Biomedical subjects

Takeshi Shirayama

Publications and source records attributed to Takeshi Shirayama.

16 recordsLinked to original sources

PubMed2006

Usefulness of paroxetine in depressed men with paroxysmal atrial fibrillation.

The occurrence and the duration of paroxysmal atrial fibrillation (AF) are influenced by vagal tone. Paroxetine, an antidepressant, can modulate vagal tone at the level of the mid-brain and inhibit the vasovagal reflex. In this study, oral paroxetine 10 mg/day was administered to patients with multidrug-resistant paroxysmal AF. Nine consecutive men responded favorably to the drug. In 3 patients, AF resolved completely. One patient could not tolerate the drug because of nausea and nervousness. These preliminary results suggest that paroxetine could be a choice in the pharmacologic treatment of paroxysmal AF.

Adult↗

PubMed2006

Cardiac hypertrophy diminished the effects of isoproterenol on delayed rectifier potassium current in rat heart.

We investigated the association between sympathetic nerve activity and delayed rectifier potassium current (I(K)) in hypertrophic rat hearts. Left ventricular hypertrophy was induced by a 50% constriction of suprarenal abdominal aorta for 6 weeks. The effects of isoproterenol on action potential duration (APD), I(K), and L-type calcium current (I(Ca)) were investigated using the whole-cell patch clamp technique. In hypertrophic rats, I(K) was decreased by 28.2%, resulting in significant APD(90) (90% repolarization) prolongation (sham: 55 +/- 3.9, hypertrophy: 98 +/- 11 ms, P = 0.01). Isoproterenol (100 nM)-stimulated I(K) was increased by 54.9% +/- 0.10% in sham-operated rats, but not in hypertrophic rats. On the other hand, isoproterenol increased I(Ca) in both sham-operated (77.7% +/- 7.6%) and hypertrophic rats (69.6% +/- 9.7%). Consequently, isoproterenol prolonged further APD in hypertrophic rats (98 +/- 11 vs. 145 +/- 8.6 ms, P < 0.01), but not in sham-operated rats (55 +/- 3.9 vs. 61 +/- 5.6 ms, n.s.). Forskolin (1 microM, an adenylyl cyclase stimulator) did not enhance I(K) in hypertrophic rats, but IBMX (100 microM, a nonselective phosphodiesterase inhibitor) enhanced the current (30.2 +/- 0.05%), as much as in sham-operated rats. We concluded that in hypertrophic hearts, I(K) was not increased by isoproterenol because of the enhanced activity of phosphodiesterase, which leads to excessive APD prolongation.

1-Methyl-3-isobutylxanthine↗

PubMed2005

Efficacy of biventricular pacing for dialysis-related hypotension due to idiopathic dilated cardiomyopathy.

A 45-year-old man who had been undergoing maintenance hemodialysis for end-stage renal failure, caused by chronic glomerulonephritis 4 years before, was admitted to our hospital for biventricular pacemaker implantation (BVP). Ten years ago, he was diagnosed with idiopathic dilated cardiomyopathy, and had been suffering from dialysis-related hypotension (DRH) due to low cardiac function over the past year. An electrocardiogram revealed complete left bundle branch block with a QRS duration of 180 ms, and echocardiography showed moderate hypokinesis of the left ventricular wall and systolic asynchronized motion of the septum and free wall. After BVP, the left ventricular ejection fraction had increased from 29% to 40%, and the transmitral rapid left ventricular filling (E wave) and atrial contraction (A wave) ratio (E/A) had improved from 1.3 to 1.0. Before and after BVP, we measured hemodynamic parameters during hemodialysis by successive echocardiography. Before BVP, systemic vascular resistance had decreased, cardiac output had not changed, and hypotension was noted. In contrast, after BVP, cardiac output had increased and systemic vascular resistance had not changed, which caused an increase in blood pressure. We conclude that BVP improved the cardiac function which resulted in an improvement in dialysis-related hypotension (DRH).

Blood Pressure Determination↗

PubMed2005

The association between cholesterol and mortality in heart failure. Comparison between patients with and without coronary artery disease.

