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Biomedical subjects

H Mitamura

Publications and source records attributed to H Mitamura.

At least 55 records · Page 3Linked to original sources
PubMed1997

Increase in heart rate after radiofrequency catheter ablation is mediated by parasympathetic nervous withdrawal and related to site of ablation.

To assess the mechanism for the increased sinus rate after radiofrequency catheter ablation performed for atrioventricular nodal reentrant tachycardia (AVNRT), we studied heart rate variability before and after radiofrequency catheter ablation in 17 patients with AVNRT and in 38 patients with an accessory pathway. The accessory pathway was located at the left ventricular free wall, the right ventricular free wall, or the posterior interventricular septum. An increased sinus rate was observed in patients with AVNRT or with the accessory pathway at the posterior septum or left free wall after radiofrequency ablation. In these groups, high-frequency power, root mean square of successive difference and percent of adjacent cycles that were more than 50 ms apart, all of which are indices reflecting parasympathetic nervous activity, were decreased. The ratio of low-frequency to high-frequency power reflecting sympathovagal balance, was increased in patients with AVNRT or with an accessory pathway at the posterior septum or left free wall. Increases in sinus rate were correlated with decreases in high-frequency power, and percent of adjacent cycles more than 50 ms apart that the increase in heart rate was due to parasympathetic nervous withdrawal.

Adolescent↗
PubMed1997

A case of widely split double P waves with marked intra-atrial conduction delay.

We report a 78-year-old man as the first documented case of double P waves separated by 400 msec on 12-lead ECG. These P waves had different polarities on lead V1. The first P wave represented activation of the lateral wall of the right atrium, and the latter P wave represented activation of the medial right atrium and the left atrium. Widely spaced double potentials were recorded craniocaudally along the line, presumably corresponding to the crista terminalis during sinus rhythm. For this to occur, conduction disturbance has to be present both in the upper and lower right atrium. Conduction disturbance in the upper right atrium would interrupt excitation from the sinus node to the medial wall, and conduction disturbance in the lower right atrium would interrupt excitation spreading from the lower lateral right atrium to the isthmus area where fragmented potentials were recorded. These multiple discrete lesions appear to constitute a unique electrical atriopathy in this patient.

Aged↗
PubMed1997

[Chest radiographic diagnosis of dissecting thoracic descending aorta].

Widening of the aortic shadow on chest radiography is one of the first indicators of aortic dissection. The degree of widening of the aortic shadow was estimated on two successive chest radiographs (mean [+/-SD] interval 0.8 +/- 0.7 years) before and after aortic dissection in 11 patients (four with DeBakey classification type I, seven with type III dissection). The distance between the center of each thoracic vertebra and the lateral margin of the descending aortic shadow (L) was measured. Since only a supine frontal film is usually available in acute aortic dissection, chest radiographs in both erect and supine positions were compared in 18 patients with hypertension. On supine films, L was larger than that on erect films, but the difference (delta L) was minimal (+2.6 mm) at the level of the tracheal bifurcation. Therefore, the L at the level of tracheal bifurcation (Lb) was best suited for comparing films taken in different positions. On supine films, Lb was significantly longer in patients with aortic dissection than in patients with hypertension (60.5 +/- 8.2 vs 46.0 +/- 7.9 mm, p < 0.001), and none with dissection showed Lb < 50 mm. Serial change of L over the follow-up of 1.4 +/- 0.7 years in patients with hypertension was also examined in erect films and was less than +1 mm. When the index film in a supine position was compared with the previous films in an erect position, delta Lb in patients with aortic dissection was +12.7 +/- 5.6 mm, which was significantly greater than that in patients with hypertension (+2.9 +/- 2.8 mm, p < 0.001). All 11 patients with aortic dissection showed delta Lb > or = +7 mm, but only one patient with hypertension (6%) exhibited this finding. Chest radiography is useful for identifying patients with aortic dissection, who characteristically show Lb > or = 50 mm on presentation and delta Lb > or = +7 mm, compared with previous films.

Aged↗
PubMed1997

[Effect of barnidipine hydrochloride on the autonomic nervous system: difference between short- and long-acting components of calcium antagonist].

