Search PubMed⌕ Search

Biomedical subjects

H Mitamura

Publications and source records attributed to H Mitamura.

At least 91 records · Page 5Linked to original sources
PubMed1987

Ventricular tachyarrhythmia initiation in a canine model of recent myocardial infarction. Comparison of unipolar cathodal, anodal and bipolar stimulation.

Ventricular tachyarrhythmia initiation was compared using unipolar cathodal, anodal and bipolar programmed stimulation at 21 sites in 5 normal adult mongrel dogs and 67 noninfarct sites in 16 dogs 3-5 days after experimental myocardial infarction. For this purpose, the minimum number of extrastimuli required for tachyarrhythmia initiation was determined in each pacing mode using twice cathodal threshold current for the drive beats and all extrastimuli except the last. The current and pacing mode were varied for the last extrastimulus (S2, S3 or S4). In the 5 normal dogs, ventricular fibrillation was reproducibly inducible from only 1/21 sites, and only in the cathodal mode. In 15/16 (94%) of the myocardial infarction dogs, a sustained ventricular tachycardia or ventricular fibrillation could be reproducibly initiated with either one (4 dogs), two (5 dogs) or three extrastimuli (6 dogs). Diastolic excitability thresholds were 0.08 +/- 0.03, 0.30 +/- 0.17, and 0.09 +/- 0.04 mA (median +/- SD) for unipolar cathodal, anodal and bipolar pacing, respectively (p less than 0.001 for anodal vs. cathodal and bipolar). The median absolute current required for ventricular tachyarrhythmia initiation was also highest with anodal pacing (0.72 +/- 0.77 mA), versus both the cathodal and anodal modes (0.18 +/- 0.28 and 0.20 +/- 0.28 mA, respectively, each p less than 0.001) but was comparable in all three modes relative to the threshold current (2.0, 2.4 and 2.6 mA for cathodal, anodal and bipolar pacing, respectively) required for initiation. Overall, ventricular tachyarrhythmia initiation was concordant in all three modes at 58/67 (87%) sites and discordant at only 9/67 (13%) sites (p less than 0.001). Moreover, there was no difference in either the pattern of arrhythmia initiated in each of the pacing modes with respect to ventricular tachycardia versus ventricular fibrillation, or in the median current required to initiate ventricular tachycardia (0.30 +/- 0.36 mA) versus ventricular fibrillation (0.31 +/- 0.44 mA; p greater than 0.1). Thus, ventricular tachyarrhythmia initiation was comparable in all three pacing modes with respect to overall success rate, number of ventricular extrastimuli required and the pattern of ventricular tachyarrhythmia initiated. Bipolar pacing with similar size anodal and cathodal electrodes appear to be appropriate for electrophysiologic ventricular tachyarrhythmia studies and are not likely to induce spurious arrhythmias resulting from stimulation at the anodal pole.

Animals↗
PubMed1987

Interactive negative chronotropic actions of adenosine and verapamil on the canine sinus node in vivo.

To study the interaction between adenosine and verapamil, adenosine (3 mumol/kg) was administered rapidly into the right atrium before and following verapamil (0.2 mg/kg, i.v.) in 25 pentobarbital anesthetized dogs divided into 4 groups: I (n = 7) - intact dogs; II (n = 6) - dogs pretreated with atropine (0.2 mg/kg, i.v.); III (n = 6) - dogs pretreated with propranolol (1 mg/kg, i.v.) and IV (n = 6) - bilateral stellectomized and cervical vagotomized dogs. Arterial blood pressure, standard lead II ECG, as well as right atrial, right ventricular and His bundle electrograms were continuously monitored and recorded. The negative chronotropic effect of adenosine was determined as the maximal prolongation in sinus cycle length (SCL). Verapamil maximally prolonged SCL by 70 +/- 14 msec (p less than 0.005) in Group I, 39 +/- 15 msec (0.1 greater than p greater than 0.005) in Group II, 86 +/- 18 msec (p less than 0.01) in Group III and by 100 +/- 12 msec (p less than 0.001) in Group IV. In Group I, control dogs, adenosine increased SCL by 82 +/- 21 msec before vs. 185 +/- 35 msec 15 minutes after verapamil, respectively (p less than 0.05). This potentiating effect of verapamil was completely abolished by atropine and markedly attenuated by propranolol. In stellectomized + vagotomized dogs, adenosine-verapamil interaction was more complex. In this group adenosine prolonged sinus cycle length maximally by 270 +/- 41 msec before verapamil, but following verapamil this effect of adenosine was transiently attenuated with a maximal sinus cycle length prolongation of only 165 +/- 24 msec (10 minutes following verapamil) (p less than 0.05, vs. before verapamil). These data indicate that the autonomic nervous system modulate the interactive negative chronotropic effects of adenosine and verapamil in the canine sinus node. Hence, the adenosine-verapamil interaction has clinical implications for conditions in which release of adenosine is increased (e.g. myocardial ischemia) or adenosine is administered in the presence of verapamil.

