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Biomedical subjects

Takeshi Ueyama

Publications and source records attributed to Takeshi Ueyama.

10 recordsLinked to original sources

Effect of endoscopic transthoracic sympathicotomy on plasma natriuretic peptide concentrations in humans.

BACKGROUND: The effects of endoscopic transthoracic sympathicotomy (ETS) on plasma natriuretic peptides concentrations in humans were examined in order to elucidate the role of the sympathetic nervous system in their regulation. METHODS AND RESULTS: Thirty-seven patients with palmar hyperhidrosis underwent ETS. Cardiac functional indices were assessed by echocardiography, and plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations were measured before and after ETS. ETS caused decreases in heart rate, mean arterial pressure, systemic vascular resistance, and increases in left ventricular (LV) end-diastolic volume, stroke index, ejection fraction, and left atrial diameter. LV end-systolic volume and cardiac index remained unchanged. Following ETS, ANP increased from 10.7+/-5.9 to 24.7+/-16.8 pg/ml (p < 0.01), and BNP increased from 5.1+/-4.2 to 19.7+/-21.5 pg/ml (p < 0.01). From the multivariate regression analysis, ETS, age and gender were determined to be significant predictors of changes in the ANP and BNP concentrations. None of the hemodynamic parameters were useful as independent predictors. CONCLUSION: The plasma concentrations of ANP and BNP increased after ETS, independent of hemodynamic changes, and apparently because of the release of the inhibitory effects of the cardiac sympathetic nerves on natriuretic peptide secretion.

Adult↗

[Diagnosis and treatment for limb edema due to venous disease].

We described the diagnosis and treatment for limb edema due to venous disease in this paper. Venous limb edema is caused by vein pressure elevation, which is induced by venous reflux, flow disturbance and overflow. Valve incompetence causes varicose vein and deep venous insufficiency of lower extremities. Deep vein thrombosis is the most popular disease among the venous obstruction morbidity. Arterio-venous fistula for hemodialysis sometimes induces venous arm edema due to overflow. Arm edema due to venous hypertension appears more clearly when it is associated by subclavian vein stenosis or occlusion. There are several causes for venous edema. So, we have to make an appropriate treatment based on the clear diagnosis.

Adolescent↗

Differentiation of the electrophysiological effects on the atrial myocardium between the pure Na channel blocker, pilsicainide, and flecainide.

UNLABELLED: The purpose of this study was to identify the difference between the pure Na channel blocker, pilsicainide and Ic-antiarrhythmic drug, flecainide, on the atrial electrophysiological characteristics. METHODS: The subjects consisted of 24 patients (48 +/- 12 years-old: P-group) in whom pilsicainide was administrated intravenously (1 mg/kg/10 min) and 31 patients (47 +/- 15 years-old: F-group) in whom flecainide was administrated intravenously (2 mg/kg/10 min). The atrial effective refractory period (ERP-A), intra-atrial conduction time (CT), max intra-atrial conduction delay (Max CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAZ) and intra-atrial conduction delay zone (CDZ) were measured before and after the drugs. RESULTS: Pilsicainide and flecainide significantly prolonged the ERP-A (211 +/- 27 msec to 246 +/- 39 msec; p < 0.001, 217 +/- 25 msec to 244 +/- 33 msec; p < 0.001, respectively) and CT (121 +/- 33 msec to 149 +/- 43 msec; p < 0.001, 122 +/- 22 msec to 153 +/- 27 msec; p < 0.001, respectively) to the same degree. However, the Max CD was shortened by pilsicainide, but not by flecainide. The RAFZ, FAZ and CDZ decreased in the P-group (21 +/- 25 msec to 4 +/- 10 msec; p < 0.01, 24 +/- 24 msec to 14 +/- 18 msec; p < 0.05, 56 +/- 29 msec to 43 +/- 32 msec, p < 0.05, respectively), but not in the F-group. CONCLUSIONS: The effects of atrial conduction delays may differ between pilsicainide and flecainide. Further examination will be needed to explain this mechanism.

Adult↗

Thoracoscopic sympathetic surgery for hand sweating.

Recently, thoracoscopic surgery has been shown to be effective for the relief of hand sweating. Although it is not fatal if left untreated, the treatment aim is to improve the quality of daily life. Therefore, it is important to understand the complaints of the patient, and provide an adequate explanation regarding postoperative sequelae. Surgeons should also recognize that thoracoscopic surgery might cause problems when performed, as the general risk of surgery remains. Many patients have been helped by the procedure, as their choices in life have expanded, and satisfactory results can be obtained when indication is determined by a full examination of the patients condition. Between December 1999 and September 2002, we performed thoracoscopic sympathetic surgery in 556 consecutive patients. Five-hundred seventeen (93%) of these complained of profuse hand sweating. Based on the new concept presented, we consider that this method of operation is an effective treatment.

Ganglia, Sympathetic↗

Effects of flecainide on the electrophysiological properties of atrial vulnerability in humans.