Short-acting calcium antagonists have a deleterious effect on the prognosis for patients with myocardial ischemia, possibly caused by overactivation of sympathetic nerves due to vasodilatation, negative inotropism, or coronary steal. However, there is considerable debate about whether long-acting calcium antagonists as well as the short-acting calcium antagonists have the same effect. Barnidipine-HCl is a newly-developed calcium antagonist with 1:2 short- and long-acting particles. This study evaluated the changes of autonomic tone due to barnidipine. Both the short- and long-acting effect of the calcium antagonist was evaluated. Eleven patients with primary hypertension underwent 24-hour ambulatory electrocardiogram and blood pressure monitoring before and after the treatment with barnidipine. Heart rate and blood pressure were compared before and after the medication. Heart rate variability was analyzed with a Marquette 8000/T. High frequency power (HF), as a parameter of vagal tone, and the ratio to low frequency power (LF), as a parameter of sympathetic tone, were obtained. Twenty-four-hour average blood pressure decreased significantly during the day, but nocturnal hypotension was not observed. Heart rate did not increase. HF decreased at the peak of the short- and long-acting components. LF/HF increased at the peak of the short-acting component. Short-acting particles of barnidipine had a deleterious effect on the autonomic tone, that is overactivation of sympathetic tone and suppression of vagal tone. Long-acting particles of barnidipine suppressed the vagal tone. These findings suggest that short-acting calcium antagonists may cause arrhythmia or deterioration of coronary ischemia.

Autonomic Nervous System↗
PubMed1996

Assessment of reverse use-dependent blocking actions of class III antiarrhythmic drugs by 24-hour Holter electrocardiography.

OBJECTIVES: This clinical study was designed to compare rate-dependent effects of class III agents on QT prolongation. BACKGROUND: Clinical data that compare the electrophysiologic differences among class III agents with different selectivity for potassium channels are still lacking. METHODS: QT intervals were measured over a wide range of preceding RR intervals during sinus rhythm by 24-h Holter electrocardiography before and after oral administration of four class III agents: E4031, dofetilide, MS551 and d-sotalol. Rate-dependent changes in the QT interval were assessed by the slope of the linear regression line estimating the QT-square root of RR relation. RESULTS: All agents significantly increased the mean slope: E4031 increased the mean [+/- SD] value from 0.32 +/- 0.05 to 0.42 +/- 0.13 (p < 0.01), dofetilide from 0.32 +/- 0.03 to 0.50 +/- 0.12 (p < 0.03), MS551 from 0.35 +/- 0.06 to 0.45 +/- 0.10 (p < 0.02) and d-sotalol from 0.31 +/- 0.05 to 0.33 +/- 0.04 (p < 0.05). However, in those patients given either E4031, dofetilide or MS551, the degree of QT prolongation was smaller at shorter square root of RR intervals and was better preserved at shorter square root of RR intervals by d-sotalol, with a smaller increase in slope (p < 0.02 vs. dofetilide and MS551). CONCLUSIONS: On ambulatory electrocardiography, reverse use dependence in QT prolongation was least prominent with d-sotalol among the four study drugs. In the range of physiologic heart rates, class III agents could manifest different profiles of rate dependence in their QT-prolonging effect.

Adult↗
PubMed1996

Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome.

OBJECTIVES: We examined the modulatory effects of autonomic nervous system and antiarrhythmic drugs on the ST segment in patients with Brugada syndrome to gain an insight into the mechanism of ST segment elevation. BACKGROUND: Right bundle branch block, ST segment elevation and ventricular tachyarrhythmias define a distinct clinical and electrocardiographic (ECG) syndrome (Brugada syndrome). However, the mechanism of ST segment elevation and the causes of this syndrome are unknown. METHODS: The study included four patients in whom structural heart or coronary artery disease was excluded by noninvasive and invasive tests. High take-off ST segment elevation of either the coved or saddle-back type in precordial leads V1, V2 and V3 was seen in all patients. Three patients experienced recurrent episodes of syncope or aborted sudden cardiac death, and the remaining patient had palpitation. Autonomic receptor stimulation and blockade and intravenous administration of antiarrhythmic drugs were performed during sinus rhythm while the 12-lead ECG was recorded. Metaiodobenzylguanidine (MIBG) scanning and Holter monitoring were also performed. RESULTS: Beta-adrenoceptor stimulation by intravenous isoproterenol consistently reduced (> or = 0.1 mV) ST segment elevation at or 80 ms after the J point in all four patients. Selective alpha-adrenoceptor stimulation by intravenous norepinephrine in the presence of propranolol or by intravenous methoxamine consistently augmented, whereas alpha-adrenoceptor blockade reduced, ST segment elevation in three patients. Intracoronary acetylcholine or intravenous edrophonium or neostigmine augmented ST segment elevation without inducing coronary spasm in three of four patients. Class IA antiarrhythmic drugs also consistently augmented (three patients), whereas class IB drugs had no effect on (two patients) ST segment elevation. No abnormality was found on MIBG imaging or heart rate variability in three patients, suggesting that autonomic dysfunction is not a primary disease process. Class IA drugs had no effect on ST segment in three control patients, suggesting that the ST segment elevation seen in patients with Brugada syndrome in response to the drugs is not a nonspecific response. CONCLUSIONS: ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alpha-adrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alpha-adrenoceptor blockade. These responses might be explained by postulating the presence of an area of early repolarization or a local "depolarized" area in the ventricle causing ST segment elevation in this syndrome. Because only a small number of patients were studied, these possibilities need further evaluation.

