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PubMed1981

["Slowing" right bundle-branch block in reciprocating tachycardia from a latent right lateral Kent bundle].

The authors report the case of a 56 year old man with paroxysmal reciprocating tachycardia. The participation of a right lateral Kent bundle, latent in sinus rhythm and with retrograde atrioventricular conduction during tachycardia was proved by : 1) the slowing of the tachycardia rhythm and lengthening of the ventriculo-atrial conduction time by 50 ms during right bundle branch block ; 2) atrial mapping during tachycardia showing right lateral atrial pre excitation ; 3) the spontaneous termination of some attacks after a blocked Hisian depolarisation. Analysis of the mechanisms of spontaneous termination of tachycardia showed a block in the accessory pathway in 80% of cases, leading to the successful use of Amiodarone. The particular electrophysiological mechanism of functional bundle branch block makes it the most reliable positive diagnostic criterion in reciprocating tachycardia. A review of previously reported series shows participation of right lateral and septal accessory pathways to be uncommon during reciprocating tachycardia. Functional bundle branch block does not necessarily lengthen the ventriculo-atrial interval with septal accessory pathways. Left lateral Kent bundles are much more common. These points are analysed together with the mechanism of functional bundle branch block in the discussion.

Bundle-Branch Block↗
PubMed1984

Catheter ablation of atrioventricular conduction.

35 patients with refractory supraventricular arrhythmias were treated in three centres by high-energy shocks delivered to the atrioventricular conduction system from a conventional transvenous pacing catheter. After a mean interval of ten months, 26 patients (74%) had persistent complete heart block, 2 (6%) had intermittent complete heart block, and 3(9%) had first-degree heart block. 3 patients continued to have conducted atrial fibrillation, but with slower ventricular rates than previously, and 1 had normalisation of dual atrio-His conduction. In 1 patient a septal accessory pathway was ablated. 30 patients (86%) are completely symptom-free without additional therapy. There were no important long-term complications. Transvenous ablation of atrioventricular conduction is a safe and effective technique for treating a wide range of refractory atrial and junctional arrhythmias.

Adolescent↗
PubMed2003

Atrial fibrillation: hypertension as a causative agent, risk factor for complications, and potential therapeutic target.

Atrial fibrillation and hypertension are 2 prevalent, and often coexistent, conditions in the North American population. Their incidence increases with advancing age, and they are responsible for considerable morbidity and mortality. Although the relation between the 2 conditions has long been known, the treatment of hypertension is not currently a focus in the clinical management of atrial fibrillation. Hypertension is associated with left ventricular hypertrophy, impaired ventricular filling, left atrial enlargement, and slowing of atrial conduction velocity. These changes in cardiac structure and physiology favor the development of atrial fibrillation, and they increase the risk of thromboembolic complications. Conventional therapy of atrial fibrillation has focused on interventions to control heart rate and rhythm and the prevention of stroke through the use of anticoagulant medications. In patients with atrial fibrillation, aggressive treatment of hypertension may reverse the structural changes in the heart, reduce thromboembolic complications, and retard or prevent the occurrence of atrial fibrillation. Specific pharmacotherapy could potentially play a major role in the primary and secondary prevention of atrial fibrillation and its complications.

Antihypertensive Agents↗
PubMed2006

Progressive and persistent atrial inexcitability.

Sinus node disease is characterized by the presence of significant sinus bradycardia or prolonged sinus pauses, and is attributed to either primary failure of sinus node automaticity or sino-atrial conduction disturbance. We present two patients with symptomatic bradycardia due to idiopathic global atrial inexcitability.

Adolescent↗
PubMed1977

Bradycardia-dependent interatrial block with retrograde left atrial activation.

A patient with a peculiar interatrial block is reported. The electrocardiogram showed a short PR interval and negative P waves in II, III, and aVF, which were preceded, 0-07 s earlier, by another positive P wave present in the right praecordial leads which were absent in the limb leads. From the study with His bundle electrograms, high right atrial electrograms, and bipolar oesophageal electrocardiograms, it could be proved that atrioventricular, His-Purkinje, and right intra-atrial conduction were normal, and that P waves recorded in limb leads represented left atrial depolarization; whereas the ones in the right praecordial leads corresponded to right atrial activation. The vectorial analysis from both P waves and atrial potentials showed that the left atrium was activated in a retrograde fashion, because of an interatrial block. This block was bradycardia dependent and it disappeared in the cycles shorter than 800 ms.