Adenosine↗
PubMed1986

Effects of adenosine and adenosine 5'-triphosphate on ventricular escape rhythm in the canine heart.

The effects of adenosine and adenosine 5'-triphosphate (ATP) on ventricular escape rhythms were studied in 16 closed chest dogs after electroablation of the His bundle region. All dogs exhibited complete atrioventricular (AV) block and stable ventricular escape rhythm with a mean cycle length of 1,210 +/- 80 ms and a QRS width of 91 +/- 5 ms. Physiologic AV sequential pacing was operative during experiments and was interrupted for rapid (less than or equal to 1 second) administration of either adenosine or ATP (3 mumol/kg) into the right atrium. Adenosine and ATP effectively depressed ventricular escape rhythms in a similar manner both qualitatively and quantitatively (cycle length from 1,210 +/- 80 to 1,764 +/- 132 ms and from 1,274 +/- 84 to 2,000 +/- 150 ms, respectively; each p less than 0.01). These effects were not significantly altered by either physostigmine (an acetylcholinesterase inhibitor) or atropine (a muscarinic cholinergic blocker), but were slightly attenuated by propranolol (a beta-adrenoceptor blocker). In the presence of autonomic blockade, the adenosine transport blocker dipyridamole markedly enhanced the depressant effects of adenosine and ATP. The adenosine competitive antagonist aminophylline reversed the action of dipyridamole. Thus, both adenosine and ATP depress ventricular escape rhythms in vivo, independent of the autonomic nervous system. Moreover, the effects of ATP can be accounted for in large part by its rapid breakdown to adenosine.

Adenosine↗
PubMed1986

Effects of AV sequential versus asynchronous AV pacing on pulmonary hemodynamics.

We studied the effects of various pacing modes on cardiac hemodynamics and pulmonary gas alterations in chronic heart blocked dogs. Changing the pacing mode from an atrioventricular interval of 100 ms (AV100) to a ventriculo-atrial interval of 100 ms (VA100) caused a significant fall in left ventricular pressure (117.64 +/- 11.91 to 95.60 +/- 16.58 mmHg) and cardiac output from 2.18 +/- 0.24 to 1.46 +/- 0.20 L/min. Following the change in pacing mode from AV100 to VA100, there was an increase in the alveolar-arterial O2 gradient from 23.28 +/- 6.97 to 28.74 +/- 8.43 mmHg and a decrease in the arterial CO2 tension from 32.42 +/- 3.22 to 29.42 +/- 3.22 mmHg. There was also a decrease in arterial CO2 tension when the AV100 pacing mode was compared to asynchronous ventricular pacing (32.42 +/- 3.22 versus 30.56 +/- 2.82 mmHg). The minute volume of O2 also decreased when the pacing mode was changed from AV100 to asynchronous ventricular pacing (0.134 +/- 0.01 versus 0.126 +/- 0.01 L/min) and decreased further at VA100 to 0.114 +/- 0.01 L/min. Other significant changes were also observed: the percent of expired CO2 decreased when the pacing mode was changed from AV100 to VA100 (3.68 +/- 0.13 versus 3.37 +/- 0.26%) or to asynchronous ventricular pacing (3.40 +/- 0.31%). The end-expiratory O2 increased and CO2 decreased when the pacing mode was changed from AV100 to VA100. The breath-by-breath correlation of end-expiratory O2 and CO2 with left ventricular systolic pressure showed an almost immediate increase in O2 and reduction in CO2 concentration associated with decreasing systolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Nonarrhythmogenicity of therapeutic cryothermic lesions of the myocardium.