The aims of this study were to evaluate the changes in the electrophysiological characteristics of the right atrium after the administration of flecainide and to clarify whether flecainide has a selective effect on human atrial tissue. Electrophysiological measurements were made in 38 patients, before and after intravenous administration of flecainide (2 mg/kg per 10 min). The effective refractory period of the right atrium (ERP-A), maximum conduction delay (Max.CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduction delay zone (CDZ) were studied in the patients who were divided into 2 groups based on whether repetitive atrial firing (RAF) was induced in the baseline study. Flecainide significantly prolonged the ERP-A (202+/-22 to 238+/-33 ms, p<0.001) and shortened Max.CD (77+/-17 to 63+/-32 ms, p<0.05) in the patients with RAF, but not in those without RAF in the baseline study. After flecainide administration, there were significant reductions in the RAFZ (43+/-22 to 13+/-19 ms, p<0.0001), FAAZ (51+/-22 to 28+/-26 ms, p<0.001) and CDZ (70+/-21 to 48+/-30 ms, p<0.01) in the patients with RAF. However, atrial fibrillation (AF) was induced by stimulation after flecainide in 2 patients without RAF in the baseline study. There was a significant negative correlation between the ERP-A in the baseline study and the change in the ERP-A upon flecainide administration (r=0.45, p<0.01). Flecainide may preferentially activate the substrate for AF and RAF, but that action is mainly based on the electrophysiological characteristics found in the baseline study.

Anti-Arrhythmia Agents↗

Decrease in the spatial dispersion at the termination of atrial fibrillation by intravenous cibenzoline.

Atrial electrograms were recorded from the high right atrium, coronary sinus, and right lateral wall in 15 patients with induced atrial fibrillation (AF). Intravenous cibenzoline terminated AF in 8 patients (T group), but not in 7 patients (non-T group). The cycle length of the AF (AFCL) obtained by the autocorrelation function was measured every 5 s during the 30 s prior to the cibenzoline administration, and just before the termination of AF or at the end of the cibenzoline infusion in the non-T group. The mean AFCL, and spatial and temporal dispersion of the AFCL were then compared between the 2 groups (dispersion = standard deviation x 100 /mean AFCL). Cibenzoline significantly increased the mean AFCL and decreased the spatial dispersion in both groups. No significant difference in either the mean AFCL or temporal dispersion before or after cibenzoline was observed between the 2 groups. In addition, no significant difference in the spatial dispersion before the cibenzoline was observed, but the spatial dispersion after the cibenzoline was significantly smaller in the T group than in the non-T group. The mean AFCL, and the spatial and temporal dispersion before the cibenzoline did not predict the termination of AF. The decrease in the spatial dispersion may be the most important mechanism by which intravenous cibenzoline terminates AF.

Aged↗

Endoscopic thoracic sympathicotomy for Raynaud's phenomenon.

PURPOSE: For many years, thoracic sympathectomy via open surgery was not used to treat Raynaud's phenomenon because of the invasiveness of this procedure and the poor long-term outcomes associated with it. However, with the introduction of endoscopic surgery, thoracic sympathectomy (or sympathicotomy) has been performed by some surgeons as a less invasive surgical option for patients with Raynaud's phenomenon. The less invasive procedure has the possibility of emphasizing merits of sympathectomy. The purpose of this study was to reevaluate the efficacy of sympathicotomy for Raynaud's phenomenon with endoscopic technique and its range of applicability. METHODS: Between December 1992 and August 2001, endoscopic thoracic sympathicotomy (ETS) was performed in 28 patients with Raynaud's phenomenon (of a total of 502 patients with autonomic disorders who underwent ETS) at National Kanazawa Hospital. We considered indications for surgical treatment of Raynaud's phenomenon to include severe chronic symptoms or nonhealing digital ulceration refractory to intensive medical therapy. All patients were mailed a self-assessment questionnaire after surgery to determine the immediate and long-term results of the procedure. Data from both initial and long-term follow-up examinations were obtained. RESULTS: Fifty-four ETS procedures were performed in 28 patients. No operative mortality was seen, and no occurrence of major complications necessitated open surgery. Initial resolution or improvement of symptoms was achieved in 26 of 28 patients (92.9%). However, later in the postoperative period, symptoms recurred in 23 of 28 patients (82.1%), although no recurrence of digital ulceration was seen throughout our observation. At the final follow-up examination (median follow-up period, 62.5 months), 25 patients (89.3%) reported overall improvement of the frequency and severity of their symptoms. CONCLUSION: Despite the high rate of recurrence, ETS clearly produced a high rate of initial relief. ETS did indeed promote healing of digital ulcers, and the procedure shows potential for reducing the severity of refractory symptoms. We consider ETS to be the method of choice for treatment of severe or refractory Raynaud's phenomenon, and especially for Raynaud's involving digital ulcer, because of its safety and efficacy.

