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PubMed1983

Sinus node electrogram recording in 59 patients. Comparison with simultaneous estimation of sinoatrial conduction using premature atrial stimulation.

Directly measured sinoatrial conduction time was compared with sinoatrial conduction time assessed simultaneously by the single premature atrial stimulus technique in 59 patients: 20 with normal sinus function, 35 with sinus dysfunction, and four with sinus bradycardia but negative indirect methods. In patients with normal sinus function direct sinoatrial conduction time was 102.5 +/- 34 ms (mean +/- 2 SD) and was identical to indirect sinoatrial conduction time. Neither direct sinoatrial conduction time in the basal and return cycle, nor post-return and basal cycle lengths were different. Sinoatrial and atriosinus conduction durations were similar. In sinus dysfunction direct sinoatrial conduction time (average 160 +/- 47 ms) was longer than in normal sinus function. Prolonged direct sinoatrial conduction time may therefore be considered as a criterion of sinus dysfunction. In sinus dysfunction no significant correlation was observed between direct and indirect sinoatrial conduction times. Direct sinoatrial conduction time was equal to (17 patients), longer than (12 patients), or shorter than (six patients) indirect sinoatrial conduction time. These differences can be explained by delayed or incomplete premature depolarisation penetration into the sinus node rather than by the classical pacemaker shift.

Adolescent↗

PubMed2006

Pilsicainide for atrial fibrillation.

Pilsicainide is a class IC antiarrhythmic drug, which has a pure sodium channel blocking action with slow recovery pharmacokinetics. In experimental studies, pilsicainide has a depressant effect on intra-atrial conduction and a prolonging effect on the atrial effective refractory period (ERP). In patients with paroxysmal atrial fibrillation (AF), pilsicainide significantly prolonged the ERP of the distal pulmonary vein (PV), PV-left atrium (LA) junction and LA, and the conduction time from the distal PV to the PV-LA junction. In some patients, PV-LA conduction block has been observed just before pilsicainide-induced termination of AF; this isolation of the PV may provide a new insight into the mechanism of pharmacological conversion of AF. Hybrid therapy with pilsicainide and PV isolation (by radiofrequency catheter ablation) appears to be an effective therapeutic approach for AF. The pharmacological PV isolation by pilsicainide and its suppression of focal discharges from atrial tissue may prevent the development of AF after unsuccessful ablation.

Animals↗

PubMed1998

Unipolar waveforms and monophasic action potentials in the characterization of slow conduction in human atrial flutter.

Anisotropic propagation may be involved in the development of areas of slow conduction in atrial flutter. We evaluated monophasic action potentials (MAPs) and simultaneous unipolar (0.2-400 Hz) and bipolar electrograms from multiple atrial sites of patients undergoing RF ablation of idiopathic atrial flutter. Nine patients (mean age 46 +/- 20 years) with typical atrial flutter (one with both types) were studied. Unipolar electrograms with triphasic complexes of small amplitude and with a slow, negative deviation of the baseline preceding the rS deflection indicated transversal conduction in relation to the orientation of cardiac fibers; smooth rS complexes longitudinal conduction; QS complexes onset of activation; and R complexes end of activation or collision. In all patients with typical atrial flutter, slow conduction occurred in the corridor between the inferior vena cava, the tricuspid annulus, and the coronary sinus. Transversal conduction was observed in this area, whereas the remaining sites showed longitudinal conduction. Anatomically guided RF ablation was successful in five patients. Transversal conduction was recorded in all successful sites. In the patient with atypical atrial flutter, slow conduction was noted in the high lateral right atrium, also exhibiting transversal conduction. Ablation at this area terminated the arrhythmia. All the areas of transversal conduction during flutter displayed longitudinal conduction after restoration of sinus rhythm. MAPs were normal in all patients during atrial flutter and sinus rhythm, even at the areas where transversal conduction was recorded. These findings suggest that anisotropic propagation is involved in the genesis of functionally determined areas of slow conduction during typical atrial flutter.

