Characteristics and coexistence of two forms of ventricular echo phenomena.

During the scanning of paced basic ventricular cycle lengths (V1V1) with extrastimulus method (V2) two forms of ventricular echo phenomena (Ve) were recognized. The Ve resulting from A-V nodal re-entry (VeAVN) occurred in 12 of 45 patients, from re-entry in the His-Purkinje system (Ve-HPS) in 20 of 45 patients, and simultaneous dual re-entry (Ve-AVN and Ve-HPS) occurred in five of 45 patients. The Ve-AVN (1) appeared at longer V1V2 intervals, (2) was dependent on retrograde A-V nodal conduction delay, (3) had normal QRS complexes and H-V intervals, and (4) did not occur when V2 blocked in the A-V node. (5) Ve-AVN had aberrant QRS complexes when preceded by Ve-HPS. The Ve-HPS (1) appeared at shorter V1V2 intervals, (2) was dependent upon retrograde conduction delay in the HPS, (3) its QRS morphology and axis orientation resembled V2, i.e., left bundle branch block pattern, when right ventricular apex was the site of stimulation, (4) persisted when V2 blocked in the A-V node and was abolished when V2 blocked below the bundle of His, and (5) rarely occurred in patients with pre-existing right bundle branch block. It is concluded that (1) at least two forms of Ve can result from induced premature ventricular beats, (2) Ve-HPS is more common than Ve-AVN in the presence of normal QRS complexes, and (3) coexistence of Ve-AVN and Ve-HPS can give rise to complex ECG pattern mimicking multiple multifocal premature ventricular beats.

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.

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.

A comparative analysis of antegrade and retrograde conduction patterns in man.

Patterns of antegrade and retrograde conduction and refractory periods were studied using His bundle electrogram recordings, incremental atrial and ventricular pacing and the extrastimulus technique. In 36/50 patients antegrade conduction was "better" than retrograde conduction (group I), as evidenced by a) onset of retrograde atrioventricular (A-V) nodal Wenckebach phenomenon at a slower rate compared to the antegrade counterpart (25 patients: group IA) or b) no ventriculo-atrial conduction at all ventricular paced rates (11 pts: group IB). The site of retrograde block in group IB patients was the A-V node. In eight patients (group II), antegrade and retrograde conduction appeared to be equal up to maximum paced rates of 160 beats/min. In six patients (group III) retrograde conduction was "better" than antegrade conduction, as indicated by onset of antegrade A-V nodal Wenckebach periods at slower rates than retrograde Wenckebach periods. During antegrade refractory period studies the area of maximum refractoriness was the A-V node in 19/40 patients, the His-Purkinje system (HPS) 6/40, and the atrial muscle in 15/40. During retrograde refractory period studies the A-V node was the area of maximum refractoriness in 12/36 pts (4/40 patients had A-V dissociation during ventricular pacing), the HPS in 12/36, and the ventricular muscle in 10/36. In 2/36 patients the site of maximum refractoriness retrogradely could not be determined: The area of maximum refractoriness during both antegrade and retrograde refractory period studies was the same in 11 patients (A-V node in seve and HPS in four), was different (i.e., A-V node or HPS) in 18 patients, and was the artrial or ventricular muscle in six patients. In five patients, including four patients in whom V-A conduction failed to occur, the above comparisons were not made. It is concluded that 1) antegrade conduction is better than retrograde conduction in most patients; 2) it is not always possible to predict area of maximum refractoriness during premature stimulation (both atrium and ventricle) from observations made during incremental pacing; 3) it is equally difficult to extrapolate patterns of retrograde conduction and refractory periods from results of antegrade conduction and refractory period studies.

Sinus node re-entrant tachycardia in man.

Sinus node re-entry (SNR) usually appears as a single beat. Tachycardias (SNRT) consistent with sustained SNR were seen in six patients and were initiated by premature stimulation of the high right atrium (six patients) and coronary sinus (four patients), and after continuous pacing from the high right atrium (four patients) or right ventricle (one patient) at rates of 130 to 200 per minute. During SNRT: (1) atrial beats exhibited a high-to-low atrial activation sequence, (2) the P-waves were similar in morphology to P-waves during sinus rhythm, and (3) re-entry in the A-V node or at the site of stimulation could be excluded. The cycle length of SNRT ranged from 625 to 320 msec. and SNRT either terminated spontaneously (six patients) or after premature atrial capture and/or vagal maneuvers (two patients). The electrophysiologic characteristics of SNRT and differentiation of SNRT from A-V nodal re-entry are discussed.