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Biomedical subjects

G Kirkorian

Publications and source records attributed to G Kirkorian.

87 records · Page 5Linked to original sources
PubMed1984

Clinical electrophysiology of intravenous sotalol, a beta-blocking drug with class III antiarrhythmic properties.

The electrophysiologic changes produced by the intravenous administration of 0.6 mg/kg of sotalol were studied in 12 patients aged 45 to 85 years (mean 68 years). Effects upon atrioventricular (AV) nodal conduction time (AH interval) and His-Purkinje conduction time (HV interval) were assessed at identical rates. The Wenckebach cycle length was determined by rapid atrial stimulation. Refractory periods before and after the drug were compared at the same cycle length. Retrograde conduction was studied, with special reference to reentry phenomena within the His-Purkinje system. Sinoatrial function was evaluated using sinus node recovery time and sinoatrial conduction time. The following changes were noted: (1) decrease in sinus rate, (2) prolongation of QT interval, (3) depression of AV nodal conduction (prolonged AH interval) and increase in effective and functional refractory periods of the AV node, (4) increase in relative refractory period of the His-Purkinje system with no associated change in HV interval, (5) prolongation of effective refractory period in the atrium and ventricle, and (6) increase in retrograde refractory period of specialized ventricular tissue and depressed conduction of premature ventricular responses. Reentry phenomena in the His-Purkinje system were not significantly affected by the drug. Thus certain of the electrophysiologic effects of sotalol in humans were found to be in favor of a class III antiarrhythmic mechanism of action. These results justify further studies to evaluate the usefulness of this drug as an antiarrhythmic agent.

Aged↗
PubMed1983

Bundle branch reentry: a possible mechanism of ventricular tachycardia.

Electrophysiologic studies were performed in three patients suffering from attacks of paroxysmal tachycardia with wide QRS complexes. Two patients had atrioventricular dissociation. The arrhythmia could be initiated and terminated by premature ventricular stimulation in all three patients. One patient developed the arrhythmia after rapid atrial stimulation. In each subject, the QRS complexes during tachycardia were identical to recorded supraventricular beats (left bundle branch block pattern in two cases and right bundle branch block pattern in one). A His bundle potential was noted before the QRS complex; the HV interval was equal to or longer than that of the sinus beats. The following observations suggested the presence of a bundle branch reentry mechanism: (1) the relationship between bundle branch block development and tachycardia initiation; (2) the occurrence of tachycardia after electrically induced His-Purkinje reentry; (3) the ability of premature ventricular stimulation during tachycardia to advance the timing of the His deflection and QRS complex, with an unchanged or slightly increased HV interval; and (4) the termination of arrhythmia by premature ventricular depolarization blocked within the bundle branch system. Our results support the idea that bundle branch reentry can play a role in the genesis of ventricular tachycardia.

Aged↗
PubMed1981

[Effects of mexiletine in the Wolff-Parkinson-White syndrome].

The effects of intravenous mexiletine were studied by His bundle recordings and programmed stimulation in 7 patients aged from 20 to 40 years old (average age : 32 years), 5 of whom had an overt WPW syndrome (4 type A, and 1 type B), and 2 of whom had concealed pre excitation. All had reciprocating tachycardia. Electrophysiological investigation was performed under basal conditions, and then several times in the hour following intravenous mexiletine (3,5 mg/Kg in 5 minutes) followed by an infusion of 0,07 mg/Kg/min. The following results were obtained : 1. mexiletine did not cause any significant changes in the normal AV conduction pathway; 2. the refractory periods of the atria and ventricles were unaffected by the drug; 3. pre excitation regressed in 2 of the 5 patients with overt WPW. In a third patient, the effective anterograde refractory period of the accessory pathway increased by 210 ms. The retrograde refractory period of the accessory pathways increased in three patients and remained unchanged in the others; 4. there was little change in the ability to induce reciprocating tachycardia by stimulation. However, in two patients, the attacks were shortened, terminating spontaneously within a few seconds. This study shows the electrophysiological basis of the use of mexiletine in the WPW syndrome. Although the results do show some variability, they justify the use of mexiletine in patients with paroxysmal tachycardia in the WPW syndrome.