Action Potentials↗

PubMed1988

[Late complications of VVI electric stimulation in patients with sick sinus syndrome].

Forty-nine patients, including 38 with documented bradysystolic sick-sinus syndrome (type I) and 11 with bradytachycardiac sick-sinus syndrome (type II) were studied. Follow-up of 24 patients with VVI stimulation (34 +/- 4 months) and 7 patients with AAI stimulation (23 +/- 1.2 months) demonstrated that VVI stimulation was associated with retrograde ventriculo-atrial conduction in 71% of patients, causing paroxysms of atrial fibrillation (5 patients, 4 of those having type I sick-sinus syndrome). Six patients developed permanent atrial fibrillation (including 5 with type I sick-sinus syndrome). Retrograde conduction slowed down the pulse rate because of ineffective ventricular response in 6 patients. Nine patients with retrograde conduction developed circulatory insufficiency.

Adult↗

PubMed1997

[Can 1/1 atrial flutter be foreseen by class I anti-arrhythmics?].

1/1 atrial tachycardia or "quinidine" flutter under class I antiarrhythmic drugs is a serious complication of these agents which, unfortunately, cannot be anticipated. The aim of this study was to review the cases of 11 patients who had suffered this complication of class I antiarrhythmic therapy to see if it could have been prevented. All drugs of this class were included. The 11 subjects were aged 57 to 78: 7 had no apparent underlying cardiac disease and the others had valvular (n = 1), hypertensive (n = 1) and ischaemic (n = 2) heart disease. They were treated for episodes of paroxysmal atrial fibrillation or tachycardia. In the absence of treatment, 7 patients had a short PR interval on the ECG (PR between 0.11 and 0.14 s). In the other 4, the PR interval was normal (0.16 to 0.20 s), but the P wave was widened with appearances of left atrial hypertrophy or an intra-atrial conduction defect. High amplification ECG performed in 3 patients showed continuity of atrial and ventricular depolarisation. Atrial stimulation showed excellent nodal conduction with a Wenckebach point of 200/min. The authors conclude that a short PR interval is predisposing factor to 1/1 atrial tachycardia with class I antiarrhythmics. High amplification ECG which allows identification of the end of the P wave with respect to the QRS complex could help identify subjects at risk when the P wave is widened and that, consequently, the PR interval appears to be normal.

Aged↗

PubMed1978

[Electrophysiological effects of the combined administration of digoxin and propranolol in man].

The electrophysiological effects of the combined administration of digoxin and propranolol were studied in 40 patients, compared with the effects of digoxin alone and considered in relation to anomalies of the conduction pathways. The cycle of the sinus node was only lengthened by digoxin in patients who had an anomaly of sinus node function. In contrast the addition of propranolol always increased it (from 1 109 +/- 53 ms to 1 232 +/- 58 ms). Sinus node recovery time was only increased by combined administration (from 1 331 +/- 101 ms to 1 450 +/- 68 ms). Changes in sino-atrial conduction intervals were not very marked. The AH interval was increased by digoxin (from 97 +/- 4 ms to 109 +/- 6 ms), with propranolol exerting a synergistic effect (119 +/- 6 ms). When there was pre-existing supra-His block only combined administration increased the conduction defect. The HV interval and QRS duration were not altered. The effective atrial refractory period was increased by combined administration (from 264 +/- 10 ms to 304 +/- 14 ms) except in subjects who had supra-His block. The effective refractory period of the AV node (385 +/- 26 ms) was increased by digoxin (450 +/- 37 ms). This effect was potentiated by propranolol (478 +/- 34 ms) except in those subjects who had supra-His block. In three cases in which there were two conduction pathways at A V node level the refractory periods of the rapid and slow pathways were increased by digoxin, with a synergistic effect from propranolol. The ventriculo-atrial conduction time changed from 151 +/- 24 ms to 172 +/- 22 ms following digoxin, then to 193 +/- 34 ms after the addition of propranolol.