Adult↗
PubMed1996

Early reduction of neurohumoral factors plays a key role in mediating the efficacy of beta-blocker therapy for congestive heart failure.

This study examined the role played by neurohumoral factors in mediating the effects of beta-blocker therapy for congestive heart failure. Fifteen patients with congestive heart failure underwent beta-blocker therapy. Plasma norepinephrine and alpha-atrial natriuretic peptide concentrations decreased 2 weeks after initiation of beta-blocker therapy. Decrease in plasma norepinephrine level persisted for 6 months. Lymphocyte beta-adrenoceptor density increased 2 weeks after therapy but was not increased 6 months later. Left ventricular ejection fraction was unchanged 2 weeks after therapy, but it increased 6 months after introduction of beta-blockers. Plasma norepinephrine level decreased 2 weeks after the therapy in the responders (increase in ejection fraction > 0.10) but not in the nonresponders. Thus early reduction of neurohumoral factor levels preceded the late improvement of left ventricular contractile function and may therefore be partly responsible for the efficacy of beta-blocker therapy for congestive heart failure.

Adrenergic beta-Antagonists↗
PubMed1996

Effect of a new beta-blocker, nipradilol, on cardiac function and neurohumoral factors in idiopathic dilated cardiomyopathy.

This study investigated the therapeutic efficacy of a new beta-blocker, nipradilol, a non-selective agent with vasodilating activity, for the treatment of idiopathic dilated cardiomyopathy (DCM). The New York Heart Association functional class improved in the nipradilol group (n = 9, p < 0.01), but not in the control group who received conventional therapy (n = 9). The observation period was 19 +/- 7 months in the nipradilol group, and 20 +/- 9 months in the control group. Before therapy there was no difference in heart rate between the 2 groups (76 +/- 12 vs 79 +/- 15 beats/min). The end-diastolic and end-systolic left ventricular dimensions decreased in the nipradilol group (p < 0.05), but not in the control group. Radionuclide ventriculography revealed that the left ventricular ejection fraction increased in the nipradilol group (27 +/- 8 to 41 +/- 18%, p < 0.05), but not in the control group (27 +/- 11 to 27 +/- 8%). Plasma norepinephrine tended to be lowered, although not significantly, whereas plasma alpha atrial natriuretic peptide significantly decreased after the therapy (p < 0.01) in the treatment group. Lymphocyte beta-adrenoceptors were up-regulated in the nipradilol group (p < 0.05). None of these parameters changed during the observation period in the control group. Thus, nipradilol improved symptoms and cardiac function with a favorable effect on neurohumoral factors in patients with DCM.

Adrenergic beta-Antagonists↗
PubMed1996

Sustained monomorphic ventricular tachycardia in a patient with Brugada syndrome.

We report a patient with Brugada syndrome who developed sustained monomorphic ventricular tachycardia (SMVT). The patient was a 29-year-old man who experienced recurrent episodes of palpitation and syncope after drinking alcohol. Electrocardiogram showed right bundle branch block and ST-segment elevation in precordial leads V1-3 without Q-Tc prolongation. Organic heart disease and coronary artery disease were excluded by noninvasive and invasive tests. Ventricular fibrillation was induced by the application of a single extra-stimulus to the right ventricular outflow tract. During isoproterenol infusion, SMVT of left bundle branch block morphology (240/min) was induced by the application of a single extrastimulus to the right ventricular apex. SMVT also developed spontaneously. Pace mapping disclosed that SMVT originated at the free wall of the right ventricular outflow tract. Head-up tilt test and an alcohol provocation test both induced similar SMVT that was associated with hypotension and near syncope. SMVT was not terminated by intravenous administration of lidocaine, procainamide or adenosine triphosphate (10 mg), but was terminated by propranolol. Thus, a beta-adrenoceptor-mediated mechanism appears to play an important role in SMVT in this patient. The site of origin of SMVT might be closely related to the lesion that causes ST-segment elevation.

Adult↗
PubMed1996

Myasthenia-like syndrome induced by overdosage of cibenzoline.

A case of cibenzoline-induced myasthenia-like syndrome is reported. A 67-year-old woman with renal failure and no previous disorder of neuromuscular junction complained of fatigue during climbing up a flight of stairs and experiencing heavy eyelids after administration of 100 mg/day of cibenzoline. Repetitive nerve stimulation tests revealed decrement at 5-10 Hz. After reduction of the dosage, myasthenia-like signs and symptoms disappeared. The peak cibenzoline concentration was still high even after the dose reduction (666.4 ng/ml). In conclusion, cibenzoline, at a high plasma level, may induce myasthenia-like syndrome without any disorder of the neuromuscular junction.