Adult↗
PubMed1981

[Electrophysiologic effects of lorcainide (R 15889) in man].

The electrophysiological effects of lorcainide (R 15 899) were studied in 15 patients. Atrioventricular conduction was analysed by His bundle recording and cardiac refractory periods were determined by the extra stimulus method. The assessment of sino atrial function was performed by measuring sinus node recovery times and sino atrial conduction times. The electrophysiological data was recorded before and 10 minutes after a slow intravenous injection of 1,5 mg/Kg of lorcainide followed by a continuous infusion at 0,02 mg/Kg/min. The following results were obtained; 1) The HV interval increased in all cases (average : II ms) 2) The QRS and QT intervals were significantly prolonged 3) Lorcainide produced a slowing of conduction and an increase in the refractory periods at atrial level 4) AV nodal conduction was unaffected 5) The sinus rate slightly increased. There were no significant changes in sinus node recovery time or sino atrial conduction. It must be concluded that, in man, lorcainide produces electrophysiological effects of antiarrhythmic agents of the quinidine type.

Adolescent↗
PubMed1980

Electrophysiological properties in man of L 9394, a substance chemically related to amiodarone.

The effects of L 9394, a new compound closely related to amiodarone, were investigated in 44 patients by electrophysiological studies. Thirty two patients were given an intravenous injection of one of the following doses: 0.5, 1, 1.5 or 2 mg/kg. Conduction times of the A-V node (A-H interval) and of the His-Purkinje system (H-V interval) were measured by recording the His bundle potential. Refractory periods were determined by the extrastimulus technique. In the remaining 12 subjects, the action of L 9394 on sinus node was assessed. Sinus node recovery time was measured by rapid atrial stimulation and estimated atrial-sinoatrial conduction time deduced from the effects of atrial premature stimulation on sinus node activity. Results were as follows: (1) A-V nodal conduction was depressed after L9394. The A-H interval increased in direct proportion to the dose. Similarly, the effective and functional refractory periods of the A-V node were prolonged, more markedly after higher doses. (2) No change was shown in the His-Purkinje system. The H-V interval was unaltered. (3) L 9394 had no significant effects on the atrial or ventricular muscle. (4) Sinus cycle length as well as sinus node recovery time did not change significantly. In 7/12 patients, results of premature atrial stimulation suggested the formation of a sinoatrial block.

Adult↗
PubMed1980

Effects of contrast media on circulating blood volume. A comparative investigation of various sites of injection.

Changes in the circulating blood volume following injection of different contrast media and at different sites have been measured in the dog. The results confirm that osmoreceptors in the right atrium play a role for changes in blood volume following injection of a contrast medium. The differential response to individual agents was mainly a function of their osmolality. Atropine appears to moderate the changes.

Animals↗
PubMed1980

[Role of accessory atrioventricular pathways in the genesis of permanent junctional tachycardia. Apropos of 2 cases].

Electrophysiological studies were performed in two patients with permanent junctional tachycardias. In both cases, the heart rate was 160/mn and standard ECG showed negative P waves in leads D2, D3 and AVF, isobiphasic or negative P waves in the left precordial leads and a PR interval of 0.12 and 0.13 secs. respectively. The tachycardia started without lengthening of the PR interval or preceding extrasystoles. Shortening of the sinus cycle before the tachycardia was inconstant. The reciprocating mechanism was shown by stimulation studies. Premature ventricular depolarisations not conducted to the atria were capable of terminating the attacks. Proof of His bundle bypass was obtained by the recording of the early atrial activity after ventricular stimulation at the time of His bundle depolarisation. The emergence of retrograde excitation in the left atrium in one of the cases was strongly suggestive of an accessory AV pathway. Atrial participation in the reentry loop was shown in both patients by premature atrial stimulation during tachycardia. This resulted in an earlier appearance of the His potential and QRS complex without affecting the reentrant excitation of the opposite atrium. The present study shows that accessory AV pathway with long retrograde conduction times may play a role in the initiation of permanent reciprocating junctional tachycardia. The functional characteristics of such pathways are suggestive of the presence of tissue with properties similar to that of the AV node. This data adds to our present knowledge of the mechanism of supraventricular tachycardia.