Adolescent↗

PubMed1977

Electrophysiologic properties of intravenous oxprenolol in man.

Electrophysiologic modifications produced by intravenous administration of 0.1 mg/Kg Oxprenolol were studied in 16 subjects with estimated normal impulse formation and conduction. Significant effects were sinus bradycardia, mild increase of sino-atrial conduction time, depression of intranodal conduction and prolongation of A-V node refractory periods. Sinus node recovery time and atrial refractory periods were unchanged. Infranodal conduction and the refractory periods of the His-Purkinje system, as well as of the bundle branches, were unchanged. These effects are compared with those observed after intravenous Propranolol and Prindolol.

Adult↗

PubMed1986

Lymph vessels of the rabbit heart: distribution and fine structure in atria.

The distribution and fine structure of lymph capillaries in the atria of the rabbit heart were examined. A lymph capillary network extends into both the right and left atria but its distribution is not uniform. It is developed in the subepicardium but not in the myocardium and subendocardium of the atrial wall; overall it is less extensive than the corresponding network in the ventricles. In the atrial conduction system and in particular the sino-atrial node and the crista terminalis, the lymph network is more widely distributed; small lymph capillaries are also detected between the myocardial cells of the conduction system. A large lymph channel consistently runs along the medial side of the crista terminalis. The morphologic characteristics of atrial lymph capillaries include irregular shape, thinness of the endothelial wall, superimpositions and interlockings of the cells in the contact areas with complex junctional processes, thin and discontinuous basal membrane.

Animals↗

PubMed1995

Signal-averaged P wave in patients with Wolff-Parkinson-White syndrome after successful radiofrequency catheter ablation.

OBJECTIVES: We attempted to establish a relation between the atrial conduction time assessed by the signal-averaged P wave electrocardiogram and episodes of paroxysmal atrial fibrillation in patients with the Wolff-Parkinson-White syndrome. BACKGROUND: The incidence of paroxysmal atrial fibrillation is higher in patients with the Wolff-Parkinson-White syndrome than in normal persons. However, the role of intraatrial conduction delay in precipitating the disorganization of atrial rhythm is not completely understood. METHODS: The total duration of the signal-averaged P wave and the P wave in standard lead II was evaluated after successful radiofrequency catheter ablation in 28 patients with the Wolff-Parkinson-White syndrome. The data obtained from 17 patients (61%) with a documented history of prior paroxysmal atrial fibrillation (group I) were compared with those obtained from 11 patients (39%) without a history of atrial fibrillation (group 2). Both groups were further compared with a normal control population. RESULTS: The mean +/- SD signal-averaged P wave duration in group 1 was 141.94 +/- 9.47 ms (range 130.0 to 171.0). Fourteen patients (82%) in this group showed a P wave duration > 135.0 ms. In group 2, the signal-averaged P wave duration was 126.64 +/- 8.72 ms (range 111.0 to 136.0). Only one patient in this group (9%) showed a P wave duration > 135.0 ms (p < 0.000, group 1 vs. group 2). The signal-averaged P wave duration in the control group was 124.46 +/- 4.49 ms (range 115.0 to 129.5; p < 0.000, group 1 vs. the control group; p < 0.454, group 2 vs. the control group). The P wave duration in lead II was 92.06 +/- 8.85 ms in group 1 and 92.27 +/- 7.86 ms in group 2 (p < 0.949). Using a cutoff value of < 135.0 ms for a normal signal-averaged P wave duration, the method had a sensitivity and specificity and positive and negative predictive values of 82%, 91%, 93% and 77%, respectively, for identifying patients with clinical paroxysmal atrial fibrillation. CONCLUSIONS: In the current study, the signal-averaged P wave showed a prolonged intraatrial conduction time in patients with the Wolff-Parkinson-White syndrome and paroxysmal atrial fibrillation. These patients can be differentiated from those with the pre-excitation syndrome without clinical atrial fibrillation as well as from normal subjects. The prolonged intraatrial conduction time may serve as an atrial substratum for development and maintenance of the fibrillatory state.