There is increasing interest in the application of surgical methods to the treatment of refractory ventricular tachyarrhythmias (VT). Cryothermic ablation is one of the more promising techniques. However, there is clinical concern that a cryothermic lesion may lead to later arrhythmias. Previous studies have shown that dogs with nonhomogeneous, transmural infarctions are susceptible to VT initiation using programmed electrical stimulation (PES). The purpose of this study was to compare the incidence of inducing VT in dogs with transepicardial cryothermic myocardial damage (Group A) versus dogs with nonhomogeneous transmural infarctions resulting from 2-hr occlusion of the left anterior descending coronary artery (LAD) and subsequent reperfusion (Group B). Twelve dogs in each group were studied 10-14 days later using PES with unipolar cathodal ventricular pacing and two ventricular extrastimuli. Initiation of VT was attempted from at least six normal intramyocardial sites in each dog along the distribution of the LAD and in close proximity (less than or equal to 1 cm) to areas of chronically cryoablated damaged tissue. All dogs survived the initial procedure. VT was not inducible in any dog in Group A. Histological as well as electrophysiological evaluation, including determination of regional excitability thresholds and refractory periods employing strength-interval curves, revealed that all of the Group A dogs had homogeneous transmural infarcts with variable subendocardial sparing. In conclusion (1) cryothermal injury produces homogeneous damage; and (2) the lesion produced is not arrhythmogenic at 7-14 days.

Animals↗
PubMed1985

Importance of the pacing mode in the initiation of ventricular tachyarrhythmia in a canine model of chronic myocardial infarction.

The use of unipolar anodal or bipolar pacing, as compared with unipolar cathodal pacing, purportedly increases the likelihood of inducing inadvertent ventricular fibrillation in susceptible patients. In this study, the ability to initiate sustained ventricular tachycardia or fibrillation with unipolar cathodal, unipolar anodal and bipolar pacing modes was compared using programmed ventricular stimulation at 82 subendocardial periinfarction sites in 11 dogs with chronic myocardial infarction. The late diastolic excitability threshold was significantly higher and the ventricular refractory period was significantly shorter (p less than 0.001) with anodal pacing (mean 0.62 mA, 156 ms, respectively) than with pacing in either the cathodal (0.12 mA, 174 ms) or the bipolar (0.13 mA, 173 ms) mode. At a current intensity twice that of the excitability threshold, the introduction of one or two extrastimuli induced ventricular tachycardia and ventricular fibrillation comparably among the three pacing modes. However, when three extrastimuli were used, ventricular fibrillation was induced with anodal pacing twice as frequently (50 [61%] of 82 sites) as with either of the other two pacing modes (each 23 [28%] of 82 sites, p less than 0.001), whereas the induction of ventricular tachycardia remained comparable with anodal pacing (15 [18%] of 82 sites) and cathodal and bipolar pacing (each 14 [17%] of 82 sites). Furthermore, a similarly high incidence of inducibility of ventricular fibrillation was observed with both cathodal pacing (56 [68%] of 82 sites) and bipolar pacing (40 [49%] of 82 sites) when an increased current equal to twice the anodal excitability threshold (1.23 mA) was used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Evidence for vagal involvement in the electrophysiologic actions of exogenous adenosine and adenosine triphosphate in the canine heart.

A closed chest canine model was used to study the electrophysiologic effects of adenosine and adenosine triphosphate (ATP) on the sino-atrial (SA) and atrioventricular (AV) nodes. Exogenous adenosine and ATP, when rapidly administered into the right atrium, caused transient negative chronotropic and dromotropic effects on the SA and AV nodes, respectively. These effects reached a maxima in 10-15 sec and dissipated in less than 120 sec. The electrophysiologic effects of ATP were more pronounced than those of adenosine. Physostigmine enhanced the chronotropic effects of adenosine and ATP and the dromotropic effects of ATP. Atropine abolished the enhancement of the electrophysiologic effects of adenosine and ATP caused by physostigmine. In the pentobarbital anaesthetized dog, ATP triggers a vagal reflex which plays a major role in mediating its electrophysiologic effects. Vagal involvement in the electrophysiologic action of adenosine is more modest, but does not appear to be mediated via reflex mechanisms.

Adenosine↗
PubMed1985

Histopathologic factors conducive to experimental ventricular tachycardia.

