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Introduction: The incidence and characteristics of dissociated arrhythmia confined to the pulmonary vein (PV) following disconnection have not been described in a large number of patients with paroxysmal atrial fibrillation., Methods and Results: This was a prospective study of 152 patients (29 female, mean age 51 +/- 11 years) referred for catheter ablation of drug-refractory paroxysmal atrial fibrillation. Following ostial ablation, the rate and regularity of any dissociated venous activity was analyzed with and without isoproterenol infusion (to achieve a heart rate of 120-140 beats/min). Patients then were classified according to their venous dissociated activity. Group 1 consisted of patients in whom the dissociated PV spike had a slow rhythm >1,200 ms. Group 2 consisted of patients with spontaneous repetitive dissociated discharges confined in the vein with a cycle length <400 ms. A total of 384 PVs were ablated in 152 patients. Disappearance of all venous potentials was observed in 88% of the treated veins; at least one dissociated venous potential was observed in the remaining 12%. Group 1 activity was seen more often than group 2 (23 patients, mean cycle length 2,300 +/- 1,100 ms vs 13 patients, mean cycle length 179 +/- 77 ms). Dissociated PV arrhythmia was seen most often in the right superior PV (19%)., Conclusion: Dissociation as the endpoint of PV disconnection was observed in 12% of PVs. Due to the capricious nature of this activity, the actual incidence is almost certainly higher. The dissociated venous rhythm usually is slow and, less commonly, is rapid and repetitive.

In order to evaluate the effects of increases of sympathetic tone in ventricular response during atrial fibrillation and in the relationship between the accessory pathway effective refractory period (ERP) and ventricular rate during atrial fibrillation, 20 male subjects, aged 19 +/- 6 years, were studied electrophysiologically in basal conditions, after isoproterenol infusion (2-4 micrograms/min) and during submaximal bicycle exercise test, at a constant workload equal to that which increases the sinus rate to the same extent (140 beats/min) induced by isoproterenol infusion. Accessory pathway ERP was evaluated at the same driven rate (150 beats/min) in both instances. In the control study as during both tests atrial fibrillation paroxysms were induced by burst stimulation. In control conditions the rate increase from 100 to 150 beats/min induced a reduction of accessory pathway ERP from 266 +/- 27 msec to 244 +/- 22 msec (P less than 0.005). At the same driven rate of 150 beats/min, isoproterenol infusion and exercise test induced a more marked shortening of accessory pathway ERP to 211 +/- 28 msec (P less than 0.005) and to 214 +/- 29 msec (P less than 0.005), respectively. Atrial fibrillation paroxysms lasting more than 10 seconds were induced in 20/20 cases in the control study, in 15/20 during isoproterenol infusion and in 13/19 cases during exercise test. The shortest cycle length during atrial fibrillation was reduced from a basal value of 253 +/- 72 msec to 204 +/- 27 msec (P less than 0.05) during isoproterenol infusion and to 236 +/- 32 msec (NS) during exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

The article deals with the modern approaches to the treatment of supraventricular tachycardia . The authors analyse the results of operations in ectopic atrial tachycardias, the Wolff-Parkinson-White syndrome, modal re-entry tachycardias, and atrial fibrillation . The last-named is of most interest because the authors possess experience in a new operation for isolation of the internodal tracts. In all conditions the authors obtained convincing evidence on the efficacy of modern surgical treatment in supraventricular tachycardias.

In patients with nodal tachycardia refractory to medical therapy, transcatheter or surgical ablation is necessary. From January 1989 to December 1990, in 26/42 patients with nodal tachycardia, referred to our institution for electrophysiologic evaluation, transcatheter ablation by radiofrequency (20 patients) or surgical ablation by perinodal cryo (6 patients) was performed. In all these cases, a total refractoriness to several antiarrhythmic drugs alone or in association had been observed. The radiofrequency current, generated by the Osypka HAT 100 device, was administered through a tripolar USCI 7 F catheter. The ideal site for energy delivery was defined on the basis of a mapping, performed in the A-V junction area. In order to find out the most premature retrograde atrial activation, the following areas were explored: right bundle, atrial His bundle, peri-nodal region, proximal His bundle and coronary sinus ostium. Local atrial activation time was evaluated during nodal tachycardia by delivering a premature ventricular extrastimulus to discover the atrial deflection from the ventricular one. In the selected area, 5 applications (range 1-12) of 20-25 W power radiofrequency energy for 5-30 s were delivered on average. A complete prevention of nodal tachycardia was achieved in 18/20 patients (90%). Only in 2 patients a total A-V block was induced. The pre- and post-procedure values are as follows: AH: pre 71 +/- 19, post 113.6 +/- 50; HV: pre 45.5 +/- 8, post 47 +/- 6; aWP: pre 353 +/- 57, post 391 +/- 87; rWP: pre 322 +/- 58, post 411 +/- 58. In 10/18 cases the AH interval was normal after radiofrequency application.(ABSTRACT TRUNCATED AT 250 WORDS)