Adult↗

PubMedDate not supplied

Effects of phenytoin on refractoriness and conduction in the human heart.

Using His bundle electrograms and the atrial (A2) and ventricular extrastimulus (V2) techniques, anterograde and retrograde refractory period studies were performed (in 9 and 12 patients, respectively) before and 10 min after intravenous infusion of phenytoin (DPH; mean plasma level, 17.3 micrograms/ml). DPH had no effect on the duration of the QRS complex or the H-V interval of the sinus beats; it had variable but insignificant effects on the sinus rates and the atrial, A-V nodal, and ventricular muscle refractoriness. With the use of the A2 technique, the effective refractory period (ERP) of the His-Purkinje system (HPS) could not be determined in any patient; the relative refractory period (RRP) of the HPS could be determined in 2/9 patients and shortened in both patients after DPH. With the use of the V2 technique, retrograde functional refractory period (FRP) and RRP of the HPS could be determined in all 12 patients and the retrograde ERP of the HPS in 7/12; DPH significantly shortened all these parameters (p less than 0.001, less than 0.001, and less than 0.005, respectively). Functional refractory period of the ventriculo-atrial conduction system (VACS) could be determined in 11/12 patients during control studies (the remaining one patient had complete ventriculo-atrial block). DPH significantly shortened the FRP of the VACS in those (4) patients (Group I) in whom it was determined primarily by the HPS (p less than 0.025), and had variable but insignificant effects on FRP of the VACS in the other seven patients (Group II) in whom it was determined almost exclusively by the A-V node. DPH significantly decreased the retrograde HPS conduction times of the premature impulses (V2H2 intervals) for the same coupling (V1V2) intervals (p less than 0.001). It is concluded that, in the human heart, DPH exerts its most important effects on the HPS where it significantly decreases refractoriness and enhances conduction of the premature impulses. This study also demonstrates that the V2 technique is far superior to the A2 technique for evaluating the effects of drugs on refractoriness and conduction in the HPS.

Adult↗

PubMed2006

Effects of cardioactive medications on retrograde conduction: continuing relevance for current devices.

INTRODUCTION: Retroconduction (ventriculo-atrial conduction) remains a problem for patients with implanted cardiac rhythm devices. Pacemaker algorithms can detect and terminate endless loop tachycardia (ELT), but actual prevention of ELT may require anti-arrhythmic drugs (AADs). Similarly, AADs can affect ICD rhythm discrimination algorithms that depend on atrio-ventricular ratios. There is concern whether these drugs remain effective during stress situations. METHODS: Electrophysiologic studies that included retroconduction testing using slow ramp pacing were done in 1332 patients. The presence or absence of retroconduction at baseline and with drug was recorded, as was the rate at block. As a stress surrogate, isoproterenol was used to test retroconduction and reversal of drug-induced block. RESULTS: Procainamide, mexiletine, phenytoin, disopyramide, quinidine, beta-blockers, encainide, and amiodarone caused complete retrograde block or decreased the rate at which block occurred (mean 76% of patients, p < 0.008), whereas digoxin, lidocaine, diltiazem, and verapamil did not. Isoproterenol (in the absence of AADs) increased the rate at block in 82% of 404 patients with retroconduction at baseline (p < 0.005). Of 319 patients without retroconduction at baseline, 134 (42%) developed retroconduction after isoproterenol. Isoproterenol reversed retrograde block in 39% of patients with block on an AAD. Amiodarone, digoxin, and the combination of digoxin plus a beta-blocker were most effective at resisting this reversal of ventriculo-atrial block (80%, 68%, and 75% respectively). CONCLUSION: Most of the AADs reviewed increase the cycle length at block or abolish retroconduction, while isoproterenol has the opposite effect. Anti-arrhythmic medications, particularly amiodarone, digoxin, and the combination of digoxin plus a beta-blocker may be considered for a patient with multiple ELT episodes or certain ICD detection problems.