Aged↗
PubMed2002

[Etio-pathogenetic mechanisms of recurrences of atrial fibrillation of toxic alcoholic origin].

The following conditions in patients with alcoholic cardiac involvement predispose to recurrences of atrial fibrillation: atrial dilatation, shortening of refractory period, slowing of atrial conduction, increased vulnerability to extra stimuli, appearance of fragmented electrical activity i.e. late atrial potentials on high resolution ECG, autonomic influences on the heart, hypokalemia and hypomagnesemia.

Alcoholism↗
PubMed1991

[Atrial tachyarrhythmias in sinus node disease: diagnostic and therapeutic problems].

It is known that sinus node dysfunctions can, in some instances, be accompanied by paroxysmal supraventricular arrhythmias. It is however not completely understood if, in these patients, it is present a situation of electrical atrial vulnerability or an electrophysiological condition which may represent the substrate for these arrhythmias. With the aim to solve this issue, 23 patients with sinus node dysfunction (8 of whom with atrial tachyarrhythmias) underwent a complete electrophysiological study, according to the protocol of the Italian Group of Cardiac Electrophysiology. The results of the electrophysiologic study allowed to demonstrate that in 75% of patients with atrial tachyarrhythmias it was possible to reproduce the arrhythmia by means of a low aggressive protocol. Also, in these patients, an inter- and intra-atrial conduction disturbance was demonstrated and, with respect to those patients without arrhythmias, the atrial refractory period was shorter in basal conditions and during induced atrial rhythm with cycle length of 600 ms, it was longer in left atrium than in high right atrium, and it shortened to a lesser extent with the shortening of the cardiac cycle.

Anti-Arrhythmia Agents↗
PubMed1984

[Electrophysiological effects of encainide in man].

Encainide is an antiarrhythmic agent under evaluation; it is effective in ventricular and supraventricular arrhythmias. Its electrophysiological effects seem to differ according to the route of administration, oral or intravenous, probably because of the effects of active metabolites. Two electrophysiological studies were carried out in 20 patients, under basal conditions, and after 4 to 10 days oral administration at doses ranging from 75 to 300 mg/day. Encainide depressed intra-atrial conduction (prolongation of the P-A interval from 29,7 +/- 2,2 to 36 +/- 4,5 ms, p less than 0,01), slowed conduction in the atrioventricular mode (prolongation of the A-H interval from 74 +/- 14 to 98 +/- 15 ms, p less than 0,01) and the His-Purkinje system (lengthening of H-V from 50 +/- 3 to 70 +/- 6,2 ms, p less than 0,001). The sinus node function was depressed with lengthening of the corrected sinus node recovery time (297 +/- 64 to 387 +/- 71 ms, p less than 0,01) and of the sinoatrial conduction time (173 +/- 25 to 219 +/- 43, p less than 0,01). The atrial and ventricular refractory periods were significantly longer (245 +/- 16 ms to 273 +/- 10 ms, p less than 0,001, and 237 +/- 12 to 266 +/- 19 ms, p less than 0,01, respectively). This new antiarrhythmic agent therefore seems to act at all levels which suggests that it may have wide ranging antiarrhythmic effects.

Administration, Oral↗
PubMed2006

Atrial tachycardia originating from the upper left atrial septum: demonstration of transseptal interatrial conduction using the infolded atrial walls.

We report a rare case of atrial tachycardia (AT) originating from the upper left atrial septum. Electroanatomic mapping of both atria demonstrated that the earliest atrial activation during AT occurred at the upper left atrial septum 26 msec before the onset of the P wave, followed by the mid-right atrial septum (10 msec before the onset of the P wave) and then the upper right atrial septum just adjacent to the left septal AT site (1 msec before the onset of the P wave), indicating detour pathway conduction from the upper left to the upper right atrium. Embryologically, it was suggested that the superior components of the secondary atrial septum are made by the infolded atrial walls and could develop a transseptal detour pathway involving the left-side atrial septal musculature, the superior rim of the oval fossa and the right-side atrial septal musculature. A single radiofrequency application targeting the upper left atrial septum successfully abolished the AT.