Adolescent↗
PubMed1979

[Nutritional status in critically ill patients. Relationship with mortality (author's transl)].

Plasma proteins, triglyceridemia, body composition and delayed hypersensitivity were determined in 154 critically ill patients after admission. Plasma proteins levels were significantly increased in patients that were subsequently discharged vs. those that died: albumin: 33 +/- 6 g/l vs 28 +/- 6 g/l (p < 10(-6)); transferrin 2,18 +/- 0,65 g/l vs. 1,54 +/0 0,55 g/l (p < 10(-7)); prealbumin: 14,32 +/- 7,79 mg/100 ml vs. 7,28 +/-5,36 mg/100 ml (p < 10(-7)) and triglyceridemia was decreased: 1,07 +/- 0,38 g/l vs. 1,66 +/- 1,12 g/l (p not equal to 10(-3)). Body weight, fat weight and lead body mass were not correlated to subsequent mortality. Muscle cell mass was decreased (-17%, p < 10(-2)) and extracellular water was increased (+14%, p < 10(-4)), in patients who subsequently died. Total body water and visceral cell mass did not change. Initial anergy (tested with 3 antigens: candidin, tuberculin, varidase) did correlate with mortality: 35/62 died when delayed hypersensitivity was negative vs. 13/71 when it was positive (p < 10(-4)). Mortality was associated with decreased total lymphocyte count: 884 +/- 1025 vs. 1270 +/- 870 (p < 0,02) and serum iron: 51 +/- 40 micrograms/100 ml vs. 74 +/- 45 micrograms/100 ml (p < 10(-2)). Sepsis correlated with mortality (p < 10(-3)) and could produce these changes. These results suggest that critically ill paients have a protein-calorie malnutrition syndrom marktly different from that observed in simple starvation. Nutritional therapy must be, in this group of patients, adapted to this concept.

Adolescent↗
PubMed1979

Effects of amiodarone on sinus node in man.

The effects of amiodarone on the sinuatrial node were studied in 24 patients after an intravenous injection of the drug (5 mg/kg). Sinuatrial function was assessed by rapid atrial pacing and premature atrial stimulation. Sinus cycle length did not change significantly, but the corrected sinus node recovery time was prolonged. While there was no significant change in sinuatrial conduction time, prolongation of the non-reset zone in 14 cases, as well as the abolition of the platesu in 2/24 patients, suggested that conduction of the atrial responses to the sinus node might have been depressed.

Aged↗
PubMed1979

The estimation of sinoatrial conduction time in rabbit heart by the constant atrial pacing technique.

This study compared estimates of sinoatrial conduction time (SACT) obtained by constant atrial pacing (CAP) and premature atrial stimulation (PAS) with measured SACT in isolated rabbit right atrial preparations. Transmembrane potentials and surface electrograms were recorded from the sinus node and crista terminalis, respectively. The crista terminalis was paced 5, 10 and 15 beats/min faster than the spontaneous sinus rate with a train of eight pulses. Estimate of SACT by CAP was taken as the difference between the first atrial return cycle and the mean spontaneous cycle length. SACTs at 5, 10 and 15 beats/min faster were 76 +/- 10, 86 +/- 10 and 96 +/- 10 msec (mean +/- SEM; n = 12), respectively; correlation coefficients with the true SACT were 0.7, 0.54 and 0.4. Consecutive determinations of SACT by PAS and CAP in the same preparation (n = 6) at 10 beats/min faster gave SACTs of 86 +/- 13 and 79 +/- 14 msec, respectively, compared with true SACTs of 79 +/- 10 msec. Shortening of sinus node action potential, depression of automaticity and shifts in the site of the primary pacemaker contributed to the errors in both techniques. Estimation of SACT by CAP may be further complicated by failure of sinus node capture. Principles to minimize some of these errors are also presented.

Animals↗