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PubMedDate not supplied

Heterodromia in accessory A-V connections.

In 15 patients with WPW-syndrome the atrio-ventricular and ventriculoatrial conduction was studied by recording of intracardiac potentials during atrial and ventricular pacing. Typical differences in the patterns of normal and accessory A-V conduction identified accessory V-A conduction in 13 patients. According to the evaluation of accessory A-V and V-A conductivity by high rate pacing the patients studied can be divided into three groups: Group I (5 pat): equally good accessory A-V and V-A conductivity. Group II (5 pat): good accessory A-V and impaired accessory V-A conductivity. Group III (5 pat): impaired accessory A-V and good V-A conductivity. In group I the course of investigation was repeated after the application of Ajmaline. The distinct heterodromia in group II and III and the different behaviour of the accessory A-V and V-A conduction after Ajmaline can be explained by the in vitro experiments of Fuente (3). According to our results and to the finding that an excellent accessory V-A conduction is a presupposition for the initiation of supraventricular re-entry tachycardia, it seems mandatory to analyze accessory A-V and V-A conduction properties as well.

Adolescent↗
PubMed1982

Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia.

Ten patients are described with two discrete discontinuities in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean +/- SD, 48 +/- 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion, triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.

Adolescent↗
PubMed1985

Prolongation of refractoriness and activation time in normal canine ventricular myocardium following bolus administration of lidocaine.

This study examines the electrophysiologic effects of an intravenous bolus of lidocaine in the normal canine ventricle. In 14 open-chest dogs, left ventricular effective refractory period, ventricular repolarization time, and activation time were measured continuously during ventricular pacing (150/min) before, during, and after intravenous lidocaine given over 4 minutes. Lidocaine doses of 1.25, 2.5, and 5.0 mg/kg transiently prolonged the ventricular effective refractory period from 177 +/- 4 (X +/- standard error of the mean) to 185 +/- 5 msec (p less than 0.05), 176 +/- 3 to 188 +/- 6 msec (p less than 0.05), and 176 +/- 5 to 197 +/- 5 msec, (p less than 0.05), respectively, at 6 +/- 1.5 minutes from the onset of the bolus. Serum lidocaine levels obtained at the peak of the effective refractory period prolongation averaged 4.3 +/- 1.0, 9.0 +/- 3.0, and 22.3 +/- 4.7 micrograms/ml, respectively. Ventricular repolarization time was not prolonged. Activation time also transiently increased from 43 to 45 msec (p less than 0.05) and from 47 to 52 msec with the 2.5 mg/kg and 5.0 mg/kg doses, respectively. Cardiac denervation and administration of propranolol, 1 mg/kg intravenously, did not influence these responses to lidocaine. We conclude that a bolus of lidocaine transiently prolongs the effective refractory period and activation time in the normal canine ventricle because of its direct membrane rather than autonomic effects.

Anesthesia↗
PubMed1986

Clinical electrophysiology of flestolol, a potent ultra short-acting beta blocker.

We measured the electrophysiologic effects of flestolol, an ultra short-acting beta blocker, in 15 patients at two infusion rates: a 45 micrograms/kg loading dose followed by a 5 micrograms/kg/min infusion and a 60 micrograms/kg loading dose followed by a 10 micrograms/kg/min infusion. Electrophysiologic measurements were made after 15 minutes at each infusion rate (plasma concentrations 46 +/- 11 and 94 +/- 23 ng/ml). Flestolol produced dose-dependent effects on the sinus node, the atrioventricular (AV) node, and right ventricular refractoriness, whereas atrial refractoriness and infranodal conduction were unchanged. At the 10 micrograms/kg/min dose, flestolol prolonged sinus cycle length by a mean of 20% (p = 0.0001), corrected sinus node recovery time by 42% (p = 0.02), AH interval by 21% (p = 0.0001), AV node effective refractory period by 28%, AV node Wenckebach cycle length by 30% (0.0001), and right ventricular effective refractory period by 5% (p = 0.03). A significant concentration-effect relationship (p less than or equal to 0.03) was present for all variables which had significant dose-effect relationships. No patient developed hypotension, bradyarrhythmias, or other toxicity. Sinus cycle length decreased linearly with time in the post infusion period (r = 0.99); by 30 minutes post infusion, measured electrophysiologic variables had returned to control values and flestolol plasma concentration had decreased to 4 +/- 2 ng/ml. Flestolol's electrophysiologic effects are similar to those of other beta blockers. In doses up to 10 micrograms/kg/min, it is safe in selected patients, has rapid onset and offset of action, and does not cause acute rebound.

