Biomedical subjects

Hiroyuki Kakugawa

Publications and source records attributed to Hiroyuki Kakugawa.

5 recordsLinked to original sources

PubMed2004

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↗

PubMed2003

New method of determining the atrial fibrillation cycle length during human atrial fibrillation.

INTRODUCTION: The aim of this study was to investigate the usefulness of the autocorrelation function (reversed fast Fourier transform analysis) in determining the atrial fibrillation cycle length (AFCL) during human atrial fibrillation (AF). METHODS AND RESULTS: From 30 episodes of atrial electrograms recorded for 30 seconds from the high right atrium during type I AF in 16 patients, the mean, 5th percentile (p5), and 95th percentile (p95) of the AFCLs were measured by using a computer-picked activation time. The peak, minimum, and maximum AFCLs also were measured by using the autocorrelation function. The mean AFCL was retrieved at the point of the maximum peak of the coefficient of the first positive autocorrelogram. The minimum AFCL (min AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from negative to positive, and the maximum AFCL (max AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from positive to negative. There was a significantly strong correlation between the mean and peak AFCLs (r = 0.995, P < 0.0001), p5 and min AFCLs (r = 0.953, P < 0.0001), and p95 and max AFCLs (r = 0.98, P < 0.0001). CONCLUSION: The autocorrelation function was useful in determining the AFCLs, at least during type I AF. The min AFCL may be used as an index of the refractory period during AF when the p5 AFCL approximates the refractory period.

Aged↗

PubMed2003

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↗

PubMed2003

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↗

PubMed2002

[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↗