Adrenergic beta-Agonists↗

PubMed2004

Electrophysiologic predictors of the recurrence of persistent atrial fibrillation within 30 days of cardioversion.

Patients with recurrence of persistent atrial fibrillation within 30 days of cardioversion had slower atrial conduction, a slower sinus rate, no difference in the absolute value of the effective refractory period, greater early reverse remodeling of the effective refractory period, and more premature atrial contractions than those who did not. These findings highlight the role of slow conduction and premature atrial contractions in the pathophysiology of atrial fibrillation and suggest a possible proarrhythmic effect of reverse remodeling.

Aged↗

PubMed1991

Electrophysiologic effects of verapamil metabolites in the isolated heart.

The electrophysiologic effects of the metabolites of verapamil are unknown and may contribute to the observed differences between intravenous and oral verapamil. We examined the electrophysiologic effects of verapamil and its metabolites (norverapamil, N-dealkylverapamil (D617), and N-dealkylnorverapamil (D620)) at estimated, free therapeutic concentrations, in the retrogradely perfused, isolated rabbit heart. Verapamil at 5 and 10 ng/ml significantly prolonged anterograde (11 and 27%, respectively) and retrograde (10 and 25%, respectively) atrioventricular (AV) nodal block cycle lengths. Anterograde and retrograde AV nodal conduction times and refractory periods were also prolonged. Norverapamil at 100 ng/ml had qualitatively similar effects equivalent to 20-50% that observed with verapamil at 10 ng/ml. D620 had small but statistically significant effects on some AV nodal parameters. D617 had no effect. The combination of verapamil plus its principal metabolite, norverapamil, had additive effects. None of the compounds had any measurable effect on atrial conduction, His-Purkinje conduction, or atrial refractoriness. Ventricular refractoriness was significantly prolonged only by norverapamil. In conclusion, some of the metabolites of verapamil have important electrophysiologic AV nodal effects and may contribute to the clinical effects observed during chronic oral verapamil dosing.

Animals↗

PubMed1980

Electrophysiological effects of hypoglycaemic sulphonylureas on rabbit heart.

The hypoglycaemic sulphonylurea drugs glibenclamide and carbutamide were compared as to their influence on the electrical activity of isolated rabbit heart preparations. Carbutamide (10(-5)-10(-3) M) was found to depress slightly the nomotopic and junctional automaticity, while in Purkinje fibres it enhanced automaticity and conduction velocity. On the other hand, glibenclamide (10(-6)-10(-3) M) had no significant influence on the nomotopic and junctional automaticity, and markedly depressed automaticity and conduction velocity in the Purkinje fibres. The atrial conduction system was not much influenced by the sulphonylureas tested. Carbutamide depressed the electrical threshold in Purkinje fibres. It follows that the hypoglycaemic sulphonylurea compounds carbutamide and glibenclamide differ considerably with respect to their influences on cardiac electrical activity.

Action Potentials↗

PubMed1978

Supraventricular tachyarrhythmias in acute myocardial infarction.

Onset of atrial tachycardia, flutter or fibrillation occurred in 11% of 274 consecutive patients with acute myocardial infarction (AMI). Atrial tachycardia started about 24 hours and atrial flutter/fibrillation about 72 hours after onset of AMI symptoms. Left heart failure, diagnosed as pulmonary rales or frank pulmonary edema, was not more common in these patients before onset of tachyarrhythmias than among the rest of the patients. On the other hand, a notching of the P wave in lead CR-was significantly more common in the patients with atrial fibrillation (67%). In most of these cases the terminal P force in lead CR1 was not negative as in so-called left atrial enlargement. These findings suggest that atrial conduction disturbances might be a basis of atrial fibrillation in AMI.

Acute Disease↗

PubMed1993

Unusual electrocardiographic findings associated with type A Wolff-Parkinson-White syndrome.

