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

Electrophysiologic studies in a case of AV nodal re-entrant tachycardia showed that a programmed atrial 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 AV nodal tissue.

Indications for His bundle recordings.

While the extrapolation of data derived from His bundle studies performed over the past 10 years has lessened the need to apply the technique for diagnostic clinical purposes, His bundle recordings remain a useful clinical research tool for better understanding of cardiac electrophysiology. Some of the areas of continued research to which the technique will most certainly be applied are: (1) study of reentrant phenomena involving the atrial, junctional, and ventricular regions of the heart, (2) investigation of the mechanisms of action of new and old drugs on the heart, (3) evaluation of effectiveness of drug treatment in resistant cardiac arrhythmias, and (4) understanding of complex arrhythmias.

Congenital pulmonary artery branch stenosis: association with renal artery stenosis.

A patient had multiple bilateral stenoses of the pulmonary artery and its branches with systemic hypertension associated with mild stenoses of the renal arteries. Cardiac catheterization and angiocardiography are important in the evaluation of the degree of stenoses and pulmonary hypertension. This case suggests that in a child or young person with hypertension and a loud precordial murmur, lesions other than coarctation of the aorta may be present. Unexplained systemic hypertension requires further investigative workup which is essential for proper treatment and long-term management of these patients.

Effects of phenytoin on refractoriness and conduction in the human heart.

Using His bundle electrograms and the atrial (A2) and ventricular extrastimulus (V2) techniques, anterograde and retrograde refractory period studies were performed (in 9 and 12 patients, respectively) before and 10 min after intravenous infusion of phenytoin (DPH; mean plasma level, 17.3 micrograms/ml). DPH had no effect on the duration of the QRS complex or the H-V interval of the sinus beats; it had variable but insignificant effects on the sinus rates and the atrial, A-V nodal, and ventricular muscle refractoriness. With the use of the A2 technique, the effective refractory period (ERP) of the His-Purkinje system (HPS) could not be determined in any patient; the relative refractory period (RRP) of the HPS could be determined in 2/9 patients and shortened in both patients after DPH. With the use of the V2 technique, retrograde functional refractory period (FRP) and RRP of the HPS could be determined in all 12 patients and the retrograde ERP of the HPS in 7/12; DPH significantly shortened all these parameters (p less than 0.001, less than 0.001, and less than 0.005, respectively). Functional refractory period of the ventriculo-atrial conduction system (VACS) could be determined in 11/12 patients during control studies (the remaining one patient had complete ventriculo-atrial block). DPH significantly shortened the FRP of the VACS in those (4) patients (Group I) in whom it was determined primarily by the HPS (p less than 0.025), and had variable but insignificant effects on FRP of the VACS in the other seven patients (Group II) in whom it was determined almost exclusively by the A-V node. DPH significantly decreased the retrograde HPS conduction times of the premature impulses (V2H2 intervals) for the same coupling (V1V2) intervals (p less than 0.001). It is concluded that, in the human heart, DPH exerts its most important effects on the HPS where it significantly decreases refractoriness and enhances conduction of the premature impulses. This study also demonstrates that the V2 technique is far superior to the A2 technique for evaluating the effects of drugs on refractoriness and conduction in the HPS.

Multiple mechanisms of tachycardias in a patient with the Wolff-Parkinson-White syndrome.

In a patient with the Wolff-Parkinson-White Syndrome we observed atrial fibrillation and three distinct paroxysmal re-entrant tachycardias. Intracardiac electrograms obtained during the tachycardias showed the mechanisms to be A-V nodal, accessory pathway and sinus node re-entry. When P wave morphology, R-P relationship and QRS configuration are considered, it is illustrated how these four tachyarrhythmias may be successfully diagnosed on the surface electrocardiogram. The therapeutic implications of multiple arrhythmias with different mechanisms in the Wolff-Parkinson-White Syndrome are discussed.

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 microgram/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 V1 V2 from 310.0 +/- 30.5 to 292.9 +/- 25.6 msec (P less than 0.025) and critical V2 H2 intervals for Re from 201.4 +/- 18.4 to 185.0 +/- 13.8 msec (P greater than 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 less than 0.001 and less than 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.

The 1,2,3,4 phenomenon. Atrioventricular nodal gap in the dog.

