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  • Regarding the pathophysiology of HF with preserved


    Regarding the pathophysiology of HF with preserved LVEF, AF is one of the most important precipitating factors related to diastolic dysfunction [22,23]. AF might have important roles in the pathogenesis of HF with preserved EF in association with diastolic HF. Compared with JCARE-CARD, which included patients hospitalized with severe HF, the patients included in the present study had a higher prevalence of ischemic etiology and preserved EF. These differences in etiology and the prognostic significance of AF might contribute to the different results of various studies including those of our study, JCARE-CARD, and other studies performed in Western countries focusing on the prognostic value of AF in patients with HF. Therefore, we need to consider the etiology and various factors when we speculate the prognostic significance of AF in patients with HF. The present study has several limitations. In this purchase SW033291 study, enrolled patients were divided into AF and non-AF groups according to ECG recordings, including 12-lead surface ECG and 24-h Holter ECG recordings performed 3 months after the initial visit; thus, patients who had a history of asymptomatic AF but were in sinus rhythm at baseline were categorized into the non-AF group. Moreover, the present study did not obtain data about new-onset AF 3 months after the first visit, which has been reported to have a prognostic effect in patients with HF [3,6,7]. As shown in Section 3, the background characteristics of the study patients differed between groups. Thus, even after adjustment based on the covariates, the independent prognostic value of AF in outpatients with HF was not determined in this study. As such, further studies are needed. Finally, this study was based on a single-center cohort; thus, its results cannot be extended to the general population.
    Conflict of interest
    Introduction Idiopathic premature ventricular contractions (PVCs) in the papillary muscles originate on or beneath the endocardium [1]. Achieving a stable catheter location for contact with these muscles can be challenging because they are actively involved in the repeated expansion and contraction of the heart. The CARTO 3D mapping system (CARTOSOUND, Biosense Webster, Diamond Bar, CA, USA) can be used with a real-time intracardiac echocardiography (ICE) probe and a CARTO™ navigation sensor (SOUNDSTAR, Biosense Webster) to facilitate image integration during ablation.
    Case A 45-year-old man with idiopathic PVCs accompanied by symptomatic palpitations underwent catheter ablation. Echocardiography demonstrated no evidence of structural heart disease. At baseline, monomorphic PVCs were frequent, with the following characteristics: QRS width of 130ms, left bundle branch block, inferior axis, a transition zone in precordial leads V3–V4, and a positive QRS wave in lead I (Fig. 1B, right panel). To determine the origin of the PVCs, noncontact mapping (EnSite Navx system, St. Jude Medical, St. Paul, Minnesota) was performed with the EnSite Array catheter positioned in the right ventricular outflow tract. A 2-Hz high-pass filter was used with the virtual unipolar electrograms. During the procedures in the right ventricle, intravenous heparin was administered to maintain an activated clotting time of >250s. Although the electrophysiology study, based on virtual isopotential mapping with a noncontact mapping system (Fig. 1A), indicated that the PVCs originated in the mid-apical region of the right ventricular septum, their morphology at that site differed from that obtained via pace mapping in the same region (Fig. 1B). Radiofrequency current was applied to the sites that had the earliest local ventricular activation time relative to the QRS onset (17ms before) and to those with a local unipolar QS pattern during the PVCs (Fig. 2A). However, radiofrequency ablation using a non-irrigated ablation catheter with a 4-mm tip (set at 30W and with a target temperature of 55°C) failed to eliminate the PVCs, although there was a slight change in the QRS morphology.