Sun H. Lau

Catheter Technique for Recording His Bundle Activity in Man

A technique for the routine recording of His bundle (H) activity in man using a bipolar or multipolar catheter is described. The recording catheter is inserted percutaneously, via the Seldinger method, into the right femoral vein and advanced fluoroscopically into the right atrium. Placement of the pre-formed curve at the catheter tip across the tricuspid valve in nine patients resulted in stable recordings of His bundle activity in successive cardiac cycles. Right atrial pacing resulted in progressive lengthening of the P-H interval with increasing frequency but the H to S-wave interval remained constant at all rates. Similar lengthening of the P-H interval was produced during atrial pacing when pressure was applied to the carotid sinus. The use of this recording technique in man will facilitate diagnostic interpretation of the electrocardiogram and can be used in various investigations of atrioventricular and intraventricular conduction in man.

A Study of Heart Block in Man Using His Bundle Recordings

The technique of recording His bundle electrograms in man by a tripolar electrode catheter was applied in a study of patients with first, second, and third-degree heart block. In all patients with first-degree heart block (congenital, acquired, or induced by atrial pacing), the delay in A-V conduction occurred proximal to the His bundle as evidenced by a prolonged P-H interval. The enhancement of A-V conduction (shortening the P-H interval) due to isoproterenol was qualitatively similar in the three forms of first-degree block. In cases of Wenckebach phenomenon the P-H interval progressively increased until a dropped beat occurred. The nonconducted P wave was not followed by a His deflection, indicating block proximal to the His bundle. Cases of 2:1 and 3:1 block occurring proximal to the His bundle were also studied. The usefulness of His-bundle recordings in the diagnosis of cases of complete and incomplete bilateral bundle-branch block is also demonstrated.

Study of atrioventricular conduction in man using electrode catheter recordings of His bundle activity.

The technique of recording electrograms of the His bundle, using a tripolar electrode catheter positioned across the tricuspid valve, was applied in a physiological study of atrioventricular conduction in man. Increasing the heart rate to 160 beats/min by right atrial pacing produced progressive prolongation of the P-H interval while the H-Q interval remained constant. At any given paced heart rate, digitalis caused a prolongation of the P-H interval. Isoproterenol and atropine markedly shortened the P-H interval at any given heart rate. Neither drug had any significant effect on the H-Q interval. Coupled premature atrial stimulation produced prolongation of the P-H interval alone when the resultant ventricular depolarization was normal, and prolongation of both the P-H and H-Q intervals when the resultant ventricular depolarization was aberrant.

The electrophysiology of propranolol in man

Abstract The effects of intravenous propranolol (0.1 mg. per kilogram) on the electrophysiologic properties of the A-V conducting system were studied in 16 patients using His-bundle electrograms and the extrastimulus method. The drug was infused at a rate of 1 mg. per minute without significant side effects. Sinus cycle length was slowed in 15 out of 16 patients (average, 128 msec.). AVN conduction time was increased in 13 out of 16 patients (average, 10 msec.) during sinus rhythm and in all patients during atrial pacing. AVN Wenckebach block occurred at slower paced rates in 14 patients. Corrected QT interval was shortened in 9 out of 16 patients (average, 24 msec.). The functional and effective refractory periods (ERP) of the AVN were prolonged in 14 out of 14 patients (average, 29 msec.) and 9 out of 9 patients (average, 24 msec.), respectively. No significant changes were seen in His-Purkinje system (HPS) conduction time, ERP of the atrium, relative refractory period or ERP of the HPS, or ERP of the ventricle in all patients in whom these variables could be muasured. Mean end-study blood level was 13.6 ng. per milliliter. Effects on the AVN explain the efficacy of propranolol in (1) controlling the ventricular rate in atrial fibrillation and flutter and (2) the treatment and prophylaxis of re-entrant supraventricular tachycardias. Its lack of effects on the HPS make its use relatively safe in patients with infra-His conduction disturbances.

Recording of Specialized Conducting Fibers (A-V Nodal, His Bundle, and Right Bundle Branch) in Man Using an Electrode Catheter Technic

Extracellular action potentials of the A-V node (N), His bundle (H), and right bundle branch (RB) were recorded in subjects with an electrode cardiac catheter which was fluoroscopically positioned across the tricuspid valve. The N potential is a slow diphasic wave occurring between the atrial electrogram (P) and the H potential. It is characterized by slurring or notching on the upstroke. The H potential, as previously described, is a biphasic or triphasic wave of 15 to 20-msec duration. The RB potential is a fast biphasic wave of 10 to 20-msec duration occurring between the H potential and the Q wave. During single atrial pacing and premature atrial stimulation, the A-V conduction delay could be localized to the N-H interval. Evidence suggests that during aberrant ventricular conduction of the right bundle-branch block type the impulse was blocked proximally in the right bundle. During concealed conduction the nonconducted impulse was completely blocked within the A-V node or the N-H interval.

