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T Ohe

Publications and source records attributed to T Ohe.

At least 19 recordsLinked to original sources
PubMed1992

Frequency analysis of signal-averaged electrocardiogram in patients with right ventricular tachycardia.

OBJECTIVES: The purpose of this study was to analyze the frequency content of signal-averaged electrocardiograms (ECGs) in patients with idiopathic ventricular tachycardia of right ventricular origin and in patients with arrhythmogenic right ventricular dysplasia. BACKGROUND: The late potentials in the time domains are usually found in patients with arrhythmogenic right ventricular dysplasia. They are not usually found in patients with idiopathic ventricular tachycardia of right ventricular origin. METHODS: Fast Fourier transform analysis of signal-averaged ECGs was performed with the use of a Blackman-Harris window in 43 subjects: 20 normal volunteers (group I), 12 patients with idiopathic ventricular tachycardia of right ventricular origin (group II) and 11 patients with arrhythmogenic right ventricular dysplasia (group III), and the frequency spectrum was displayed in a three-dimensional graph. Area ratio (ratio of the area under the spectral plot from 40 to 120 Hz to the area from 0 to 120 Hz) was calculated in all subjects. RESULTS: Area ratio was significantly higher in group II than in group I (243 +/- 45 vs. 196 +/- 15, p < 0.01) and significantly higher in group III (396 +/- 51) than in group I or II (p < 0.001). The high frequency components in group II were confined within the QRS complex in the three-dimensional graph, whereas those in group III extended outside the QRS complex. CONCLUSIONS: Frequency analysis of the signal-averaged ECG with fast Fourier transform analysis can detect the high frequency components in patients with right ventricular tachycardia, including idiopathic ventricular tachycardia and arrhythmogenic right ventricular dysplasia.

Adult↗
PubMed1992

Y-29794--a non-peptide prolyl endopeptidase inhibitor that can penetrate into the brain.

A novel non-peptide prolyl endopeptidase (PPCE) inhibitor, Y-29794, has been identified. Y-29794 selectively and competitively inhibited rat brain PPCE (Ki = 0.95 nM) in a reversible manner. Ex vivo study demonstrated that Y-29794 could penetrate into brain to exhibit dose-dependent and long-lasting inhibition. Furthermore, Y-29794 was found to potentiate the effect of TRH on the release of ACh in the rat hippocampus. These results indicate that Y-29794 is an orally active, potent and specific PPCE inhibitor and should be of value in studies on the physiological role of the enzyme in neuropeptide metabolism especially in memory process.

Acetylcholine↗
PubMed1992

Bradycardia-induced abnormal QT prolongation in patients with complete atrioventricular block with torsades de pointes.

Fourteen patients with complete atrioventricular block with or without torsades de pointes (TdP) were included in this study. They were divided into 2 groups, 6 patients with TdP (TdP[+] group) and 8 patients without TdP (TdP[-] group). The patients were evaluated at 2 different periods, before (acute period) and after (chronic period) pacemaker implantation. In the acute period, the QRS and heart rate during the escape rhythm were not significantly different between the 2 groups; however, the QT and QTc intervals were significantly longer in the TdP(+) group than in the TdP(-) group: 753 +/- 57.5 vs 635 +/- 78.4 ms (p less than 0.01) and 585 +/- 44.8 vs 476 +/- 58.3 ms (p less than 0.01). In the chronic period (greater than 2 months after pacemaker implantation), we changed the pacemaker rate from 90 or 100 beats/min to 50 beats/min and examined the QT interval changes in relation to the heart rate. The QT interval in the TdP(+) group was significantly prolonged compared with the TdP(-) group when the pacing rate was decreased less than or equal to 60 beats/min: 551 +/- 40 vs 503 +/- 36 ms at 60 beats/min (p less than 0.05), and 700 +/- 46 vs 529 +/- 43 ms at 50 beats/min (p less than 0.001). Patients with complete atrioventricular block with TdP had a bradycardia-sensitive repolarization abnormality and this characteristic remained after pacemaker implantation. The critical heart rate that induced abnormal QT prolongation in the TdP(+) group was less than or equal to 60 beats/min.

Adult↗
PubMed1992

Induction of TU abnormalities in patients with torsades de pointes.