The electrophysiologic effects of encainide were studied in 10 patients with Wolff-Parkinson-White syndrome after intravenous (1 mg kg-1 in 60 minutes) and oral administration of two dose regimens (75 and 150 mg daily). Under control conditions atrial fibrillation (AF) with a rapid ventricular response was induced in all patients and atrioventricular reciprocating tachycardia (AVRT) in 9 patients. After intravenous encainide AF was no longer induced in 3/9 patients; in 3 of the remaining the accessory pathway (AP) was totally blocked and in the others the shortest RR interval increased from 213 +/- 6 to 297 +/- 91 ms and the mean RR interval from 293 +/- 39 to 362 +/- 79 ms. The lower dose of oral encainide prolonged the shortest RR interval from 206 +/- 24 to 273 +/- 64 ms and the mean RR interval from 280 +/- 48 to 368 +/- 52 ms in 6 patients; in 2 cases no preexcited beats were recorded and in 1 AF was not inducible. After the higher dose of oral encainide AF was still inducible in 7/8 cases; in 3 the AP was blocked and in the others the shortest and mean RR intervals increased from 202 +/- 30 to 280 +/- 24 ms and from 276 +/- 59 to 436 +/- 80 ms, respectively. After intravenous encainide antegrade conduction over the AP was blocked in 4/9 patients and the antegrade effective refractory period (ERP) was prolonged in another 4. Oral encainide blocked AP conduction in 4 cases and prolonged ERP considerably in the others.(ABSTRACT TRUNCATED AT 250 WORDS)

The electrophysiologic effects of oral encainide (75 to 150 mg daily) were evaluated in 14 patients (6 male and 8 female, aged 49 +/- 9 years) with atrioventricular (AV) node reentrant tachycardia of the slow-fast type. The patients were studied in control conditions and after 2 to 12 days of treatment. Encainide increased the AH interval from 67 +/- 10 to 82 +/- 23 ms (p less than 0.02). Anterograde Wenckebach cycle length was increased in three patients, reduced in four, unchanged in one; it was not measurable in the remaining patients because tachycardia was induced. Retrograde Wenckebach periodicity increased from 307 +/- 71 to 401 +/- 92 ms (p less than 0.005) in all nine patients in whom it was measurable; complete retrograde block was observed in one patient. At the control study, tachycardia was induced in all patients, with a mean cycle length of 341 +/- 50 ms; after encainide, tachycardia was inducible in only 1 patient, with an increase in cycle length from 270 to 320 ms; in the other patients, tachycardia was not inducible because of a lack of retrograde (11 patients) or anterograde (2 patients) conduction. The mean plasma concentrations of encainide and its metabolites O-demethyl-encainide and 3-methoxy-O-demethyl-encainide measured in 13 patients during the repeat study were 161 +/- 304, 128 +/- 100 and 95 +/- 85 ng/ml, respectively; three poor metabolizers who presented a high concentration of the parent compound were observed in this series. All patients were discharged on encainide at a mean daily dose of 112 +/- 39 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

In 10 patients with supraventricular tachycardia who underwent an electrophysiological study the ectopic atrial origin of the tachycardia could be demonstrated by the intracavitary localization of the earliest depolarized point (six cases in the right atrium and four cases in the left). Vagal stimulation and/or the i.v. infection of ATP induced or increased the degree of AV block during tachycardia; in five cases ATP interrupted the tachycardia. On the basis of their clinical and electrophysiological behavior, the patients were divided into two groups. In the first one (6 patients) tachycardia was persistent, started following late atrial beats with the same morphology of the subsequent and showed a progressive initial rate increase (warm-up phenomenon); programmed atrial stimulation failed to start and interrupt it. In the second group (4 patients) tachycardia was paroxysmal or repetitive, started following early atrial beats and could be induced and interrupted by programmed atrial stimulation. With respect to the electrophysiological characteristics of each group the authors try to define the possible mechanism responsible for the tachycardia (automaticity and micro-reentry).

The aim of this report is to attempt a definition of functional properties of Kent bundle on the basis of electrophysiologic and electropharmacologic data obtained from 89 cases of Wolff-Parkinson-White syndrome selected among a total number of 114 consecutive cases of WPW syndrome that underwent electrophysiologic intracavitary study. In 36 cases anterograde (ant) and retrograde (retr) effective refractory period (ERP) of accessory pathway were evaluated with premature (atrial and ventricular) stimulation at the same driven cycle length. The ant-ERP was longer than retr-ERP in 28/36 patients, shorter in 5 and equal in 2. This strong discrepancy between ant- and retr- ERP suggests an important role of "impedance mismatch" in the activation of ventricular (or atrial) muscle through an anomalous muscular bundle. In 11 cases an intermittent pattern of ventricular preexcitation was observed; in all these patients an anterograde supernormal conduction through the accessory pathway was observed. This aspect could be related to the activation of ventricular muscle, beyond Kent bundle, in its supernormal phase of excitability, suggesting the critical role played by ventricular activation for the appearance of preexcitation. Isoproterenol, injected in 11 cases (1 among them with intermittent ventricular preexcitation in basal conditions), produced a reduction of ant-ERP in all these cases, in spite of its well known poor effect on refractoriness of myocardial fibers. Ajmaline, injected in 32 patients, was able to block ventricular preexcitation in 81% of the cases, in spite of its poor effect on refractoriness of normal tissues. It is very likely that the disappearance of ventricular preexcitation is in this instance expression of lack of ventricular excitation (distal to Kent bundle) consequent to a drug-induced reduction of membrane responsiveness of ventricular cells. In conclusion, all these aspects strongly suggest that the appearance of ventricular (or atrial) preexcitation could be related to the activation of ventricular (or atrial) muscle distal to Kent bundle, rather than to conduction through the Kent bundle itself.

