Demonstration of a Posterior Atrial Input to the Atrioventricular Node During Sustained Anterograde Slow Pathway Conduction

AbstractObjectives. This study sought to demonstrate electrophysiologic evidence for the existence of different anatomic atrial input sites of fast and slow conduction pathways in patients with dual atrioventricular (AV) node physiology.Background. Although a separate posterior exit site exists for a retrograde slow AV node pathway, it remains unresolved whether a separate atrial input site into the AV node actually exists in patients with dual anterograde AV node pathway physiology.Methods. In 10 patients with dual AV node pathway physiology, atrial pacing at three chosen drive cycle lengths (DCL1, DCL2 and DCL3) was performed at an anterior site (A) just above the His bundle recording site and at a posterior atrial site (P) just below the coronary sinus ostium. DCL3 was chosen as the one cycle length that resulted in a long AH interval consistent with slow pathway conduction. The stimulus to His bundle conduction times (SH) at both sites (SHPand SHA, respectively) and their differences (ΔSH = SHP− SHA) at each of the three drive cycle lengths were analyzed.Results. The mean ± SD ΔSH values for DCL1 and DCL2 measured 9 ± 16 and 8 ± 18 ms, respectively, and the mean ΔSH value at DCL3 measured −34 ± 24 ms, which was significantly different from the mean ΔSH values at DCL1 and DCL2 (both p < 0.05).Conclusions. The significant change in the ΔSH (SHP− SHA) value during slow pathway conduction could be accounted for by a corresponding shift of anterograde input from an anterior to a posterior entry site to the AV node. These findings support the notion that a separate anterograde entry site of the slow pathway does exist in patients with dual AV node pathway physiology

Clinical significance of ventricular fibrillation-flutter induced by ventricular programmed stimulation

Two hundred twenty-four patients underwent ventricular programmed stimulation (VPS) without prior documentation of the clinical occurrence of sustained ventricular tachycardia (VT) or ventricular fibrillation-flutter (VF). Indications for VPS were: palpitations or nonsustained VT during ambulatory monitoring (85 patients), syncope or presyncope (137 patients), and a family history of sudden death (two patients). Sustained VF requiring transthoracic defibrillation was initiated by VPS in 18 patients (8.0%). Four patients were treated for inducible VF with antiarrhythmic agents directed by electropharmacologic testing; five patients were treated empirically; nine patients received no therapy. No patient has had a cardiac arrest or sudden death during a follow-up period of 25.2 +/- 13.8 months (mean +/- standard deviation). VF was initiated by two ventricular extrastimuli in three patients and by three extrastimuli in 15 patients. The incidence of VF was similar in patients with and without previous symptoms (8.8% vs 6.9%) or heart disease (7.1% vs 9.6%). It was significantly higher when VPS at three ventricular sites with a current of 5 mA (pulse width 2 msec) was compared to programmed stimulation at two ventricular sites with a current twice diastolic threshold (pulse width 2 msec) (15.2% vs 3.0%, p &lt; 0.05). VF initiated by VPS in patients without prior VT or VF appears to be a nonspecific finding. Antiarrhythmic therapy for VF may not be necessary in these patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25695/1/0000249.pd

A-V Nodal Reentrant Tachycardia vs Accelerated A-V Junctional Rhythm in Acute Inferior Myocardial Infarction

This report describes initiation of A-V nodal reentrant tachycardia in a patient with acute inferior myocardial infarction. The onset of tachycardia was preceded by an abortive A-V nodal Wenckebach periodicity. A-V nodal ischemia with or without vagotonia was implicated as the cause of induction of critical functional dissociation between the two A-V nodal conduction pathways. Since the tachycardia manifested its rate between 95–110 beats/min during the evolutionary phase of acute inferior myocardial infarction, it simulated, electrocardiographically, an accelerated A-V junctional rhythm. Analysis of the onset of tachycardia was of diagnostic importance

