6 results match your criteria: "Department of Cardiology and Nephrology Hirosaki University Graduate School of Medicine Hirosaki Japan.[Affiliation]"

Background: We aimed to quantify the incidence of atrial fibrillation (AF) in patients with cryptogenic stroke globally, as well as separately in patients in and outside of Japan, using an implantable loop recorder from a prospective, observational, Reveal LINQ Registry.

Methods And Results: Patients developing cryptogenic stroke and monitored by implantable loop recorder for searching AF were studied. The primary end point was incidence of AF within 36 months after insertion.

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In the case of adenosine-sensitive atrial tachycardia originating near the atrioventricular (AV) node, overdrive pacing from the anterior right atrium showed constant and progressive fusion, indicating that the pacing site is proximal to slow conduction. Shortening the pacing cycle length prolonged conduction times to the orthodromic capture sites; they remained unchanged at the antidromic capture sites. Limited decremental conduction property in the slow conduction zone supports the hypothesis that AV node-like tissue remnants along the AV annulus are involved.

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A patient with hypertrophic cardiomyopathy experienced cardiopulmonary arrest. An automated external defibrillator administered defibrillation for ventricular fibrillation (A). The pacemaker recorded atrial tachycardia with a rapid ventricular response before the patient collapsed (B).

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Introduction: During ventricular pacing, a fusion of atrial activation may occur owing to the simultaneous retrograde conduction of the atrioventricular (AV) node and accessory pathway (AP), potentially leading to an inaccurate mapping of the atrial AP insertion site.

Objective: We tested the hypothesis that landiolol, an ultra-short-acting intravenous β1-blocker, could dissociate a fusion of atrial activation.

Methods: We conducted a prospective before-and-after study to investigate the effect of landiolol on retrograde conduction via the AV node and AP.

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Background Although PAR-1 (protease-activated receptor-1) exerts important functions in the pathophysiology of the cardiovascular system, the role of PAR-1 signaling in heart failure development remains largely unknown. We tested the hypothesis that PAR-1 signaling inhibition has protective effects on the progression of cardiac remodeling induced by chronic renin-angiotensin system activation using renin-overexpressing hypertensive (Ren-Tg) mice. Methods and Results We treated 12- to 16-week-old male wild-type (WT) mice and Ren-Tg mice with continuous subcutaneous infusion of the PAR-1 antagonist SCH79797 or vehicle for 4 weeks.

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Background An enhanced renin-angiotensin system causes hypertensive renal damage. Factor Xa not only functions in the coagulation cascade but also activates intracellular signaling through protease-activated receptors ( PAR ). We investigated the effects of rivaroxaban, a factor Xa inhibitor, on hypertensive renal damage in hypertensive mice overexpressing renin (Ren-TG).

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