Hypercholesterolemia is a risk factor for development of coronary artery disease (CAD), however, several reports have suggested that low serum cholesterol is associated with a worse prognosis in patients with congestive heart failure (CHF). The objective of this study was to determine the prognostic value of cholesterol for CHF. The study subjects consisted of 133 consecutive patients hospitalized in our institution for progressive heart failure from April 2000 to March 2003. Thirty-two percent of the patients had CAD. After improvement of congestive heart failure and discharge from the hospital, lipid profiles, including serum total cholesterol (TC), triglycerides, and high and low density lipoprotein cholesterol (HDL, LDL, respectively), were obtained. During the follow-up period (2.3 +/- 0.9 years), 21 patients died. There was a significant difference between survivors and nonsurvivors in HDL (53 +/- 15, 43 +/- 15 mg/dL, P = 0.01), but no differences were observed in other variables. In patients with CAD, survivors had significantly lower TC concentrations (179 +/- 30 versus 246 +/- 55 mg/dL, P = 0.004), although in patients without CAD, survivors had significantly higher TC concentrations (203 +/- 37 versus 170 +/- 40 mg/dL, P = 0.02). Multivariate analysis showed high TC predicted a worse outcome in patients with CAD (odds ratio (OR) = 1.052, 95% confidence interval (CI) 1.002-1.104, P = 0.04), but a better outcome in patients without CAD (OR = 0.972, 95% CI 0.948-0.997, P = 0.03), independent of age, gender, medication, and complications. Thus, low serum cholesterol is associated with an improved outcome in patients with CAD, while it predicts a worse outcome in patients without CAD.

Adult↗

PubMed2004

Aldosterone directly induces myocyte apoptosis through calcineurin-dependent pathways.

BACKGROUND: Aldosterone has recently attracted considerable attention for its involvement in the pathophysiology of heart failure, in which apoptotic cell loss plays a critical role. This study examined whether aldosterone directly induces myocyte apoptosis via its specific receptors. METHODS AND RESULTS: Neonatal rat cardiac myocytes were exposed to aldosterone (10(-8) to 10(-5) mol/L). Nuclear staining with Hoechst 33258 showed that aldosterone induced myocyte apoptosis in a dose- and time-dependent fashion. Treatment of myocytes with 10(-5) mol/L aldosterone significantly increased the percentage of apoptosis (15.5+/-1.4%) compared with serum-deprived control (7.3+/-0.6%). Radio ligand binding assay revealed the existence of plasma membrane receptor with high affinity (K(d), 0.2 nmol/L) for aldosterone in cardiac myocytes but not in fibroblasts. Aldosterone rapidly (approximately 30 seconds) mobilized [Ca2+]i that was blocked by neomycin. Aldosterone induced dephosphorylation of the proapoptotic protein Bad, enhancement of mitochondrial permeability transition, decrease in mitochondrial membrane potential, and release of cytochrome c from the mitochondria into the cytosol with concomitant activation of caspase-3. These effects of aldosterone were inhibited by concurrent treatment with either an L-type Ca2+ channel antagonist, nifedipine, or inhibitors for the Ca2+-dependent phosphatase calcineurin, cyclosporin A and FK506. CONCLUSIONS: The present study demonstrates for the first time that the specific plasma membrane receptor (coupled with phospholipase C) for aldosterone is present on cardiac myocytes and that aldosterone accelerates the mitochondrial apoptotic pathway through activation of calcineurin and dephosphorylation of Bad, suggesting that the proapoptotic action of aldosterone may directly contribute to the progression of heart failure.

Aldosterone↗

PubMed2004

Rate-dependent QRS prolongation during exercise testing associated with hyperkalemia.

The present case showed gradual increase of QRS duration from 100 ms up to 180 msec during an ergometer exercise test along with the heart rate increase. After exercise, QRS duration shortened and normalized. Laboratory test showed hyperkalemia (K = 8.0 mEq/l). T1 myocardial scintigraphy revealed exercise-induced transient ischemia in posterolateral region of left ventricle. Coronary angiography showed significant stenosis in the distal portion of left circumflex coronary artery. The increase of QRS duration was possibly due to the combination of hyperkalemia and the effect of mexiletine. The rate dependent blocking effect on sodium channel of mexiletine might be intensified under hyperkalemia.

Aged↗

PubMed2004

Clinical significance of preserving spontaneous QRS wave in the therapy of DDD pacing for sick sinus syndrome.

