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Biomedical subjects

H Atarashi

Publications and source records attributed to H Atarashi.

52 records · Page 3Linked to original sources
PubMed1989

Coronary artery-left ventricular fistulae with atrial septal defect.

We describe a 65-year-old woman who had coronary artery-left ventricular fistula associated with atrial septal defect of the sinus venosus type, and left-sided heart failure. Although a cardiac valve anomaly associated with coronary artery fistula has been described, atrial septal defect has not been reported previously in this condition.

Aged↗
PubMed1989

[Long-term follow-up of the f wave amplitude in chronic atrial fibrillation].

Long-term follow-up of the amplitude of fibrillatory waves (f waves) on the standard electrocardiograms 0.6 +/- 3.3 yr, up to 20 yrs) was performed in 45 patients with chronic stable atrial fibrillation (24 men and 21 women, average age 60.2 +/- 11.5 yrs). The patients were divided into three groups on the basis of the underlying heart disease. Seventeen patients with mitral stenosis were classified as the MS group, 11 with hypertensive heart disease, old myocardial infarction, and aortic insufficiency as the HD group, and 17 without apparent heart diseases as the no heart disease (NHD) group. The f wave amplitude was measured at lead V1 according to the technique employed by Peter. The initial f wave amplitudes of the MS group (0.24 +/- 0.12 mV, mean +/- SD) and of the HD group (0.19 +/- 0.08 mV) were significantly larger than that of the NHD group (0.13 +/- 0.08 mV, p less than 0.05). The f wave amplitudes were significantly decreased during the observation period in each group, and the terminal f wave amplitudes (expressed as the percent of the initial f wave amplitude) were 61 +/- 34% in MS group, 59 +/- 26% in the HD group and 67 +/- 34% in the NHD group. In the NHD group, there was no significant difference in the terminal f wave amplitude between the cases with (n = 10) and without (n = 7) maintenance dose of digitalis. These results showed the apparent reduction of the f wave amplitude with perpetuation of this arrhythmia, and suggested that maintenance doses of digitalis had little effect on this process.

Aged↗
PubMed1988

Clinical and electrocardiographic characteristics of responders and nonresponders to class IA antiarrhythmic drugs.

A retrospective analysis of 44 patients was carried out to evaluate the efficacy of class IA antiarrhythmic drugs (disopyramide and/or procainamide), and of drugs of one or more other classes by means of 24-hour Holter recording. This study included only patients who exhibited 5000 or more ventricular premature complexes (VPCs) during a 24-hour pretrial baseline recording. The drugs that reduced the frequency of VPCs by at least 50% were considered effective. Eighteen patients (41%) responded to class IA drugs (responders) and 26 patients (59%) did not (nonresponders). There was a significant difference between the two groups in relation to the types of disease (p less than 0.01), but no significant difference with regard to other clinical and electrocardiographic characteristics. There was a significant discordance between trials of class IA drugs and class IC drugs (p less than 0.05). The efficacy of class IA drugs is very similar to that of class IB drugs, and only class IC drugs represent the highest efficacy in patients refractory to both class IA and class IB drugs. In conclusion, when ventricular arrhythmias do not respond to class IA or IB drugs, class IC drugs could be chosen as the next regimen.

Adult↗
PubMed1985

Dispersion of ventricular repolarization and arrhythmia: study of two consecutive ventricular premature complexes.

The effect of two consecutive ventricular premature stimuli (S1S2) during atrial pacing on dispersion of repolarization and inducibility of ventricular arrhythmias was studied in 16 dogs under control conditions and in four dogs in the presence of an increased dispersion of repolarization during atrial pacing induced by general hypothermia and regional warm blood perfusion via selective cannulation of the distal branch of left anterior decending coronary artery. Dispersion of repolarization was measured as the maximal difference between the ends of six simultaneously recorded monophasic action potentials (MAPs) from anterior ventricular surface, and consisted of MAP duration difference and activation time difference. Dispersion of repolarization during atrial pacing at control was 29 +/- 7 msec (activation time difference 4 +/- 6 msec, MAP duration difference 25 +/- 8 msec), that after S1 at paraseptal the site was 81 +/- 8 msec (activation time difference 73 +/- 12 msec, MAP duration difference 8 +/- 5 msec), and that after S1S2 was 148 +/- 27 msec (activation time difference 103 +/- 21, MAP duration difference 44 +/- 26 msec). Neither S1 nor S1S2 induced ventricular arrhythmia. Hypothermia and regional warm blood reperfusion increased dispersion of repolarization during atrial pacing to 70 +/- 22 msec (activation time difference 9 +/- 3 msec, MAP duration difference 61 +/- 19 msec). During hypothermia and regional warm blood reperfusion, S1 produced a dispersion of repolarization of 149 +/- 29 msec (activation time difference 85 +/- 8 msec, MAP duration difference 64 +/- 23 msec) and did not induce ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effects of mexiletine on action potential duration and its restitution in guinea pig ventricular muscles.