Adrenergic beta-Antagonists↗
PubMed1976

Modification by manganese ions and verapamil of the responses of the atrioventricular node to norepinephrine.

In isolated and cross-circulated canine A-V node preparations single injections of Mn2+ (1-30 mumol) and verapamil (0.3-10 nmol) into the posterior septal artery (PSA) caused a dose-dependent increase in the A-V conduction time and, in large doses, produced A-V conduction block. The A-V conduction time increased by Mn2+ and verapamil is resotred by 1-norepinephrine (1-NE) injected into the PSA. The A-V nodal tachycardia induced by 1-NE is suppressed by Mn2+ but not by verapamil. These indicate the following: (1) the slow Ca2+ channel plays an important role in A-V conduction; (2) the positive dromotropic response of the A-V node to 1-NE may have some relations to the Ca2+ channel; (3) the A-V nodal tachycardia induced by 1-NE may be mediated by the Ca2+ channel. Possible causes which produced differences between Mn2+ and verapamil in the effects in antagonizing the 1-NE-induced A-V nodal tachycardia are discussed.

Animals↗
PubMed1979

Effects of the beta-adrenergic blocking agents propranolol and timolol on canine cardiac refractory periods.

The effects of d,1-propranolol and 1-timolol on cardiac refractory periods (RP) were compared in 14 phentobarbital-anesthetized dogs using endocavitary His bundle electrograms and programmable electrical stimulation. Beta-blocking agents were injected at cumulative doses in each dog at 3 day intervals. A control group (6 dogs) received 4 successive saline injections at the same time intervals. RP measurements at a constant drive rate were done before and 10 minutes after each dose of either drug or saline. Propranolol and timolol produced a dose-dependent increase of atrial and atrioventricular nodal refractory periods; dose-response curves were parallel. Depending on the parameter chosen timolol exerted an 8--36 times more potent effect than propranolol. The effects of propanolol and timolol on ventricular effective (VERP) and functional (VFRP) RP were measured in 6 dogs. Both drugs increased VFRP significantly, but saline had the same effect. Only the higher doses of timolol increased VERP significantly. These data confirm that blockade of myocardial beta-adrenergic receptors exerts predominant effects on supraventricular refractoriness and that in anesthetized dogs timolol has more potent beta-blocking properties than does propranolol.

Animals↗
PubMed2004

Right lateral decubitus position reduces QT dispersion in patients with chronic heart failure.

A greater QT dispersion in patients with chronic heart failure (CHF) appears to be a non-invasive marker of susceptibility to malignant ventricular arrhythmias. We evaluated whether QT dispersion in CHF patients is modified by the patients' recumbent position. In 12 CHF patients, and age and sex-matched 12 normal subjects, a single 12-lead surface ECG was recorded in each postural position [left lateral decubitus position (L), supine position (S), and right lateral decubitus position (R)]. In normal subjects, the QT dispersion was comparable in the three recumbent positions [L: 47+/-15 (SD) ms, S: 40+/-9 ms, R: 38+/-14 ms, P=NS]. In contrast, in CHF patients, QT dispersion was significantly shorter in R than those in L and S (L: 93+/-42 ms*, S: 81+/-29 ms*, R: 63+/-24 ms, *P <.05 vs. R). In conclusion, reclining in R reduces the prolonged QT dispersion in CHF patients.

Aged↗
PubMed1978

The effect of hypoxia on the refractoriness of the canine ventricular muscle.