The aim of this clinical crossover study was to elucidate the effects of atrioventricular (AV) synchronous pacing on cardiac function in patients with sick sinus syndrome (SSS). Thirty SSS patients, each with dual chamber pacemaker (DDD), were enrolled and divided into two groups based on echocardiographic findings. Group A (n = 16) had hypertensive heart disease (wall thickness 11 approximately 12 mm) or mitral or aortic regurgitation (Grade I or II). Group B (n = 14) had no organic heart disease. Three successive 3-month pacing periods were tested. For the first 3 months, long AV delay that achieved > 80% ventricular sensing was chosen. For the next 3 months, AV delay was abbreviated to achieve > 80% ventricular pacing at an optimal AV interval. For the final 3 months, the first setting was resumed. At the end of each period, M mode echocardiography, pulsed-Doppler study, and measurement of plasma brain natriuretic peptide (BNP) level were conducted. In both groups, echocardiographic parameters were not significantly changed during the evaluation. In group A, plasma BNP level was significantly higher at the end of the short AV delay period than at the long AV delay period (P = 0.009), while in group B it did not differ during each period. AV synchronous pacing (> 80% ventricular pacing) in the SSS patients with a DDD pacemaker implanted could increase the ventricular load, and it is better to preserve the spontaneous QRS with the DDD mode with prolonged AV delay in patients with mild hypertensive or valvular disease.

Aged↗

PubMed2004

Idiopathic long QT syndrome with early afterdepolarization induced by epinephrine. Acase report.

A patient with idiopathic long QT syndrome had repeated syncopal episodes. The QTc interval on the electrocardiogram at rest was 530 ms and was prolonged by exercise up to 740 ms with T wave alternation. Intravenous epinephrine (0.1 microg/kg weight per min), but not isoproterenol (0.7 microg/min), produced early after depolarization of the monophasic action potential recorded at the right ventricular apex. Epinephrine prolonged the QTc interval to 710 ms. After the addition of propranolol to the epinephrine, the QTc (580 ms) was longer than at baseline. Methoxamine also prolonged the QTc to 580 ms. The QT interval in long QT syndrome is generally considered to be prolonged by a beta-adrenergic effect, but in the present case alpha-adrenergic stimulation had an additional effect on the prolongation of the QT interval.

Adrenergic alpha-Agonists↗

PubMed2004

Ebstein anomaly associated with unusual conduction delay and sick sinus syndrome.

A 64-year-old man was admitted to our hospital because of palpitation, dyspnea on effort, and facial edema. The echocardiographic diagnosis was Ebstein anomaly. Although the 12-lead electrocardiogram showed an atrial rate of 150 beats/min and no typical flutter wave, the electrophysiological study showed counterclockwise rotation of excitation along the tricuspid annulus. Because of sinus arrest and syncope, a permanent pacemaker was implanted, but the right atrium was not captured by electrical stimulation at 5 V/0.4 ms, except for the orifice of coronary sinus, and the intracardiac P wave was only 0.2 mV or less. This is a rare case of Ebstein anomaly characterized by unusually prolonged conduction in the atrium, the basis of which was global myocardial damage, including the ventricles.

Ebstein Anomaly↗

PubMed2003

Role of atrial fibrillation threshold evaluation on guiding treatment.

Atrial fibrillation could be induced reproducibly by 50 Hz rapid stimulation which was given through systolic and early diastolic phase of atrial excitation. Duration of atrial fibrillation induced in this way was roughly dependent on the current amplitude of the stimulation. The minimum current that could induce long-lasting atrial fibrillation (30 sec in the clinical setting, 2 sec in the rabbit or rat model) was defined as atrial fibrillation threshold (AFT). AFT was larger in patients who had history of atrial fibrillation than those who did not. Anti-arrhythmic drugs raised AFT by various degrees both in experimental and clinical cases. Long-term efficacy of a drug could be predicted in a patient, measuring how much the drug increased AFT (cut-off point = 5 mA increase). AFT is a useful marker to evaluate atrial vulnerability and to guide pharmacological treatment of atrial fibrillation.

Journal Article↗

PubMed2003

Cardiac sarcoidosis mimicking right ventricular dysplasia.

