19 research outputs found

    Electrical storm after cardiac resynchronization therapy in a patient with nonischemic cardiomyopathy: Signal-averaged vector-projected 187-channel electrocardiogram-based risk stratification for lethal arrhythmia

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    AbstractWe describe treatment of atrial flutter and electrical storm presenting as incessant ventricular tachycardia (VT) after implantation of a cardiac resynchronization therapy defibrillator (CRT-D) in a patient with dilated cardiomyopathy. No prior arrhythmic event had occurred. Our treatment strategy, including amiodarone administration, was guided in part by signal-averaged vector-projected 187-channel electrocardiogram (SAVP-ECG)-based risk stratification for ventricular arrhythmia. Corrected recovery time (RTc) dispersion and Tpeak-end dispersion were used to evaluate transmural dispersion of repolarization. RTc and Tpeak-end dispersion increased during the period of electrical storm. Values were improved 2 years after CRT-D implantation, and the amiodarone was discontinued. The VT has not recurred despite discontinuation of the antiarrhythmic agent. SAVP-ECG-based risk stratification for ventricular arrhythmia proved useful for the management of antiarrhythmic therapy

    What Are the Expectations for Cardiac Resynchronization Therapy? A Validation of Two Response Definitions

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    Background: The definition of response to cardiac resynchronization therapy (CRT) varies across clinical trials. There are two main definitions, i.e., echocardiographic response and functional response. We assessed which definition was more reasonable. Methods: In this study of 260 patients who had undergone CRT, an echocardiographic response was defined as a reduction in a left ventricular end-systolic volume of greater than or equal to 15% or an improvement in left ventricular ejection fraction of greater than or equal to 5%. A functional response was defined as an improvement of at least one class category in the New York Heart Association functional classification. We assessed the response to CRT at 6 months after device implantation, based on each definition, and investigated the relationship between response and clinical outcomes. Results: The echocardiographic response rate was 74.2%. The functional response rate was 86.9%. Non-responder status, based on both definitions, was associated with higher all-cause mortality. Cardiac death was only associated with functional non-responder status (hazard ratio (HR) 2.65, 95% confidence interval (CI) 1.19–5.46, p = 0.0186) and heart failure hospitalization (HR 2.78, 95% CI, 1.29–5.26, p = 0.0111). Conclusion: After CRT implantation, the functional response definition of CRT response is associated with a higher response rate and better clinical outcomes than that of the echocardiographic response definition, and therefore it is reasonable to use the functional definition to assess CRT response

    Efficacy of Cardiac Resynchronization Therapy in Patients with a Narrow QRS Complex

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    Aims. In the guidelines for cardiac resynchronization therapy (CRT), there is a gap between the Japanese Circulation Society (JCS) criteria, which specify a QRS duration of ≥120 ms, and other countries, with a QRS ≥ 130 ms. The efficacy of CRT remains controversial in patients with a narrow QRS <130 ms. The aims of this study are to evaluate the response to CRT in patients with a narrow QRS and to identify predictors of mortality. Methods. We retrospectively studied 212 patients who received CRT. They were divided into narrow QRS (<130 ms) and wide QRS (≥130 ms) groups. We compared CRT response rates and investigated whether age, gender, baseline New York Heart Association (NYHA) class, ischemic etiology, atrial fibrillation, and ventricular arrhythmias are associated with response and also predictive of mortality. Results. The CRT response rate was not significantly different between the wide QRS group and the narrow QRS group (74.6% versus 77.2%, p = 0.6876), and the response rate in the narrow QRS group was as good as that reported worldwide. NYHA class IV was shown to be a predictor of mortality (HR 9.38, 95% CI 5.35–16.3, p < 0.0001). Conclusions. The present study demonstrated that patients with a narrow QRS complex responded well to CRT. Even with QRS <130 ms, CRT should be tried if no other effective treatment is available

    Interleukin-16 promotes cardiac fibrosis and myocardial stiffening in heart failure with preserved ejection fraction.

