Antonio R. Caracta

Effect of Atrial Stimulation Site on the Electrophysiological Properties of the Atrioventricular Node in Man

The electrophysiological properties of the atrioventricular conduction system were compared in 16 patients using stimulation of the high right atrium (HRA) and a site within the coronary sinus (CS). The site of atrial stimulation significantly altered A-V nodal conduction time and refractoriness in eight patients (Group A) and did not change A-V nodal properties in the remaining patients. His-Purkinje conduction time and refractoriness were not affected by changing the atrial stimulation site. The atrial stimulation site may influence A-V nodal function by changing the site and/or mode of entry of the impulse into the A-V node.

Interventricular septal motion during preexcitation and normal conduction in Wolff-Parkinson-White syndrome: Echocardiographic and electrophysiologic correlation☆

Interventricular septal motion was studied by echocardiogram in 20 consecutive patients with documented Wolff-Parkinson-White (WPW) syndrome before and during electrophysiologic evaluation using His bundle recordings and pacing techniques. Characteristic abnormal interventricular septal motion was seen in 8 of 11 patients with type B WPW syndrome (groups I and II). All eight patients had electrocardiographic patterns consistent with an anomalous pathway located in the anterior right ventricular wall (group I). In five of these eight patients normalization of the QRS complex for one or more beats was accomplished and produced normalization of the septal motion in four; whereas in the fifth patient, who had an underlying atrial septal defect, the abnormal septal motion remained abnormal. All nine patients with type A WPW syndrome (groups III to V) had normal septal motion both during total preexcitation and during normalization of the QRS complex. The normalization of the abnormal interventricular septal motion with normalization of the QRS complex in type B WPW syndrome strongly suggests that the abnormal motion is related to an abnormal sequence of ventricular depolarization during preexcitation. Furthermore, persistent abnormal septal motion after normalization of the QRS complex suggests that other factors such as right ventricular volume overload may be responsible. Likewise, when abnormal septal motion occurs in the presence of type A WPW syndrome, an explanation other than preexcitation must be sought.

Induction of atrioventricular nodal reentrant tachycardia after atropine: Report of five cases☆

After intravenous administration of 0.5 mg of atropine sustained atrioventricular (A-V) nodal reentrant tachycardia could be produced in five patients who had no prior historical or electrocardiographic evidence of supraventricular tachycardia. During the control period single atrial echo beats could be demonstrated in four of the five patients, but no instance of sustained tachycardia occurred. Atropine, known to enhance A-V nodal conduction, allowed achievement of longer A-H intervals (Case 1) and provided the necessary balance of conduction and refractoriness within the A-V nodal reentrant pathways (Cases 1 to 5) to sustain A-V nodal reentry in these patients.

Time dependent changes in the functional properties of the atrioventricular conduction system in man.

Time dependent changes in the electrophysiological properties of the atrioventricular conducting system (AVCS) were determined at two or more cycle lengths (CL) in 22 patients using bundle of His (H) electrograms, incremental atrial pacing and atrial extrastimulus method. The atrioventricular (A-H interval) and intraventricular (H-V interval) conduction times and refractory periods (RP) of the atrium, the A-V node (AVN) and His-Purkinje system (HPS) were measured during the control period, and repeat measurements were made after a 30 minute interval in eight patients (group A), after a 60 minute interval in nine (group B) and after 30 and 60 minute intervals in five (group C). No statistically significant changes from control values were seen after 30 and 60 minute intervals in any group in sinus rate, A-V nodal conduction time and the onset of A-V nodal Wenckebach block. H-V intervals were identical to the control values in all groups. Insignificant changes from control values occurred in RP of the atrium and HPS. Only the functional refractory period (FRP) of the AVN showed a statistically significant decrease from control values in groups B and C. This decrease could be explained by changes in autonomic tone. These observations in general confirm the reproducibility of electrophysiological properties of AVCS within one hour, and further support the validity of the techniques utilized in this and previously reported studies in the evaluation of cardioactive drugs.

The Gap Phenomena During Retrograde Conduction in Man

Ventricular refractory period studies were performed in 12 consecutive and unselected patients using the ventricular extrastimulus method (V2) at basic ventricular cycle lengths (V1 V1). In six of 12 patients two types of retrograde gaps occurred. At relatively long V1 V2 intervals, ventriculo-atrial (V-A) conduction failed and then resumed at shorter V1 V2 intervals. The initial sites of retrograde block were the A-V node in two patients and the His-Purkinje system in four patients. In both groups, resumption of V-A conduction at shorter V1 V2 intervals occurred because of retrograde delay within the His-Purkinje system. Retrograde gaps differ from previously described antegrade gaps in A-V conduction: The site of initial block in A-V gaps is the His-Purkinje system and resumption of A-V conduction occurs at shorter A1 A2 intervals because of proximal delay in the A-V node (type I) or delay in the proximal His-Purkinje system (type II). In V-A gaps the site of initial block may be either the A-V node or the His-Purkinje system and resumption of V-A conduction always occurs due to delay within the distal His-Purkinje system. A common feature of both A-V and V-A gaps is the fact that delay of the more premature impulses allows time for previously refractory areas to recover excitability and both can be functional in nature. Only one of the 12 patients had both A-V and V-A gaps in conduction. Retrograde gaps in V-A conduction are more commonly observed than A-V gaps.

