Publications by authors named "Toshihiko Kubo"

Pulmonary vein isolation (PVI), which creates electrical blocks between pulmonary veins and left atrium, is an established way of catheter ablation for atrial fibrillation (AF). PVI is usually performed via the femoral vein access, using two or three long preshaped sheaths, followed by atrial-septal puncture to approach the left atrium. Here, we treated an AF patient with a permanently implanted inferior vena cava filter (IVC-F) due to deep venous thrombosis (DVT) and pulmonary thromboembolism (PTE).

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We describe the case that persistent atrial fibrillation refractory to rhythm control by pharmacotherapy and electrical cardioversions caused tachycardia-induced cardiomyopathy with low ejection fraction and hemodynamic instability. Mechanical hemodynamic support using an intra-aortic balloon pump is one of the choices of hemodynamic support during catheter ablation by pulmonary vein isolation.

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An 86-year-old man was admitted to our hospital for treatment of congestive heart failure with severe aortic stenosis and advanced atrioventricular (AV) block. Despite pharmacological therapy, he developed complete AV block and resultant acute pulmonary edema requiring temporary pacing and tracheal intubation. We urgently performed retrograde balloon aortic valvuloplasty (BAV) with a sheathless technique.

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We herein report the case of 34-year-old woman with acute tricuspid valve infective endocarditis (IE) associated with a ruptured sinus of Valsalva and multiple septic pulmonary emboli. She had no history of medical problems, except for atopic dermatitis (AD). Blood cultures identified methicillin-sensitive Staphylococcus aureus.

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Background: A nuclear accident occurred at the Fukushima Daiichi Nuclear Power Plant of Tokyo Electric Power Company (TEPCO) as a result of a mega-earthquake and tsunami in March, 2011. A large number of workers were engaged in response and recovery operations under a complex structure of involved companies. They were exposed not only to radiation but also to other health hazards.

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Background: Muscle sympathetic nerve firing rate increases as chronic heart failure (CHF) progresses, yet its oscillation, particularly within the frequency range encompassing 0.13 Hz, diminishes. The current study tested the hypothesis that chronic therapy with lipophilic β-adrenoceptor antagonists augments the modulation of muscle sympathetic nerve activity variability (MSNAV) at this frequency range.

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A 36-year-old man with underlying systemic lupus erythematosus complicated by autoimmune hemolytic anemia underwent immunosuppressive treatment. After showing a low-grade fever for two days, his fever spiked. He was confirmed to have pandemic (H1N1) 2009 by real-time reverse transcription polymerase chain reaction (PCR).

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Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking.

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We have documented a pre-junctional beta-2 adrenoceptor mediated reduction in cardiac norepinephrine spillover (CNES) in heart failure patients receiving chronic beta-blockade. Our present objective was to ascertain the consequence of this decrease for vagal heart rate (HR) regulation by determining CNES, arterial baroreflex sensitivity for HR (BRS) and arterial baroreflex modulation of muscle sympathetic nerve activity (MSNA) before and upon 4 months of beta-blockade with either carvedilol or metoprolol. In 19 heart failure patients in sinus rhythm (age: 55+/-2 [mean+/-S.

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Objectives: This study was designed to determine whether reductions in morning systolic blood pressure (BP) elicited by treatment of moderate to severe obstructive sleep apnea (OSA) in heart failure (HF) patients are associated with a reduction in sympathetic vasoconstrictor tone.

Background: Daytime muscle sympathetic nerve activity (MSNA) is elevated in HF patients with coexisting OSA. In our recent randomized trial in HF, abolition of OSA by continuous positive airway pressure (CPAP) increased left ventricular ejection fraction (LVEF) and lowered morning systolic BP.

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Objectives: To determine, in sedentary normotensive postmenopausal women, the after-effects of exercise on systemic and regional hemodynamics, and whether changes in total peripheral conductance after exercise relate to changes in brachial artery flow-mediated vasodilation (FMD).

Methods: In 13 sedentary postmenopausal women, the blood pressure (BP), cardiac output, total peripheral resistance and total peripheral conductance, calf vascular resistance and FMD were measured during baseline rest, and again commencing 45 min after treadmill exercise. Fourteen premenopausal women completed the identical protocol to obtain reference values for the after-effects of exercise in healthy females.

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Background: Obstructive sleep apnea subjects the failing heart to adverse hemodynamic and adrenergic loads and may thereby contribute to the progression of heart failure. We hypothesized that treatment of obstructive sleep apnea by continuous positive airway pressure in patients with heart failure would improve left ventricular systolic function.

Methods: Twenty-four patients with a depressed left ventricular ejection fraction (45 percent or less) and obstructive sleep apnea who were receiving optimal medical treatment for heart failure underwent polysomnography.

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Nitric oxide (NO) plays an important role in the control of vascular tone as well as structure. This study examined the possibility that the extent of restenosis 3 months after percutaneous transluminal coronary angioplasty (PTCA) might be correlated with the magnitude of NO production at the PTCA sites on the day following PTCA. In 23 consecutive patients who underwent PTCA, we examined the coronary artery diameter response to intracoronary administration of L-arginine (1 microg/kg) and isosorbide dinitrate (ISDN, 40 microg/kg) at the sites of PTCA (n = 25) and at untreated sites distal to the PTCA sites approximately 18 h after PTCA.

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