Intraventricular Dissociation due to Complete Intraventricular Block

Intraventricular dissociation due to intraventricular block occurred in a patient with cardiac arrest due to massive cerebral hemorrhage. The electrocardiogram showed complete atrioventricular block with three different types of accelerated ventricular rhythm. The ectopic beats did not interfere with each other because of the existence of an area of complete block surrounding the areas in which impulse formation occurred. Hence, the corresponding QRS complexes did not result from depolarization of all the ventricular muscle mass but only of certain regions. The latter were large enough to produce ventricular complexes of enough size to be recorded at the body surface. This phenomenon is the clinical counterpart of the multiple isolated focal contractions which may be seen directly in the ventricles of dying hearts

Ventricular Tachycardia and Ventricular Fibrillation in Patients with Short P‐R Intervals and Narrow QRS Complexes

Eleven patients with short P‐R Intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A‐H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P‐R and A‐H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an expression of the “enhanced A‐V conduction” that had been manifested in sinus beats by short P‐R and A‐H intervals. In clinical settings and physiological conditions proven to be hemodynamicaliy unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R‐on‐T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studie

Body Surface and Intracardiac Recordings in a Patient with Wolff-Parkinson-White Syndrome (type A) with Complete Infra-His Bundle Block

Electrocardiograms, vectorcardiograms and His bundle electrograms were recorded in a patient with Wolff-Parkinson-White syndrome (type A) who developed complete infra-Hisian block and advanced A-V block in the Kent bundle. The atrial impulses reaching the ventricles exclusively through the Kent bundle produced QRS complexes and vector loops showing diffuse (leftward initial and rightward pre-terminal) delays and slurrings. These abnormalities were not due to Wolff-Parkinson-White type A coexisting with right bundle branch block, but reflected the activation sequence characteristic of arrival of excitation; spontaneous impulse formation; or electrical stimulation, at the postero-superior wall of the left ventricle. Intracardiac recordings were a complement to body surface recordings in the study of Wolff-Parkinson-White syndrome complicated by A-V conduction disturbances

His bundle electrocardiography in digitalis-induced “atrioventricular junctional” Wenckebach periods with irregular H-H intervals

His bundle electrograms were recorded during catheter insertion for prophylactic demand pacing in two patients with accelerated or nonaccelerated “atrioventricular (A-V) junctional” rhythms associated with A-V junctional Wenckebach periods. This appears to be the first published report of so-called A-V junctional Wenckebach periods in which the characteristic irregularities of the H-H intervals were recorded. Patient 1 had an additional area of “complete” anterograde A-V nodal (A-H) block. In Patient 2 the rate of impulse formation was consistent with nonparoxysmal A-V junctional tachycardia. The His bundle recordings were obtained in patients with digitalis toxicity and should be interpreted in that context. The integration of clinical and intracardiac findings with extrapolations from microelectrode and pharmacologic studies and with deductions from the clinical electrocardiograms suggests that the conduction disturbances probably occurred within the A-V node itself (in its AN region). This hypothesis implies that automaticity also originated in the A-V node because the site of impulse formation must have been proximal to the site of the Wenckebach periods. However, conclusive proof of these postulates will require further studies with refined techniques

Complete abolition of the reentrant supraventricular tachycardia zone using a new modality of cardiac pacing with simultaneous atrioventricular stimulation

In an attempt to prevent recurrent reentrant supraventricular tachycardia, an experimentally designed new pacemaker has been developed. The pacemaker, when connected to both atrial and ventricular electrodes, is capable of sensing either an atrial or ventricular signal and, in turn, triggers simultaneous atrioventricular (A-V) stimulation. Efficacy of this pacemaker was tested in four patients with recurrent paroxysmal A-V nodal reentrant tachycardia during electrpphysiologic studies. After connection of the electrodes to the new pacemaker, all atrial or ventricular premature stimuli elicited simultaneous A-V stimulation with resultant impulse collision in the A-V junction. Consequently, the reentrant tachycardia zone was completely abolished in all patients. This study has thus demonstrated the clinical feasibility of simultaneous A-V pacing to abolish the supraventricular tachycardia zone in man