A 59-year-old woman with skin sarcoidosis was admitted to hospital for assessment of complete atrioventricular block. Cross-sectional echocardiography showed that the apical free wall of the right ventricle was thin and dyskinetic with dilation of the right ventricle. Thallium-201 myocardial imaging revealed a normal distribution. Both gallium-67 and technetium-99m pyrophosphate scintigraphy revealed no abnormal uptake in the myocardium. Right ventriculography showed chamber dilation and dyskinesis of the apical free wall, whereas left ventriculography showed normokinesis, mimicking right ventricular dysplasia. Cardiac sarcoidosis was diagnosed on examination of an endomyocardial biopsy specimen from the right ventricle. A permanent pacemaker was implanted to manage the complete atrioventricular block. After steroid treatment, electrocardiography showed first-degree atrioventricular block and echocardiography revealed an improvement in the right ventricular chamber dilation. Reports of cardiac sarcoidosis mimicking right ventricular dysplasia are extremely rare and as this case shows, right ventricular involvement may be one of its manifestations.

Arrhythmogenic Right Ventricular Dysplasia↗

PubMed2003

Subepicardial aneurysm associated with ventricular septal perforation showing a normal coronary angiogram.

Subepicardial aneurysm is a rare complication of acute myocardial infarction and the present case was associated with ventricular septal perforation. Echocardiography showed the subepicardial aneurysm adjoining the true apico-anteroseptal aneurysm, with the former being discontinuous with the myocardium at its neck, which was narrower than the diameter of the aneurysm. In addition, color Doppler imaging showed shunt flow from the aneurysm to the right ventricle. Coronary angiography revealed extension only of the anterior descending artery without any discernible stenosis. The apical aneurysm was excised and the defect closed with an epicardial patch. The myocardial infarction was probably caused by coronary spasm. Echocardiography was useful for diagnosing the anatomy and hemodynamic condition of the subepicardial aneurysm.

Aged↗

PubMed2002

A case of cardiomyopathy induced by premature ventricular complexes.

Tachycardia-induced cardiomyopathy is a well-known and reversible condition, but the left ventricular dysfunction caused by frequent isolated premature ventricular complexes (PVCs) has been rarely reported. Apparent dilated cardiomyopathy was resolved in a patient after the focal source of PVCs was eliminated by radiofrequency catheter ablation. Echocardiography showed progressive improvement of the abnormal wall motion. Frequent PVCs could be the cause of left ventricular dysfunction in a subset of patients with dilated cardiomyopathy and radiofrequency ablation should be the choice of therapy in those patients.

Cardiomyopathy, Dilated↗

PubMed2002

Neurally mediated syncope manifesting during atrial fibrillation: a case report.

A 64-year-old male was admitted to hospital because of repeated episodes of syncope and palpitation. Ambulatory monitoring revealed paroxysmal atrial fibrillation (AF) as the cause of palpitation; he did not have structural heart disease. The induction of AF by rapid pacing (50 Hz for 1 s) in an upright position provoked syncope with a vasodepressor response. Atropine sulfate blocked the induction of syncope. The possible etiology was neurally mediated syncope that manifested only during AF, which suggests that the abnormal vagal activity during AF in this case exaggerated the vasodepessor response while upright.

Atrial Fibrillation↗

PubMed2002

Swallowing syncope: complex mechanisms of the reflex.

A 69-year-old woman was admitted to our hospital for the examination of syncope. When she ate solid food, she had dizziness or loss of consciousness. The ambulatory ECG suggested sino-atrial block during swallowing with a maximum sinus pause of 6 seconds. An electrophysiologic study revealed pre-existing sinus node dysfunction, which was exaggerated by the balloon inflation in the esophagus. Atropine counteracted the slowing of the basal sinus rate induced by esophageal pressure, but it did not block the effect on the maximum sinus node recovery time. This observation suggested that the syncope was mediated partly by a non-vagal mechanism.

Deglutition↗

PubMed2002

Two cases of polymorphic ventricular tachycardia induced by the administration of verapamil against paroxysmal supraventricular tachycardia.

Verapamil is widely used for the termination of paroxysmal supraventricular tachycardia (PSVT) with little proarrhythmic effect. We describe two cases of PSVT that changed to non-sustained polymorphic ventricular tachycardia after administration of verapamil. Electrophysiological study revealed atrioventricular nodal reentrant tachycardia in the first case, and atrioventricular reentrant tachycardia due to a concealed left lateral accessory pathway in the second case. Catecholamine-induced automaticity was one of the possible mechanisms of VT in the first case, but the mechanism is unknown in the second case.

Anti-Arrhythmia Agents↗