Aged↗
PubMed1976

Clinical studies on the sick sinus syndrome.

1) Overdrive suppression is clinically useful to evaluate depressed cardiac automaticity in the sick sinus syndrome. 2) His bundle electrograms revealed frequent association of atrioventricular conduction defects with the depressed automaticity in this syndrome. 3) Especially in BTS, marked intra-atrial conduction defect was observed, and this conduction defect may play a role for development of re-entrant tachycardia. 4) Pathologic changes in the sick sinus syndrome are supposed to involve the whole atrial tissues including not only the S-A nodal region but the A-V node and its approaches.

Adams-Stokes Syndrome↗
PubMed2000

Potent and reversible effects of ATI-2001 on atrial and atrioventricular nodal electrophysiological properties in guinea pig isolated perfused heart.

We recently demonstrated that the short-acting analog of amiodarone, ATI-2001, caused favorable effects in guinea pig ventricular myocardium on electrophysiological substrates underlying tachyarrhythmia initiation, perpetuation, and termination. Here, the acute effects of 1.0 microM ATI-2001 and 1.0 microM amiodarone (90-min infusion followed by 90-min washout period) on atrial and atrioventricular (AV) nodal electrophysiological properties were studied in guinea pig isolated hearts. Neither ATI-2001 nor amiodarone significantly prolonged atrial conduction time. Compared with amiodarone, ATI-2001 caused significantly more rapid and greater prolongation of atrial monophasic action potential duration at 90% repolarization (maximal change 21.4 +/- 3.7 versus 19.0 +/- 4.0 ms) and atrial effective refractory period (ERP, 27.8 +/- 6.1 versus 9.2 +/- 2.3 ms). Shortening of the atrial cycle length from 250 to 200 ms did not significantly alter drug-induced changes in atrial repolarization and refractoriness. ATI-2001 prolonged the atrium-to-His bundle interval (22.1 +/- 2.6 versus 8.8 +/- 2.3 ms), His bundle-to-ventricle interval (2.8 +/- 0.4 versus 0.9 +/- 0.3 ms), AV nodal ERP (72.5 +/- 7.3 versus 31.4 +/- 4.1 ms), and Wenckebach cycle length (69.6 +/- 5.2 versus 35.8 +/- 4.1 ms) significantly more than did amiodarone. Unlike amiodarone, the effects of ATI-2001 were markedly reversed upon discontinuation of drug infusion. Given these data, ATI-2001 should not only be useful for terminating ongoing and preventing reoccurrence of atrial tachyarrhythmias but also to treat supraventricular tachycardias involving the AV node and to control ventricular rate during atrial tachyarrhythmias. Whether the observed differences in the pharmacokinetic properties render ATI-2001 superior to amiodarone in acute tachyarrhythmia management and less likely to accumulate into tissues during chronic therapy remains to be established.

Action Potentials↗
PubMed1982

Atrial excitability and conduction in patients with interatrial conduction defects.

Prolongation of P-wave duration is an accepted indicator of an interatrial conduction disturbance and may predispose patients to atrial arrhythmias. This study was performed to monitor electrophysiologic characteristics of the atria in patients with a prolonged P-wave duration. Atrial excitability and conduction times were compared in 7 patients with a P-wave duration of less than 115 ms (Group I), and 13 patients with a duration of greater than of equal to 115 ms (Group II). In contrast of the Group I patients, most of the 13 patients in Group II had atrial arrhythmias, including sinus nodal dysfunction (3 patients) and a history of atrial fibrillation or ectopic atrial tachycardia (6 patients). Electrophysiologic differences between the 2 groups included a higher late diastolic threshold in Group II (0.8 +/- 0.2 mA versus 1.3 +/- 0.2 mA; p less than 0.005), and a greater increase in intraatrial conduction time (5 +/- 10 ms versus 30 +/- 20 ms; p less than 0.005) and interatrial conduction time (5 +/- 15 ms versus 30 +/- 15 ms; p less than 0.05) of early premature responses. There were no differences between the 2 groups in refractory periods, shape of the strength interval curve, or conduction times of premature responses occurring late in diastole. These abnormalities in conduction time and excitability found in patients with a prolonged P-wave duration may predispose to the initiation of certain atrial tachyarrhythmias.