A 50-year-old woman with Wolff-Parkinson-White (WPW) syndrome presented with unusual electrocardiographic (ECG) findings following the termination of paroxysmal supraventricular tachycardia. The ECG showed three different QRS complexes and irregular R-R intervals. These QRS complexes consisted of: (1) narrow QRS; (2) wide QRS with delta wave; and (3) wide QRS with left bundle branch block (LBBB). The mechanisms of these findings, revealed by electrophysiological study, were: (1) intermittent anterograde left-sided accessory pathway conduction; (2) rate-dependent ipsilateral LBBB; and (3) intermittent retrogradely conducted atrial echoes that occurred due to intraventricular conduction delay resulting from LBBB. Cases of WPW syndrome with these unusual ECG findings, which were clearly interpreted by electrophysiological study, are rare.

Bundle-Branch Block↗

PubMed2005

Biatrial epicardial pacing prevents atrial fibrillation and confers hemodynamic benefits after coronary artery bypass surgery.

Biatrial pacing (BIP) can be more effective than standard right atrial pacing (RAP) in preventing atrial fibrillation (AF) after coronary artery bypass graft surgery (CABG). However, the mechanisms and hemodynamic benefits of BIP have not been studied in detail. This study examined the efficacy and hemodynamic benefits conferred by overdrive epicardial BIP in preventing post-CABG AF. After undergoing CABG, 72 patients (mean age = 66 +/- 12 years, 48 men) were randomly assigned to triggered BIP (BIP-AAT; n = 50) versus single RAP (RAP-AAI; n = 22). The hemodynamic effects of BIP were measured by right heart catheterization and echocardiography. The patients were monitored for 8.8 +/- 2.4 days after CABG to detect episodes of AF. The incidence of AF was significantly lower in the BIP-AAT group (22.0%) than in the RAP-AAI group (59.1%, P < 0.01). Cardiac output was significantly higher and pulmonary artery wedge pressure (PAWP) significantly lower during BIP-AAT than during RAP-AAI. The E-wave (65.2 +/- 37.8 vs 57.8 +/- 37.8 cm/s, P < 0.05) was significantly higher during BIP-AAT, and the interval between atrial pacing spike and the end of A-wave (241 +/- 18.4 vs 286 +/- 17.2 ms, P < 0.001) was significantly shorter during BIP-AAT than during RAP-AAI. Triggered BIP was well tolerated and significantly reduced the incidence of post-CABG AF compared to single-site RAP. The hemodynamic improvements conferred by BIP-AAT were due to a shortening of the inter-atrial conduction delay and greater contribution of left atrial contraction. These hemodynamic benefits may play a role in lowering intra-atrial pressure and in preventing AF.

Aged↗

PubMed2002

New insights into onset mechanisms of atrial fibrillation and flutter after coronary artery bypass graft surgery.

OBJECTIVE: To determine by means of a monitoring study the onset mechanisms of atrial fibrillation (AF) after coronary artery bypass graft surgery (CABG). PATIENTS AND DESIGN: During elective CABG, 81 patients had one bipolar atrial and one ventricular epicardial electrode attached. These were connected to a Vitatron 900E external pacing device, which monitored the patients for four consecutive days. 12 lead ECGs were obtained if AF was clinically detected and Holter ECGs were obtained in 8 (33%) of these patients. RESULTS: 24 patients (30%) developed paroxysmal AF (50%), atrial flutter (17%), or both (33%). The number of AF episodes varied from 1-169 a day (median 5) and were usually of short duration (median 2.25 minutes). Pacemaker diagnostics showed much intrapatient and interpatient variability in onset mechanisms but the majority of AF onsets (71%) were preceded by either short runs of AF or multiple atrial extrasystoles. The final trigger was a conducted atrial extrasystole in 72% of cases. There were no bradycardic triggers. The Holter ECGs confirmed the device's data. CONCLUSIONS: The onset mechanisms of post-CABG AF are dominated by atrial extrasystoles with multiple atrial extrasystoles and short runs of AF preceding the main AF onset in the majority of cases. These results have major implications for the development of new preventive pacing algorithms.

Angina Pectoris↗