1. TU abnormalities could be induced by the specific interventions in the majority of the patients with TDP in chronic stage: isoproterenol in congenital long QT patients, disopyramide in Ia-related TDP patients, and slow heart rate in bradycardia-related TDP patients. 2. Humps in MAP could be recorded in all patients with congenital long QT syndrome by isoproterenol, in half of the patients with Ia-related TDP by disopyramide, but in none of the control patients by these agents. 3. The results suggested that TU abnormalities and the occurrence of hump in MAP were hypersensitive reactions. 4. The results also suggested that specific intervention was not enough for the appearance of marked TU abnormalities in some TDP patients, especially in Ia-related TDP patients. Additional aggravating factors were probably required for marked TU abnormalities and the occurrence of TDP in these patients.

Action Potentials↗
PubMed1992

Effects of a combination of disopyramide and mexiletine on the anterograde accessory pathway conduction in patients with Wolff-Parkinson-White syndrome.

In order to evaluate the electrophysiological effects of the combined administration of disopyramide and mexiletine on anterograde accessory pathway conduction, we studied 11 patients with Wolff-Parkinson-White (WPW) syndrome. Disopyramide was first infused intravenously at 1 mg kg-1 for 5 min followed by a continuous infusion at 0.025 mg kg-1 min-1. After the infusion rate of disopyramide was decreased to 0.004 mg kg-1 min-1 to maintain a lower serum concentration, mexiletine was infused at 2 mg kg-1 for 5 min followed by a continuous infusion at 0.008 mg kg-1 min-1 (protocol 1). The shortest atrial paced cycle length with 1:1 anterograde accessory pathway conduction (shortest CL with 1:1) and the anterograde effective refractory period of the accessory pathway (ERP) were measured: (1) before drug administration, (2) after disopyramide was given alone, and (3) after disopyramide and mexiletine were combined at lower concentrations. The same protocol was repeated with the order of drug administration reversed (mexiletine followed by disopyramide) in all patients (protocol 2). Both disopyramide and mexiletine lengthened the shortest CL with 1:1 and the ERP to the same degree. The combination of disopyramide and mexiletine at lower concentrations further lengthened the shortest CL with 1:1. It was longer than with disopyramide (protocol 1) or mexiletine (protocol 2) alone [protocol 1: 412 +/- 169 ms (combination) vs 356 +/- 117 ms (disopyramide); P less than 0.05, protocol 2: 409 +/- 166 ms (combination) vs 355 +/- 119 ms (mexiletine); P less than 0.01].(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Significance of ventricular pacing site in manifest entrainment during orthodromic atrioventricular reentrant tachycardia with left-sided accessory pathway.

We examined entrainment by ventricular pacing in six patients during orthodromic atrioventricular reentrant tachycardia (AVRT) utilizing a left-sided lateral accessory pathway. Constant fusion and progressive fusion were demonstrated in all patients by left ventricular pacing during tachycardia, but in none of the patients by right ventricular pacing. When left ventricular pacing was performed during AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous pacing beat (n - 1) within the ventricle, therefore, constant fusion and progressive fusion were demonstrated in the surface electrocardiographic QRS complexes. On the other hand, when right ventricular pacing was performed during orthodromic AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous paced beat (n - 1) within the normal atrioventricular pathway, and constant fusion and progressive fusion were therefore not demonstrated. These phenomena were explained by the relationship of the ventricular pacing site and the reentrant circuit. This study demonstrates the importance of the pacing site in manifest entrainment of orthodromic AVRT during ventricular pacing.

Adult↗
PubMed1992

Spectral analysis of signal-averaged electrocardiograms in patients with idiopathic ventricular tachycardia of left ventricular origin.

BACKGROUND: The signal-averaged ECG has been used to detect late potentials, and it is considered a noninvasive marker for areas of slow conduction requisite for reentrant arrhythmia. Late potentials are not usually found in patients with idiopathic ventricular tachycardia (VT); nevertheless, fragmented electrograms are often recorded in those patients during endocardial mapping. The purpose of this study was to investigate the spectral content of the signal-averaged ECGs with use of fast Fourier transform analysis (FFT) in patients with idiopathic VT of left ventricular origin. METHODS AND RESULTS: Signal-averaged ECGs were recorded in 12 patients with idiopathic VT originating from the left ventricle (group 1) and 25 age-matched normal volunteers (group 2). Frequency analysis with FFT was performed with a Blackman-Harris window in a segment length of 120 msec from 40 msec before the end of the QRS complex, and the frequency spectrum was displayed in a three-dimensional graph. Area ratio 1 (area of 20-50 Hz/area of 10-50 Hz) and area ratio 2 (area of 40-100 Hz/area of 0-40 Hz) were calculated in all subjects. Late potentials defined by the time domain were negative in all subjects. The area ratios of group 1 were significantly higher than those of group 2. High-frequency components in the three-dimensional graph were confined within the QRS complex. CONCLUSIONS: These results suggest that frequency analysis of signal-averaged ECGs with FFT is an available method for detecting the high-frequency component within the QRS complex in some patients with idiopathic VT of left ventricular origin.