Electrophysiologic effects of procainamide in subtherapeutic to therapeutic doses on human atrioventricular conduction system

The effects of single intravenous infusions of 50 to 400 mg of procainamide on the functional properties of the atrioventricular (A-V) conduction system were studied in 36 patients and correlated with plasma concentrations. A 50 mg dose of procainamide resulted in a plasma concentration of less than 1.0 mug/ml and produced no electrophysiologic changes. Doses of 100, 200, 300 and 400 mg resulted in progresively increasing plasma concentrations (1.2, 1.8, 3.5 and 4.2 mug/ml, respectively). The effects of procainamide on the sinus rate were variable and not dose-related. The effects of doses of up to 300 mg on A-V nodal conduction were variable and not dose-related. Only in a dose of 400 mg did procainamide prolong A-V nodal conduction in six of seven patients. Whereas 100 mg had no effect on His-Purkinje system conduction, doses of 200, 300 and 400 mg prolonged His-Purkinje system conduction time by 6, 8 and 9 msec, respectively. Dose-related increases in atrial refractoriness started with a dose of 200 mg and became statistically significant with doses of 300 and 400 mg. The effects of procainamide on A-V nodal functional refractoriness were variable and not dose-related, but in doses of 100 to 400 mg, procainamide produced significant and progressively dose-related increases in His-Purkinje system refractoriness. Suppression of some types of ventricular arrhythmia by small doses of this drug may be explained by changes in refractoriness of the His-Purkinje system produced by doses of procainamide as small as 100 mg.

Unmasking and Conversion of Gap Phenomenon in the Human Heart

Two types of gap phenomena (types I and II ) have been described in human hearts and their electrophysiologic bases have been delineated. In both types of gap phenomena relatively early premature atrial impulses are blocked within some portion of the His-Purkinje system (HPS). By increasing the prematurity of the atrial depolarization, conduction to the ventricles resumes due to delay of the premature impulse with the atrioventricular node (A-VN) (type I gap) or within the proximal HPS (type II gap). Gap phenomena are not observed when the refractory period of the A-VN exceeds that of the HPS. Since atropine decreases refractoriness of the A-V node, its effect on the gap phenomena was studied in nine subjects. After administration of atropine (0.2-0.5 mg i.v.) type I gap was demonstrated in six subjects and type II gap in three subjects. When atropine shortened the functional and effective refractory period (ERP) of the A-V node, premature atrial impulses arrived at the HPS during its ERP. By a similar mechanism, type I gap was converted into type II gap in three subjects following atropine administration. Decreasing the basic atrial drive rate converted type II gap into type I (two subjects) and ultimately abolished both types of gap phenomena in all subjects. These results suggest that the gap penomenon may be functional in nature and may be readily manifested or abolished by varying the refractoriness of the A-V node relative to that of the HPS.

Gap Phenomena: Antegrade and Retrograde

The phenomenon of ‘Gap in A-V Conduction’ was originally described by Moe and associates (559). During experiments designed to evaluate conduction characteristics with the canine heart, it was noted that premature atrial beats evoked progressively earlier in the cardiac cycle conducted to the ventricles with prolonged P-R intervals. With decreasing prematurity a zone within the cardiac cycle was reached where in premature atrial responses no longer conducted to the ventricles. However, as the atrial responses were made even more premature, conduction resumed. Within this context, the term ‘gap in A-V conduction’ as originally used, defined a zone within the cardiac cycle where in premature atrial impulses failed to evoke ventricular responses while atrial beats of greater and lesser prematurity did.

Evidence that AV nodal re-entrant tachycardia does not require participation of the entire AV node

Electrophysiologic studies in a case of A V nodal re‐entrant tachyca rdia showed thai a programmed alrial premature depolarization induced during the tachycardia did not change the tachycardia cycle but caused a delay in the following atrial echo. Analysis of such a phenomenon suggests that the atrial premature depolarization was conducted to the upper part of the AV node but not to the site of the re‐entry. Therefore, AV nodal re‐entry can persist without the participation of the upper part of the AV node. This case illustrates that the upper common pathway connecting the dual AV nodal pathways cranially is most likely located within the AV node and consists of A V nodal tissue.

Modification and abolition of re-entry within the His-Purkinje system in man by diphenylhydantoin.

The phenomenon of macrore-entry (Re) within the His-Purkinje system (HPS) was consistently observed in 10 of 19 patients during retrograde refractory period studies. Effects of intravenous infusion of diphenylhydantoin (DPH) on Re were studied in these 10 patients 10 minutes after completion of infusion (mean plasma level equal to 17.0 ug/ml). Diphenylhydantoin modified determinants of Re in seven patients (group I) and abolished Re in the remaining three patients (group II). In group I, DPH shortened the critical V, V2 from 310.0 ± 30.5 to 292.9 ± 25.6 msec (P < 0.025) and critical V2 H2 intervals for Re from 201.4 ± 18.4 to 185.0 ± 13.8 msec (P > 0.05). In group II, DPH abolished Re in two of three patients by precluding attainment of critical V2 H2 intervals whereas Re was abolished in the remaining one patient despite attainment of critical V2 H2 intervals (vs control). For both groups, DPH significantly shortened functional and effective refractory periods of the HPS (P < 0.001 and < 0.01, respectively) without significantly affecting the effective refractory period of the ventricular muscle. Diphenylhydantoin either completely abolished or significantly shortened the retrograde gap zones in the HPS. It is concluded that diphenylhydantoin significantly shortens His-Purkinje system refractoriness, abolishing Re in the patients with higher degree of improvement in refractoriness.