This study confirms the facility with which the so-called 1,2,3,4 phenomenon can be reproduced in intact dog hearts. When a series of three atrial premature beats (A2, A3, A4) were delivered following a constant A1-A1 drive, we demonstrated a narrow zone of A1-A3 and A1-A4 intervals in which A4 conducted to the ventricles in the presence of A3 but not in its absence. We used His bundle and multiple atrial electrograms to produce the phenomenon in nine of 16 dogs. Facilitation of conduction of A4 (1) occurred above the His bundle, (2) occurred within narrow ranges of A1-A3 and A1-A4 intervals, (3) required penetration of A3 into the atrioventricular (AV) node, (4) required critically long A2-H2 intervals, (5) always was associated with prolonged A4-H4 intervals, and (6) was limited by atrial refractoriness. An apparent or pseudo-1,2,3,4 phenomenon demostrated in five of 16 dogs occurred with (1) latency between S4 and A4, (2) a sinus nodal or atrial reentry beat, or (3) an atrial escape beat. In the absence of A3, A4 could be made to conduct by preexciting the ventricle in advance of V2. We found no evidence for dual AV nodal pathways. Our results suggest that the underlying mechanism for the 1,2,3,4 phenomenon is analogous to the phenomenon of the gap in AV conduction.

Abnormal Q waves in Wolff-Parkinson-White syndrome. Incidence and clinical significance.

Between January 1970 and January 1975 the diagnosis of Wolff-Parkinson-White syndrome was entertained in 44 patients. Thirty-one (70%) of these patients had negative sigma-deflections (Q waves) on one or more electrocardiographic leads, thereby simulating a pattern of myocardial infarction (Mi). Fifteen patients (34%) were initially referred with an erroneous diagnosis of Mi based on the presence of Q waves. In nine of these 15 patients, the referring diagnosis was Mi plus ventricular preexcitation; in six, the diagnosis of ventricular preexcitation was overlooked entirely. The incidence of misdiagnosis (34%) was exactly the same as that reportly by Wolff and White approximately 30 years ago. Erroneous diagnosis of Mi can be virtually eliminated by normalizing the QRS complex by premature stimulation of the atrium during the effective refractory period of the accessory pathway.

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.

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.

Electrophysiologic effects of tolamolol on atrioventricular conduction in man.

The electrophysiologic effects of tolamolol (UK-6558-01), a beta-adrenergic blocking agent, were studied in 13 patients by means of intracardiac electrograms and the extrastimulus method. Tolamolol (4 to 30 mg. intravenously) resulted in : (1) prolongation of sinus cycle length (SCL) in all patients (p less than 0.01); (2) prolongation of sinus escape time (SET) in 11 of 13 patients (p less than 0.001); (3) prolongation of A-V nodal conduction time during sinus rhythm in 1i of 13 patients (p less than 0.001); (4) onset of A-V nodal Wenckebach block at longer paced cycle lengths in 10 of 11 patients (p less than 0.001); (5) prolongation of the functional refractory period (FRP) of the A-V node in 11 of 11 patients (p less than 0.001); and (6) prolongation of the effective refractory period (ERP) of the A-V node in 10 of 10 patients (P less than 0.001). Tolamolol had no effect on His-Purkinje system (HPS) conduction time in any patient, including 3 patients with abnormal H-V intervals. Because of the marked increase in A-V nodal conduction time encountered by premature atrial depolarizations, the relative and effective refractory periods of the HPS could not be determined in any patient after tolamolol. Atropine (0.5 or 1.0 mg. intravenously) significantly reversed the effects of tolamolol on: sinus cycle length (4 of 5 patients); sinus escape time (3 of 3 patients); A-V nodal conduction time (4 of 5 patients); and A-V nodal refractioriness (5 of 5 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.

Echocardiographic manifestation of "false" mitral stenosis that was.

An unusual normal posterior direction of motion of the posterior mitral valve leaflet echo during diastole was detected in a patient whose clinical and hemodynamic data confirmed the presence of significant rheumatic mitral stenosis after other conditions causing echocardiographic pattern of "false" mitral stenosis were ruled out. The finding of normal direction of motion of the posterior mitral valve leaflet when associated with abnormal EF slope of the anterior mitral valve leaflet does not rule out the existence of significant mitral stenosis.

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.