Adult↗
PubMed1992

[Effects of glucose ingestion on hepatic hemodynamics in patients with liver disease by per-rectal portal scintigraphy using 99mTcO4- (direct intramural administration of radioisotope method)].

Effects of glucose (225 ml, 300 kcal) ingestion on hepatic hemodynamics was studied in ten patients with liver cirrhosis and eight patients with non cirrhotic liver disease by per-rectal portal scintigraphy using 99mTcO4- (direct intramural administration of radioisotope method). Initial portal blood flow index (IP) and collateral index (CI) were calculated from the time activity curve of heart and liver. The value of IP was not significantly changed between before and after glucose ingestion in cases with liver cirrhosis (before: 0.0160 +/- 0.0016, after: 0.204 +/- 0.106). In cases with non cirrhotic liver disease, the value of IP was significantly increased after glucose ingestion (before: 0.0381 +/- 0.0145, after: 0.0544 +/- 0.0194, p less than 0.02). These findings suggested increase in portal blood flow via inferior mesenteric vein to the cardiac blood flow. The value of CI before glucose ingestion was significantly increased in cases with liver cirrhosis (0.751 +/- 0.156) compared with that in cases with non cirrhotic liver disease (0.517 +/- 0.122), but no significant difference in values after glucose ingestion was found between these two groups.

Administration, Oral↗
PubMed1991

Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia.

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.

Adult↗
PubMed1991

Differential response of QTU interval to exercise, isoproterenol, and atrial pacing in patients with congenital long QT syndrome.

Sympathetic stimulation is well known to contribute to the genesis of QTU prolongation and ventricular tachyarrhythmias in patients with congenital long QT syndrome. In this study, we performed exercise treadmill testing, isoproterenol infusion (1-2 micrograms/min), and right atrial pacing (cycle length 500 msec) in 11 patients with congenital long QT (LQT) syndrome (LQT group) and in 12 age- and sex-matched controls (control group). The responses of the corrected QT (QTc; Bazett's method) interval and the TU wave complex were evaluated. The QTc interval was prolonged from 482 +/- 63 msec1/2 to 548 +/- 28 msec1/2 by exercise in the LQT group (n = 11; P less than 0.005), and this was associated with fusion of the T waves with enlarged U waves, whereas the QTc interval did not increase with exercise in the control group (n = 12; 402 +/- 19 msec1/2 vs 409 +/- 22 msec1/2). The QTc interval was also prolonged from 466 +/- 50 msec1/2 to 556 +/- 33 msec1/2 by isoproterenol in the LQT group (n = 7; P less than 0.005) in association with morphological changes of the TU wave complex like those seen with exercise, whereas it was only slightly increased from 399 +/- 10 msec1/2 to 436 +/- 13 msec1/2 by isoproterenol in the control group (n = 77; P less than 0.001). However, the QTc interval did not increase with atrial pacing in the LQT group (n = 8; 476 +/- 57 msec1/2 vs 486 +/- 59 msec1/2), whereas it was slightly increased from 400 +/- 21 msec1/2 to 426 +/- 18 msec1/2 by atrial pacing in the control group (n = 8; P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Repetitive nonsustained monomorphic ventricular tachycardia aborted by methoxamine and sleep "heart rate dependent ventricular tachycardia".

Methoxamine, an alpha adrenoreceptor agonist, and sleep abolished repetitive nonsustained monomorphic ventricular tachycardia in a 41-year-old man without detectable underlying heart disease. Detailed pacing studies revealed that the occurrence of ventricular tachycardia was totally dependent on the basic heart rate. Sleep and the alpha adrenoreceptor agonist abolished the ventricular tachycardia by slowing the basic heart rate. Verapamil, propranolol, and disopyramide were able to decrease the upper limit of the tachycardia-initiating heart rate, but none of them were able to increase the lower limit (75/min). Failure to increase the lower limit of the tachycardia-initiating heart rate was a major reason why these conventional antiarrhythmic drugs were unable to suppress his daytime episodes of repetitive ventricular tachycardia.

Adult↗
PubMed1991

Dominance of blood pressure in natriuresis associated with supraventricular tachycardia.