Adult↗
PubMed1994

Effect of metoprolol on atrial fibrillatory rate, atrioventricular nodal concealed conduction, and ventricular response during atrial fibrillation in pigs.

We wished to elucidate the effect of beta-blockade on fibrillatory rate and atrioventricular (AV) nodal concealed conduction during atrial fibrillation (AF). Subsequent to determination of the effect on atrial functional refractoriness with the extrastimulus technique (basic cycle length 400 ms), the effect of metoprolol (0.3 mg/kg) on atrial fibrillatory rate was determined in 8 open-chest pigs with metacholine-facilitated AF. Once stable AF was established, fibrillatory rate was recorded with a bipolar epicardial electrode, together with the ventricular response during 500 ventricular intervals. For each episode of AF, three indexes were calculated to determine the degree of concealed conduction: the ratio of the longest to the shortest ventricular interval, the ratio of the median ventricular interval to the median atrial interval, and the coefficient of variation of the ventricular intervals. Metoprolol decreased fibrillatory rate (571-432 beats/min, p < 0.01), suggesting a proportionate increase (+32%) in atrial functional refractoriness during AF that far exceeded the increase (+7%) during sinus rhythm (217-233 ms, p < 0.05). None of the indexes of concealed conduction was affected by metoprolol. Metoprolol decreases fibrillatory rate in AF, possibly due in part to its class I effect, causing rate-dependent prolongation of atrial refractoriness. Despite reducing fibrillatory rate, metoprolol does not affect AV nodal concealed conduction measurably. Our results support the assumption that the reducing effect of beta-blockers on ventricular rate during AF is due to direct prolongation of AV nodal refractoriness.

Animals↗
PubMed2005

Long-term outcome after cardioversion of atrial fibrillation: prediction of recurrence with P wave signal averaged ECG and chemoreflexsensitivity.

AIM: The recurrence of atrial fibrillation after cardioversion was a general problem in medical practice. METHODS: We wanted to test the hypothesis that the recurrence of atrial fibrillation could be predicted by measurements of P wave triggered P wave signal averaged ECG and chemoreflexsensitivity (CHRS) in 118 consecutive patients one day after successful electrical cardioversion. We measured the filtered P wave duration (FPD) and the root mean square voltage of the last 20 ms of the P wave (RMS 20) with P wave triggered P wave signal averaged ECG. The CHRS was calculated of a ratio between the difference of RR intervals in ECG and venous pO2 before and after 5-min oxygen inhalation. The pathologic CHRS was predefined as a CHRS below 3.0 ms/mm Hg. RESULTS: A recurrence of atrial fibrillation was observed in 57 patients (48%) during a 9.3-month follow-up. The left atrial size (41.9+/-4.0 vs. 39.3+/-3.1 mm, P<0.0003) was larger, the FPD (139.6+/-16.0 vs. 118.2+/-14.1 ms, P<0.0001) was longer, the RMS 20 (2.57+/-0.77 vs. 3.90+/-0.99 muV, P<0.0001) and the CHRS (2.66+/-1.18 vs. 4.01+/-1.66 ms/mm Hg, P<0.0001) were lower in patients with recurrence of atrial fibrillation. A cut-off point was defined with FPD > or =126 ms and RMS 20 < or =3.1 muV and could predict atrial fibrillation with a specificity of 77%, a sensitivity of 72%, a positive value of 75%, a negative predictive value of 75% and an accuracy of 75%. Patients with FPD > or =126 ms and RMS 20 < or =3.1 muV had nearly a 7-fold increase risk for recurrence of atrial fibrillation. CONCLUSION: The recurrence of atrial fibrillation after cardioversion could be detected by P wave signal averaged ECG and an analysis of CHRS. These methods seem to be appropriate to show a delayed atrial conduction and a neurovegetative imbalance which might be possible trigger mechanisms of reinitiating of atrial fibrillation.

Aged↗
PubMed1977

Intermittent AV conduction disturbances in patients with AV nodal bypass tracts. Possible mechanisms of unusual variant of tachycardia-bradycardia syndrome.

His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent AV conduction disturbances occurring below the site from which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent AV block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachcardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block.