A case of phase-3 (tachycardia dependent) and phase-4 (bradycardia-dependent) left bundle branch block (LBBB) which illustrates some relationships between automaticity and conduction in the intraventricular conduction system is reported. The observations made were: a) a conspicuous spontaneous variability of the conductivity and block temporal zones in the left bundle branch (LBB), i.e. of the cycle duration determining either normal intraventricular conduction or block in the LBB; b) after isoproterenol, transient shortening of phase-3 block zone and disappearance of phase-4 block zone due to escape beats which rise from the LBB; c) transient change into not rate-dependent LBBB in consequence of catheter LBB injury and gradual successive reappearance of conductivity zone; d) short periods of 2:1 phase-4 LBBB. A coexisting phase-4 block in a LBB fascicle with electrocardiographic pattern not fulfilling the agreed diagnostic criteria for hemiblocks was also demonstrated. This intraventricular conduction defect was also characterized by conspicuous spontaneous variability of the block temporal zones. After isoproterenol, the duration of the cycle decreased where it occurred. After LBB traumatic injury, it lasted not rate-dependent longer than LBBB and no escape beats rising from the LBB injured fascicle appeared. During normal intraventricular conduction the ECG showed "ischemic" alterations in V1-V4 leads of variable degree related to LBB conductivity and block zone duration. Selective coronary angiograms were normal. These findings are discussed in an attempt to clarify the electrophysiological mechanism of rate-dependent intraventricular conduction defects.

Presence of rate-dependent (RD) intraventricular conduction defects (IVCD) was documented by inducing variations in heart rate in 30 acute myocardial infarction (AMI) patients (10 right bundle branch block, six left bundle branch block, 13 left anterior hemiblocks, and two left posterior hemiblocks). Five IVCDs were tachycardia-dependent (TD), 20 were bradycardia-dependent (BD), and six were both TD and BD. In TD blocks shortest cycles showing normal intraventricular conduction ranged from 410 to 1330 msec (697 +/- 84 SE); in BD blocks longest cycles with normal intraventricular conduction ranged from 450 to 1450 msec (962 +/- 52). In 60% of cases intermittent incomplete RD blocks were also present. In one patients RD-IVCD intermittency remained until discharge; in the others it lasted from 4 minutes to 10 days. Afterwards 19 RD-IVCDs disappeared and four became stable; six patients died during RD-IVCD intermittency period. Disappearance of RD block was preceded by gradual reduction in cycle length showing TD block and lengthening of cycles stopped beats with BD block. Serial observation of RD-IVCDs provides information about sequence of electrophysiologic effects on the intraventricular conduction system in clinical AMI.

Myocardial ischemia, particularly when transmural as in variant angina pectoris, may be associated with ventricular tachycardia, ventricular fibrillation and paroxysmal atrioventricular block (15%). Syncope (7%) and sudden death (3%) due to these malignant arrhythmias are sometimes a unique marker of myocardial ischemia. Two-hundred fifty-four patients (220 males and 34 females), aged 5 +/- 9 years with transmural myocardial ischemia related to coronary artery spasm, were studied. Particular attention was paid to the role of syncopal attacks as unique clinical manifestation of silent ischemia. Patients examined were divided into 3 Groups. Group 1 includes 5/254 (2%) patients with atrial fibrillation during acute ischemia. Group 2 was divided into four subgroups: subgroup A includes 17/254 (7%) patients with syncopal attacks due to malignant arrhythmias (ventricular tachycardia and advanced A-V block); subgroup B, 15/254 (6%) patients with documented malignant arrhythmias, without syncopal attacks; subgroup C, 7/254 (3%) with ventricular fibrillation during acute ischemia and subgroup D, 18/254 (7%) patients with history of syncopal attacks without documented arrhythmias during hospital observation. Group 3 includes 17/254 (7%) patients with left anterior hemiblock in basal condition, 7/254 (3%) patients with left anterior hemiblock and one left posterior hemiblock during acute ischemia and one patient with right bundle branch block during acute ischemia. Syncopal symptoms are present in many of these cases of angina pectoris; paroxysmal A-V block is documented in nearly half of the cases with syncope (65%); ventricular tachycardia is frequently demonstrated during ischemia but leads to syncope in only a few cases; patients with syncope do not present specific clinical features.(ABSTRACT TRUNCATED AT 250 WORDS)