To clarify the mechanism of mexiletine-induced changes in action potential duration (APD), we studied the effects of mexiletine (2 micrograms/ml) on APD at 0 mV (APD0mV) and 90% (APD90%) repolarization and on restitution of premature responses in guinea pig ventricular muscle at three extracellular potassium concentrations [( K]0) and three stimulation rates using standard microelectrode techniques. The rates at which APD0mV and APD90% were shortened by mexiletine (S-APD0mV and S-APD90%) expressed as percent change from control were most pronounced at [K]0 = 5.4 mM. The percent changes at the three concentrations were 5.0 +/- 2.1% at a [K]0 of 2.7 mM, 6.0 +/- 3.2% at 5.4 mM and 1.8 +/- 1.2% at 10.0 mM for S-APD0mV and 2.0 +/- 1.9%, 4.7 +/- 2.0% and 1.3 +/- 1.5% for S-APD90% at the same concentrations, respectively. S-APD0mV and S-APD90% were more markedly affected when stimulated at a frequency of 1 Hz than when stimulated at 0.2 or 0.5 Hz. Mexiletine failed to produce any additional APD shortening beyond that produced by the introduction of tetrodotoxin (2.5 X 10(-6) M). Mexiletine and tetrodotoxin did not influence APD restitution that fitted a single exponential curve. We conclude that the shortening of APD by mexiletine results from inhibition of a tetrodotoxin-sensitive sodium current.

Action Potentials↗
PubMed1984

Cycle length-dependent action potential duration in canine cardiac Purkinje fibers.

We studied the effects of pharmacologic probes that affect predominantly the Na inward current [tetrodotoxin (TTX), lidocaine], the slow inward current [cobalt, isoproterenol, verapamil], and the potassium currents [tetraethylammonium chloride (TEA), SG-75] on the duration of the action potential (APD) of canine cardiac Purkinje fibers during steady state and restitution. A schema is proposed in which the APD during steady state or restitution is determined by three factors: maximum action potential duration (APDmax), kinetics of restitution, and "memory." The predicted APDmax was 469 +/- 34 (SE) ms (n = 27) in control. It was prolonged (P less than 0.05) by cobalt, verapamil, and TEA and shortened (P less than 0.05) by TTX, lidocaine, isoproterenol, and SG-75. In control, the kinetics of restitution were described by a sum of two exponentials with time constant T1 = 137 +/- 9 ms and T2 = 1,665 +/- 135 ms (n = 27), respectively. T1 was prolonged (P less than 0.05) by TTX, lidocaine, and verapamil but was not changed by other probes. None of the probes studied altered the T2 of restitution or the memory factor, computed at a cycle length of 500 ms from the predicted APDmax and the plateau of restitution. Low temperature (31 degrees C) prolonged APDmax and T1 and reduced the memory. We conclude that each of the proposed three factors is controlled by different mechanisms and that a TTX-sensitive current appears to contribute to the process of restitution of APD.

Action Potentials↗
PubMed1981

A case of myotonic dystrophy associated with sick sinus syndrome.

A 22-year-old man with myotonic dystrophy associated with sick sinus syndrome is described. The patient showed marked weakness of grasping power, grip myotonia, percussion myotonia, bilateral cataracts, fixed facial expression and elevation of serum CPK level, and was diagnosed as having myotonic dystrophy. The Holter ECG showed marked sinus bradyarrhythmia at the rate of 25 beats per minute and the sinus node recovery time using overdrive suppression test was significantly prolonged. These findings indicated the patient also suffered from the sick sinus syndrome. Although various kinds of ECG abnormalities have been noted in the cases with myotonic dystrophy, there have been very few descriptions concerning the involvement of sinus node dysfunction in this disorder.

Adult↗