Ventricular tachyarrhythmia is the leading cause of sudden cardiac death. Determination of the substrates conducive to the initiation of this arrhythmia remains an important clinical goal. The purpose of this study was to correlate histopathologic findings, specifically: pattern (heterogeneous versus homogeneous infarct morphology), distribution (viable epicardial and/or endocardial rim), and infarct size, with susceptibility to the initiation of sustained ventricular tachycardia employing programmed electrical stimulation in two canine models of experimental myocardial infarction. Twenty-one adult dogs were randomly divided into two groups: 12 dogs underwent two-stage, 2-hour occlusion of the proximal left anterior descending coronary artery and nine animals underwent permanent, complete occlusion of the left anterior descending coronary artery with latex embolization. With programmed ventricular pacing with two premature ventricular extrastimuli, initiation of ventricular tachycardia was attempted, open chest, two weeks after infarction. Electrophysiologic evaluation of the infarct type correlated significantly with the histologic morphology of the infarction (p less than 0.001). The presence of a viable epicardial rim was an extremely important variable for ability to induce sustained ventricular tachycardia (p = 0.04). The presence of an endocardial rim was not significant (p = 1.0). Infarct size alone was only marginally related to ventricular tachycardia inducibility (p = 0.08). Nonuniform infarcts were more conducive to the initiation of sustained ventricular tachycardia than were homogeneous infarcts (p = 0.025). The presence of a large, nonuniform infarct correlated best with inducibility (p = 0.0002). Thus in these experimental models, specific infarct morphologies correlate significantly with susceptibility to inducible sustained ventricular tachyarrhythmias.

Animals↗
PubMed1982

Evaluation of combined valvular prolapse syndrome by two-dimensional echocardiography.

The patterns of aortic and tricuspid valve motion in 50 patients with mitral valve prolapse were analyzed by wide-angle, phased-array, two-dimensional echocardiography. Twelve patients (24%) had redundant aortic leaflets bulging into the left ventricular outflow tract during diastole. Eight of 12 patients had aortic regurgitation and seven of 12 had M-mode echocardiographic evidence of aortic valve prolapse. One patient underwent mitral and aortic valve replacement, and the excised valves revealed marked myxomatous degeneration. Eight of 15 patients undergoing contrast echocardiography had tricuspid regurgitation (systolic reflux of contrast material into the inferior vena cava persisting for more than 10 beats), and prolapse in the septal leaflet of the anterior leaflet or both. A similar tricuspid valve pattern was noted in three of seven patients without tricuspid regurgitation. Tricuspid valve prolapse was identified in 20 patients (40%). Nine patients (18%) had combined prolapse of the mitral, aortic and tricuspid valves. In five patients with middiastolic high-pitched murmurs recorded along the left sternal border, tricuspid valve prolapse was demonstrated. In one of these patients, the presence of pulmonary regurgitation was confirmed by intracardiac phonocardiography. We conclude that two-dimensional echocardiography is useful for evaluating patients with combined valvular prolapse syndrome.

Adolescent↗
PubMed1981

Two dimensional echocardiographic analysis of wall motion abnormalities during handgrip exercise in patients with coronary artery disease.

Studies were made of the feasibility and value of two dimensional echocardiography in detecting left ventricular asynergy during handgrip exercise in 45 patients with suspected coronary artery disease. Resting echocardiography revealed normal wall motion in 32 patients, and in 17 of these handgrip exercise induced abnormal wall motion. All 17 patients had significant stenoses in the coronary arteries. However, only 65 percent of patients with coronary artery disease whose resting two dimensional echocardiogram revealed normal wall motion showed abnormal wall motion during handgrip exercise. The left ventricular wall visualized in the short axis plane was divided into 5 segments, and a total of 225 segments were analyzed. Of 49 segments with exercise-induced asynergy, 46 (94 percent) reflected significant stenosis in the perfusing coronary artery. In particular, 16 (89 percent) of 18 segments with exercise-induced akinesia reflected stenosis of greater than 90 percent. Resting or exercise two dimensional echocardiography (or both) was able to diagnose multivessel disease with a predictability of 92 percent. It is concluded that two dimensional echocardiography combined with handgrip exercise has high specificity in detecting coronary artery disease and would be useful for predicting severely stenotic or multivessel coronary arterial lesions.

Adult↗
PubMed1981

A case of coexisting tachycardia- and bradycardia-dependent bilateral bundle branch block.

Electrocardiograms and His bundle electrograms were presented from a patient with a rare combination of intermittent bilateral bundle branch block. Critical analyses of R-R intervals and evolution of bundle branch block patterns revealed both tachycardia dependent right bundle branch block and bradycardia dependent left bundle branch block. Evaluation of HV intervals on His bundle electrograms suggested an additional possibility of bradycardia dependent conduction delay in the right bundle branch system.

Aged↗
PubMed1981

[Two-dimensional echocardiographic approach to the localization of myocardial infarction: echocardiographic, electrocardiographic, and coronary arteriographic correlations (author's transl)].

