036 mV, P = 0.002) and P wave dispersion (56.9 ± 14.8 versus 33.5 ± 12.9 ms, P = 0.001) were significant independent factors for the prediction of new-onset AF. By using these factors, new-onset AF could be predicted with a sensitivity of 69.1% and specificity of 88.2%. P wave analysis is useful for predicting new onset AF.