Termination of atrial flutter by rapid electrical pacing of the atrium

Abstract A technic has been developed for converting atrial flutter to normal sinus rhythm utilizing an intra-atrial electrode catheter and rapid impulses 10 milliamperes in magnitude delivered directly to the atrial wall. Atrial flutter has been converted to normal sinus rhythm in 3 patients after premedication with small doses of quinidine or procainamide. No anesthesia is required, the ventricle is at no time depolarized by the shock, and there is no ventricular irritability produced.

The effect of lidocaine on atrioventricular and intraventricular conduction in man.

Abstract Atrioventricular and intraventricular conduction were studied in 10 patients with arrhythmias before and after rapid administration of lidocaine (1 to 2 mg/kg by direct intravenous injection). Standard electrocardiographic lead II and catheter recordings of His bundle electrograms (H) were obtained. Recordings were made at varied heart rates, utilizing atrial pacing. P wave to H (P-H) interval was used as a measure of atrioventricular conduction. H to onset of the Q wave (H-Q), and H to the terminal deflection of the QRS complex (H-S) were used as measures of intraventricular conduction. After administration of lidocaine, P-H intervals were essentially unchanged in 4 patients, slightly decreased in 4 and slightly increased in 2 patients. H-Q intervals remained constant in all patients and at all rates both before and after lidocaine. H-S intervals were unchanged in 6 patients and increased in 4 patients by 8 to 18 msec (4 to 18 percent of total H-S interval). Thus, lidocaine in therapeutic doses had a minimal effect on atrioventricular and intraventricular conduction. This is in contrast to quinidine and procainamide, which may prolong atrioventricular and intraventricular conduction.

Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex☆

Eighteen subjects with a short P-R interval (<0.12 second) and normal QRS complex were studied by means of His bundle recordings and programmed atrial premature depolarizations. Eight subjects had a history of supraventricular tachycardia. During sinus rhythm, the A-H interval was less than or at the lower limits of normal values (45 to 80 msec), and the H-V interval was normal (30 to 50 msec). Atrial pacing at rates of up to 160/min produced 3 types of responses. Thirteen subjects showed a progressive increase in A-H interval similar to that of normal subjects but to a lesser degree. Three subjects showed an initial increase at low pacing rates, followed by a plateau response and further increase at higher rates. Two subjects showed no significant increase in the A-H interval. In 6 of 8 subjects with supraventricular tachycardia, atrial premature depolarizations produced atrial echo beats and sustained supraventricular tachycardia in 4, indicating atrioventricular (A-V) nodal reentry as the mechanism for the supraventricular tachycardia. In 10 subjects, refractory periods of the various components of the A-V conducting system were found to be similar to those of subjects with a normal P-R interval. The data suggest the following possible explanations for the short P-R interval: (1) total or partial bypass of the A-V node; (2) an anatomically small A-V node; (3) a short or rapidly conducting intranodal pathway; or (4) isorhythmic A-V dissociation.

Atrial Fibrillation Produced by Atrial Stimulation

Twenty-six episodes of atrial fibrillation and flutter-fibrillation, each lasting less than 23 sec, were recorded in three normal subjects during atrial pacing studies. The cause of these atrial arrhythmias was determined to be the result of stimulation within the atrial vulnerable period.

Electrophysiologic properties of procainamide in man

Abstract The electrophysiologic properties of procainamide were studied in 16 patients and correlated with plasma levels. Procainamide caused a minimal prolongation of atrioventricular (A-V) nodal conduction in 11 of 16 patients during sinus rhythm, but His-Purkinje conduction time was significantly prolonged in 15 of 16 patients. The effective refractory period of the atrium was prolonged by procainamide in 14 of 16 patients. The effective refractory period of the A-V node decreased in 8 of 9 patients. This may have been due to (1) anticholinergic properties of procainamide, (2) production of an A-V nodal “gap” by procainamide, or (3) an apparent A-V nodal block that actually represented decremental conduction in the His bundle; procainamide then caused delay in the A-V node allowing improved intra-His conduction and ventricular depolarization. The relative refractory period of the His-Purkinje system was prolonged in 10 of 11 patients. The effective refractory period was prolonged in one patient, unchanged in a second and apparently shortened in a third. In this third patient, procainamide produced a marked delay in proximal His-Purkinje conduction allowing a distal area of refractoriness to recover, thus causing apparent shortening of the effective refractory period. Plasma levels averaged 7.1 mg/ liter at the end of the study; no toxicity was noted.