Arrhythmias, Cardiac↗
PubMed2001

Effects of E047/1, a new antiarrhythmic drug, on experimental atrial fibrillation in anesthetized dogs.

Effects of a new antiarrhythmic drug, E047/1, on atrial fibrillation were studied. Atrial conduction velocity and effective refractory period (ERP), electrocardiogram parameters (RR, PR, QRS, QT, and QTc intervals), systolic and diastolic blood pressure, and plasma concentrations of E047/1 were determined during the first 30 min after sequential administration of 1, 3, and 6 mg/kg of E047/1 in polysorbate 60 (Tween 60) to anesthetized, opened-chest dogs with vagally induced atrial fibrillation. Epicardial mapping (using 224 unipolar electrodes) was used to determine atrial fibrillation cycle length and activation sequence before and after drug administration. E0471, 3 mg/kg, prevented atrial fibrillation reinduction, and 6 mg/kg terminated atrial fibrillation. E047/1, 6 mg/kg, increased atrial ERP from 124 +/- 9 to 168 +/- 14 ms (p < 0.05). Conduction velocity decreased from 103 +/- 4 cm/s to 87 +/- 3 cm/s (p < 0.05). Epicardial mapping showed that under drug influence there was gradual reduction of wavelet number until termination of the reentrant excitation. Atrial fibrillation cycle length increased before atrial fibrillation termination from 93 +/- 4 to 137 +/- 12 ms (p < 0.05). The ability of E047/1 to terminate and prevent reinduction of experimental atrial fibrillation appears associated more with a significant prolongation of the atrial ERP than with a slowing of conduction. E047/1 appears to be a promising antifibrillatory agent.

Animals↗
PubMed1978

[Evaluation of sino-atrial function using the method of extrasystole induced by constant-relative premature impulses. 1. Method and normal results].

Atrial pacemaking under conditions of relative constancy (40 or 50% of the preceding cycle) enables us to calculate the immediate sino-atrial conduction time (retrograde and antegrade) (SACT). 17 patients were chosen for their normal sino-atrial function under spontaneous changes of the sinus cycle (SC). In each case, a significant inverse linear relationship was found between SACT and the corresponding SC. The mean correlation slope was -0.36 in 10 patients with no post-pacing depression (PPD). The slope was greater in 7 patients with a PPD (-0.89); if this depression is taken into account when the SACT is calculated, the slope decreases. In 5 patients, atropine (1 mg I.V. reduced the mean value of SC, and shortened (constant relative value) the SACT. The mechanisms for the spontaneous and induced variations in the sinus output are discussed; it may be that there are substitute pacemakers within the cells of the sino-artrial node, which are affected by variations in sympathetic or parasympathetic activity or by pacing. In clinical practice, automatism and conduction with the sinus node should be interpreted as inter-related functions, both under normal conditions and after vagal block.

Adult↗
PubMed1976

The effect of premature atrial depolarization on sinus node automaticity in man.

Sino-atrial conduction time (SACT) may be calculated from the difference between the length of the return cycle and the spontaneous cycle, using programmed premature atrial stimulation during spontaneous sinus rhythm. This approach to sinoatrial conduction assumes that sinus node automaticity is not changed by premature depolarization. In order to validate this assumption, we compared the length of the post-return cycles to the spontaneous cycle length in 71 patients. Patients were grouped according to clinical diagnosis and the value of calculated SACT. At long coupling intervals at which no reset of the sinus node occurred there was only a small prolongation of the post-return cycles (less than 8.4 msec, on an average) compared to the spontaneous cycle length. This suggests no or only an insignificant effect of premature depolarization on the sinus node. However, during test stimuli leading to reset of the sinus node, the post-return cycles were significantly prolonged between 20 to 30 msec, on an average. The response of the individual cases sometimes varied to a great extent. In patients who demonstrated a progressive linear prolongation of the return cycles at decremental shortening of the test interval, there was no significant prolongation of the post-return cycles versus the spontaneous cycle length. We conclude that 1) premature depolarization of the sinus node may have a depressant effect on sinus node automaticity, which, if present, is usually small; 2) calculation of SACT using the extrastimulus technique may overestimate true SACT.

Action Potentials↗