Supraventricular tachycardia was induced in 10 patients by programmed cardiac stimulation through esophageal lead. Blood pressure, heart rate, renal function, and hormonal factors were measured before, during, and after tachycardia. The patients were divided into two groups, depending on whether antinatriuresis occurred during tachycardia; one group (n = 5) with antinatriuresis during tachycardia associated with a decrease in blood pressure and the other group (n = 5) with neither antinatriuresis nor changes in blood pressure. The urinary sodium excretion tended to increase after tachycardia only in the latter group. On the other hand, urine volume and free water clearance increased during or after tachycardia in both groups. Plasma levels of atrial natriuretic peptide significantly increased and the urinary vasopressin excretion significantly decreased during tachycardia in both groups. During tachycardia, natriuresis due to atrial natriuretic peptide secretion seems to be hampered by hypotension, but polyuria is preserved despite the fall in blood pressure probably related to suppression of vasopressin release.

Adult↗
PubMed1991

Early afterdepolarizations induced by isoproterenol in patients with congenital long QT syndrome.

BACKGROUND: Several recent experimental and clinical studies have shown that early afterdepolarizations (EADs) are important in the genesis of QTU prolongation and ventricular tachyarrhythmias (VTs) in patients with long QT syndrome. On the other hand, sympathetic stimulation is well known to contribute to the genesis of QTU prolongation and VTs in patients with congenital long QT syndrome. The present study was performed to examine the influence of isoproterenol on the genesis of EADs and on the action potential durations and QTU intervals in patients with congenital long QT syndrome. METHODS AND RESULTS: We recorded monophasic action potentials (MAPs) with a contact electrode during right atrial pacing at a constant cycle length of 500 msec before and after continuous isoproterenol infusion (1 microgram/min). MAPs were obtained from the right and left ventricular endocardium in six patients with congenital long QT syndrome (LQT group, 18 recording sites) and in eight control patients (control group, 19 recording sites). Although no EADs were recorded from either group during the control state, MAP duration at 90% repolarization (MAPD90) was significantly longer in the LQT group (n = 18) than in the control group (n = 19) (275 +/- 36 versus 231 +/- 22 msec; p less than 0.0005). Isoproterenol induced EADs in four of the six LQT patients (five of 18 recording sites) but not in the eight control patients (zero of 19 recording sites). The appearance of EADs in the LQT group was associated with an increased amplitude of the late component of the TU complex, and the corrected QT (QTc) interval was prolonged by isoproterenol from 543 +/- 53 to 600 +/- 30 msec 1/2 (n = 6; p less than 0.05). Isoproterenol also prolonged the MAPD90 from 275 +/- 36 to 304 +/- 50 msec in the LQT group (n = 18; p less than 0.005), whereas it shortened the MAPD90 from 231 +/- 22 to 224 +/- 25 msec in the control group (n = 19; p less than 0.05). Moreover, isoproterenol increased the dispersion of MAPD90 (difference between the longest MAPD90 and the shortest MAPD90 in each patient) from 30 +/- 5 to 62 +/- 35 msec in the LQT group (n = 6; p = 0.08), whereas it did not change the dispersion of MAPD90 in the control group (n = 8; 25 +/- 14 versus 27 +/- 14 msec). CONCLUSIONS: These results suggest that patients with congenital long QT syndrome have primary repolarization abnormalities and that EADs induced by isoproterenol play an important role in the exaggeration of these repolarization abnormalities.

Action Potentials↗
PubMed1991

[Cardiac pacing].

Explore the source record for details and available documents.

Arrhythmias, Cardiac↗
PubMed1990

Possible role of renal prostaglandin E2 in natriuresis associated with supraventricular tachycardia.

We investigated the possible role of renal prostaglandin (PG) E2 in natriuresis associated with supraventricular tachycardia (SVT). In five female patients with paroxysmal tachycardia, SVT was artificially induced and then stopped 60 min later. Before, during, and after SVT, plasma levels of arginine vasopressin and atrial natriuretic peptide (ANP) and the urinary excretion of sodium and PGE2 were measured. Polyuria was observed during SVT. However, natriuresis did not occur until immediately after the termination of SVT. During SVT, the plasma levels of arginine vasopressin tended to decrease. When SVT was terminated, the vasopressin levels increased significantly (p less than 0.01). Urinary excretion of PGE2 tended to decrease during SVT and then increased significantly (p less than 0.01) after SVT ended. Urinary excretion of sodium was correlated (r = 0.699, p less than 0.001) with the urinary excretion of PGE2. Plasma ANP increased during SVT, but there was no correlation with urinary sodium excretion. These results suggest that renal PGE2, the biosynthesis of which may be stimulated by a increase in plasma vasopressin, is an important factor contributing to the natriuresis observed after the end of SVT.

Adult↗