The effect of hypoxia on the relationship between refractoriness and transmembrane action potential was studied in isolated canine papillary muscle preparations. Test stimuli were applied at variable intervals after every 10 to 15 driving stimuli, and action potentials were recorded through an intracellular microelectrode located near the stimulus site. During hypoxia of 30 to 90 min duration, induced by nitrogenization of the perfusate, action potential duration (APD) was tremendously decreased in association with decline in the amplitude and rising velocity. The resting potential was also reduced. Concurrently the effective refractory period (ERP) was decreased, but its decrement was smaller than that of the APD. The total refractory period (TRP) was, on the other hand, prolonged. In consequence, not only the TRP but the ERP as well fairly outlasted full repolarization as a result of the hypoxia. The duration of the relative refractory period (RRP) was increased during hypoxia as the result of the changes in ERP and TRP, and graded local responses were registered frequently in the early phase of RRP. These facts were thought to be related to the genesis of arrhythmias in the ischemic heart.

Action Potentials↗
PubMed2000

Long-term lifestyle changes maintain the autonomic modulation induced by rehabilitation after myocardial infarction.

The altered autonomic balance observed after myocardial infarction is shifted toward a higher parasympathetic tone by rehabilitation. This effect persists after 1 year, however we observed a discrete variability in the long-term sympathovagal balance among patients. We postulated that such variability derives from the disparate adherence of patients to lifestyle prescriptions regarding exercise continuance and smoking avoidance. To test this hypothesis, we reviewed the data of 40 patients, who completed with a favourable autonomic modulation the initial rehabilitation phase after myocardial infarction and underwent the annual follow-up. One year after infarction, 23 patients complied to the advice about regular exercise and smoking avoidance (adherent, Group 1); 17 did not (non-adherent, Group 2). Groups were similar for age, site of infarction, left ventricular function, stress test duration and therapy. The ratio LF/HF, derived from the power spectral density of RR intervals variability, was used as an index of the sympathovagal balance. It was obtained from 15 min of ECG at rest, assessed 1 month after MI (baseline), and repeated 3 months (rehabilitation) and 1 year (follow-up) afterwards. Rehabilitation increased parasympathetic tone in all patients, reducing LF/HF by 33%. At follow-up, this potentially favourable autonomic profile persisted only in Group 1 patients. In conclusion, after a first myocardial infarction, the persistence of the potentially beneficial effect of rehabilitation on the sympathovagal balance depends on the compliance to the lifestyle changes proposed during the initial phase.

Analysis of Variance↗
PubMed1990

Time dependence of ventricular refractory periods: implications for electrophysiologic protocols.

Cardiac refractory periods are routinely measured during electrophysiologic testing. Informal observations suggested that the effective refractory period lengthened with a prolongation of the time in sinus rhythm (basic cycle length time) between successive runs of drive stimuli (S1S1s). If this were true, failure to control the basic cycle length time could affect the results and interpretation of electrophysiologic testing. To study this phenomenon, the effective refractory period was studied in 20 patients during sinus rhythm and two ventricular paced rates with up to three extrastimuli, while varying the basic cycle length time from 2 to 3, to 10 to 20 s. With each of the stimulation sequences used, the effective refractory period lengthened as the basic cycle length time increased ("basic cycle length time-effective refractory period effect"). The effect was most pronounced when extrastimuli were used during the two ventricular paced rates. As the basic cycle length time increased from 2 to 3 to 20 s, the mean effective refractory period determined during sinus rhythm increased from 296 to 300 ms; with the first ventricular paced rate, the effective refractory period increased from 259 to 272 ms (p less than 0.0003) and with the second ventricular paced rate, the effective refractory period increased from 250 to 263 ms (p less than 0.01). The basic cycle length time-effective refractory period effect became more pronounced as the number of extrastimuli increased. With the second ventricular paced rate, as basic cycle length was increased from 2 to 3 to 20 s, the mean prolongation in the cumulative effective refractory period (S1 to final extrastimulus) as the number of extrastimuli increased from 1 to 2 to 3, was 13 (p less than 0.01), 42 (p less than 0.0003) and 82 ms (p less than 0.001), respectively. Results were confirmed in 17 instances by redetermining the effective refractory period at the 2 to 3 s basic cycle length time after the final 20 s basic cycle length time determination, and demonstrating that it was similar to the effective refractory period after the initial 2 to 3 s basic cycle length time. No further prolongation of the effective refractory period could be demonstrated by increasing basic cycle length time from 20 to 60 s, and no significant effect of medications on the basic cycle length time-effective refractory period effect could be demonstrated.

Adolescent↗