Location of infarct lesions (IL) demonstrated by two-dimensional echocardiography (2DE) was correlated with electrocardiographic patterns of myocardial infarction and with the sites of obstructive lesions in the individual coronary arteries. The left ventricular wall was displayed by phased-array 2DE in 47 patients with healed myocardial infarction, 29 of whom underwent coronary arteriography. Segmental analysis of IL was performed on 14 segments, 10 of which were obtained by the parasternal short-axis recordings at the mitral (basal) and papillary muscle (mid) levels (each level containing the anterior septum, anterior wall, lateral wall, posterior wall, and posterior septum). The remaining 4 segments (septum, anterior wall, lateral wall, posterior wall) were obtained by the apical 2-chamber and 4-chamber recordings. IL were defined as akinesis, thinning, increased echo density, or absent systolic thickening of the left ventricular wall. All 22 patients with anterior infarction (Q in V1-V4) had IL in the mid anterior septum which was specific for the lesion of the left anterior descending artery (LAD). The presence or absence of the r wave in V1 could not predict the involvement of this segment. IL in the apical anterior wall and septum were observed in 21 of 22 patients. The presence of Q waves in V5, V6 suggested the additional involvement of the apical posterior wall. Additional Q waves in I, aVL indicated the extension of IL from the mild anterior septum to the basal anterior septum, anterior wall, and mid anterior wall. The basal and mid lateral walls appeared normal in most patients. This pattern of IL distribution was observed in 5 of 6 patients with a stenosis on the proximal LAD. All 14 patients with inferior infarction (Q in II, III, aVF) had IL in the mid posterior wall and posterior septum. In contrast, 5 patients with infero-posterior infarction (Q in II, III, aVF + R in V1) and 6 patients with posterior infarction (R in V1) had IL in the mid lateral as well as the mid posterior wall without an involvement of the posterior septum. Coronary arteriography revealed that all of the 10 patients with inferior infarction had a stenosis in the right coronary artery, whereas 6 patients with infero-posterior or posterior infarction invariably had a stenosis in the left circumflex coronary artery. It was concluded that 2DE provides a reliable method for detecting IL and anatomic location of myocardial infarction reflecting a specific coronary artery disease.

Adult↗
PubMed1979

Changes in blood level of kininogen, prostaglandin E and hemodynamics during experimental acute myocardial ischemia with and without FOY-007.

Changes in kininogen, prostaglandin E and hemodynamics were studied during 2 hours after left anterior descending artery ligation in 19 anesthetized dogs with and without FOY-007, an inhibitor of kinin forming enzyme. Significant decrease in kininogen in aorta and great cardiac vein (aorta greater than great cardiac vein) and increase in prostaglandin E in great cardiac vein were observed after ligation, indicating release of kinin and prostaglandin E from ischemic area. Both kininogen and prostaglandin E changes were inhibited by FOY-007 but further decrease in cardiac output and increase in systemic vascular resistance were observed. In summary, myocardial release of both kinin and prostaglandin E was inhibited by FOY-007, with increase of afterload of the heart.

Animals↗
PubMedDate not supplied

Evidence against prostaglandin mediation of the differential electrophysiologic effects of ATP versus adenosine in the canine heart.

Adenosine triphosphate (ATP) and adenosine exert negative chronotropic and dromotropic effects on the sino-atrial and atrioventricular nodes of the canine heart. The electrophysiologic action of ATP is more pronounced due, at least in part, to vagal reflexes triggered by ATP. In addition, ATP, but not adenosine, triggers the synthesis and release of prostaglandins. To determine whether this latter action of ATP is involved in the quantitative differences between the electrophysiologic effects of ATP and adenosine, the influence of the prostaglandin synthesis inhibitor, indomethacin, was studied on the actions of ATP and adenosine in 18 dogs. Indomethacin (5 mg/kg, i.v.) alone caused slight increase in sinus cycle length (from 384 +/- 16 ms to 402 +/- 16 ms; p less than 0.025) but did not affect atrioventricular conduction. In the presence of indomethacin, the negative chronotropic effects of both ATP and adenosine (3 mumol/kg each) were significantly augmented to a similar extent, proportionally: the maximal percent increase in sinus rhythm cycle length following ATP increased from 203 +/- 33 to 266 +/- 62 ms (p less than 0.025), and following adenosine increased from 44 +/- 8 to 64 +/- 20 ms (p less than 0.001). These results indicate that prostaglandins can indirectly modulate the electrophysiologic action of ATP and adenosine; however, ATP-triggered synthesis and release of prostaglandins do not play a major role in the differential electrophysiologic actions of ATP versus adenosine.

Adenosine↗