Adult↗

Beta-blocker decreases the increase in QT dispersion and transmural dispersion of repolarization induced by bepridil.

Bepridil is effective for intractable cardiac arrhythmia, but in rare cases will induce torsades de pointes (TdP) associated with QT interval prolongation. Beta-blockers will effectively prevent TdP in some clinical settings, so the effect of beta-blocker on the change in QT interval, QT dispersion and transmural dispersion of repolarization (TDR) induced by bepridil was investigated in 10 patients (7 male, 3 female; 62+/-6 years old) with intractable paroxysmal atrial fibrillation. The QTc interval, QTc dispersion and TDR were measured before and after 1 month of administration of bepridil, and then a beta-blocker was added and the QTc interval, QTc dispersion and TDR re-measured 1 month later. Bepridil significantly prolonged the QTc interval (0.42+/-0.05 to 0.50+/-0.08; p<0.01), and increased both the QT dispersion (0.07+/-0.05 to 0.14+/-0.08; p<0.01) and TDR (0.10+/-0.04 to 0.16+/-0.05; p<0.01). The addition of a beta-blocker decreased the QTc interval (0.50+/-0.08 to 0.47+/-0.04; p=0.09) and significantly decreased both the QTc dispersion (0.14 +/-0.08 to 0.06+/-0.02; p<0.01) and TDR (0.16+/-0.05 to 0.11+/-0.04; p<0.001). Compared with the control, the combination therapy significantly prolonged the QTc interval, but did not increase either QTc dispersion or TDR, and so was effective in all patients with intractable AF. The findings suggest that beta-blocker reduces the increase in QT dispersion and TDR induced by bepridil, and combined therapy with bepridil and beta-blocker might thus be useful for intractable atrial fibrillation.

Adrenergic beta-Antagonists↗

[Up-regulation of inositol 1, 4, 5-trisphosphate receptor expression in atrial tissue in patients with chronic atrial fibrillation].

BACKGROUND: Abnormal intracellular Ca2+ homeostasis occurs in chronic atrial fibrillation(AF). The intracellular Ca2+ concentration is regulated by ryanodine and inositol 1,4,5-trisphosphate (IP3) receptors. Changes occur in ryanodine receptors in atrial tissue from patients in chronic AF. Whether AF patients have alterations in atrial IP3 receptors was investigated. METHODS: IP3 receptor expression was analyzed in the right atrial myocardium from 13 mitral valvular disease (MVD) patients with AF (MVD/AF), 5MVD patients with normal sinus rhythm(MVD/NSR), and 8 control patients with NSR(tissue obtained during coronary artery bypass surgery). Hemodynamic and echocardiographic data were obtained preoperatively, and an immunohistochemical study was performed on the atrial tissue. RESULTS: The relative expression level of IP3 receptor protein was significantly greater in MVD/AF (0.75 +/- 0.26) than in MVD/NSR (0.42 +/- 0.13, p < 0.01), and both were significantly above the control value (0.14 +/- 0.08). The relative expression level of IP3 receptor mRNA was significantly greater in MVD/AF(0.028 +/- 0.008) than in control subjects (0.015 +/- 0.004, p < 0.01), but MVD/AF patients did not differ from MVD/NSR (0.020 +/- 0.006) patients. The relative expression levels of IP3 receptor protein and mRNA were higher in patients with left atrial dimension > or = 40 mm, pulmonary capillary wedge pressure > or = 10 mmHg, and right atrial pressure > or = 5 mmHg. IP3 receptors were overexpressed in the cytosol and at the nuclear envelope of atrial myocytes in MVD. CONCLUSIONS: Since chronic mechanical overload of the atrial myocardium increases IP3 receptor expression, especially in patients with chronic AF, up-regulation of IP3 receptors may be important in modulating intracellular Ca2+ homeostasis and initiating and/or perpetuating AF.

Atrial Fibrillation↗

[Lethal arrhythmias--etiological view and therapeutic approach].

Life threatening arrhythmias may cause sudden cardiac death and are divided into bradyarrhythmias and tachyarrhythmias. Most of lethal arrhythmias result from structural (fibrosis and scar due to ischemia) and functional(heart failure and autonomic nerve) abnormalities of the myocardium. But primary electrical diseases, which are caused by the abnormalities of the gene, may also develop lethal arrhythmias without such abnormalities. The treatment of lethal arrhythmias consists of pharmacologic, non-pharmacologic therapy and combination of those. Current meta-analysis have showed the efficacy of K channel blockers as an anti-arrhythmic drug for lethal tachyarrhythmias. Pacemaker therapy for brady-arrhythmia has been established as non-pharmacologic therapy. Additionally, radiofrequency catheter ablation is useful for some lethal arrhythmias but most case should be considered for implantation of ICD. Recently, upstream approach to arrhythmia has been emphasized and recognized as a preventive method for lethal arrhythmias.

Anti-Arrhythmia Agents↗