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    BACKGROUND: Chronic heart failure (CHF) with preserved left ventricular (LV) ejection fraction (HFpEF) is observed in half of all patients with CHF and carries the same poor prognosis as CHF with reduced LV ejection fraction (HFrEF). In contrast to HFrEF, there is no established therapy for HFpEF. Chronic inflammation contributes to cardiac fibrosis, a crucial factor in HFpEF; however, inflammatory mechanisms and mediators involved in the development of HFpEF remain unclear. Therefore, we sought to identify novel inflammatory mediators involved in this process. METHODS AND RESULTS: An analysis by multiplex-bead array assay revealed that serum interleukin-16 (IL-16) levels were specifically elevated in patients with HFpEF compared with HFrEF and controls. This was confirmed by enzyme-linked immunosorbent assay in HFpEF patients and controls, and serum IL-16 levels showed a significant association with indices of LV diastolic dysfunction. Serum IL-16 levels were also elevated in a rat model of HFpEF and positively correlated with LV end-diastolic pressure, lung weight and LV myocardial stiffness constant. The cardiac expression of IL-16 was upregulated in the HFpEF rat model. Enhanced cardiac expression of IL-16 in transgenic mice induced cardiac fibrosis and LV myocardial stiffening accompanied by increased macrophage infiltration. Treatment with anti-IL-16 neutralizing antibody ameliorated cardiac fibrosis in the mouse model of angiotensin II-induced hypertension. CONCLUSION: Our data indicate that IL-16 is a mediator of LV myocardial fibrosis and stiffening in HFpEF, and that the blockade of IL-16 could be a possible therapeutic option for HFpEF

    Current use of direct oral anticoagulants for atrial fibrillation in Japan: Findings from the SAKURA AF Registry

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    Background: Large-scale investigations on the use of oral anticoagulants including direct oral anticoagulants (DOACs) in patients with atrial fibrillation (AF) have not included Japanese patients. Methods: We established the multicenter SAKURA AF Registry to support prospective observational research on the status of anticoagulation treatment, especially with DOAC, for AF in Japan. We enrolled 3266 AF patients treated with warfarin (n=1577) or any of 4 DOACs (n=1689) from 63 institutions (2 cardiovascular centers, 13 affiliated hospitals or community hospitals, and 48 private clinics) in the Tokyo area. Results: We conducted our first analysis of the registry data, and although we found equivalent mean age between the DOAC and warfarin users (71.8±9.5 vs. 72.3±9.4 years, p=0.2117), we found a slightly lower risk of stroke (CHADS2 score of 0 or 1 [46.9% vs. 39.4%, p<0.0001]) and significantly better creatinine clearance in DOAC users (70.4±27 vs. 65.6±25.7 mL/min, p<0.0001). Importantly, we documented under-dosing in 32% of warfarin users and inappropriate-low-dosing in 19.7–27.6% of DOAC users. Conclusions: Our initial analysis of the SAKURA AF Registry data clarified the real-world use of anticoagulants, which includes DOACs and warfarin in Japan. The DOAC users were at a lower risk for stroke than the warfarin users. In 20–30% of DOAC users, the dose was inappropriately reduced

    Elevated serum interleukin-16 (IL-16) levels in rats with heart failure with preserved ejection fraction (HFpEF).

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    <p><b>A,</b> Serum IL-16 levels in control rats and the rats with HFpEF. <b>B</b> through <b>D,</b> Correlations of serum IL-16 level and left ventricular end-diastolic pressure (LVEDP) (<b>B</b>), lung weight to body weight ratio (lung weight/body weight) (<b>C</b>) and myocardial stiffness constant (MSC) (<b>D</b>) in control and HFpEF rats combined. <b>E,</b> mRNA level of IL-16 in the left ventricle of control and HFpEF rats.</p
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