Aged↗
PubMed1996

Ventricular arrhythmias in heart failure.

In the management of patients with chronic heart failure, our attention is shifting from just improving left ventricular function and abolishing ventricular arrhythmias to improving personal longevity. Importantly, sudden cardiac death is a pattern of death in as many as a half of patients with chronic heart failure. Arrhythmias are common in this disorder, but may possibly be a marker of diseased heart rather than a predictor of sudden cardiac death. The mechanisms and triggers of rapid ventricular tachycardia or fibrillation responsible for sudden cardiac death have not been well established. At present, it is important to be reminded that pharmacologic augmentation of cardiac contractility or suppression of asymptomatic ventricular arrhythmias is not an effective approach to preventing sudden cardiac death, but may even be deleterious. Three groups of drugs that have shown efficacy in preventing sudden cardiac death in patients with chronic heart failure are amiodarone, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors. Although how these drugs improve prognosis of heart failure are not clear at present, myocardial protection by these agents appears to be most important.

Arrhythmias, Cardiac↗
PubMed1996

[Usefulness of the newly developed transtelephonic electrocardiogram and computer-supported response system].

The "Cardiophone System" is a system designed to expand the relationship between patients and medical services using a transtelephonic electrocardiogram and computer-assisted answering system. The transtelephonic electrocardiogram, or so-called "Cardiophone", developed by Nihon Kohden, Inc., allows the patients to carry a "Cardiophone" to record electrocardiograms during paroxysmal occurrences of palpitation, chest pain, and other symptoms. The Cardiophone may function as a terminal of the host computer at the hospital, which stores the electrocardiogram and print it as soon as the computer receives the electrocardiogram over the phone. Cardiologists can examine the electrocardiogram immediately after it is printed. Cardiologists and operators are on duty 24 hours a day. Judgments based on the electrocardiogram are made by the cardiologist on duty, and stored in the computer by the operator. The patients may listen to the judgment over the phone within 30 min of sending the electrocardiogram. In the case of potentially lethal findings on the electrocardiogram, the cardiologist on duty calls the patient directly to give a medical advice. We studied 184 outpatients who were enrolled in the Cardiophone System of our hospital. The average number of transtelephonic electrocardiograms was 10 per day. Abnormal electrocardiographic changes were observed in 42 patients, and the diagnoses were as follows: paroxysmal supraventricular tachycardia in 18 patients, paroxysmal atrial fibrillation in 17, ventricular tachycardia in 3, and angina in 7. Among seven patients in whom ST changes were documented by Cardiophone, six were diagnosed as variant angina. In several patients with diagnoses already made by Holter monitoring, the Cardiophone was used to monitor the drug effects and the correlations between symptoms and arrhythmic events. We conclude that the Cardiophone System is useful for diagnosing the causes of paroxysmal cardiac symptoms in some patients and for improving home medical services.

Adolescent↗
PubMed1996

[His bundle block].

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Electrocardiography↗
PubMed1995

Rate-dependent anisotropic conduction property in the epicardial border zone of canine myocardial infarcts and its modification by moricizine.

We evaluated anisotropic conduction properties, different conduction velocities depending on fiber orientation, in normal and infarcted myocardium and the effects of moricizine on anisotropic conduction. Various cycle lengths of stimulation were applied to 15 mongrel dogs, and epicardial mapping was performed using a 96-channel mapping electrode. Moricizine was then administered to seven dogs and the same procedure was performed. Conduction velocities were calculated from these maps. Programmed electrical stimulations were performed before and after moricizine administration to induce ventricular arrhythmias. Before moricizine administration, a rate-dependent decrease in longitudinal conduction velocity was observed in the infarcted zone. Moricizine suppressed longitudinal conduction in the normal zone significantly at 300 msec pacing, but not at slower rates. Moricizine at a dose of 4 mg/kg, on the other hand, suppressed longitudinal conduction in the infarcted zone significantly at all pacing cycle lengths. The effect of moricizine on transverse conduction was inconsistent. In three dogs, sustained ventricular tachycardia (VT) was induced either before or after moricizine administration. The mean cycle length of sustained VT was prolonged from 202 msec to 291 msec after 4 mg/kg of moricizine. Thus, the changes in cycle length of ventricular tachycardia observed were most likely the result of slowing of conduction velocity, especially in the longitudinal direction, in the infarcted myocardium. We conclude that the electrophysiologic nature of the subacute ischemic model was modified by moricizine, leading to depression of the conduction velocity of longitudinal conduction and the inducibility of ventricular arrhythmias.

Analysis of Variance↗