Bundle Electrogram Research Articles

Coronary Sinus Activation Pattern in Patients with Atrioventricular Nodal Reentrant Tachycardia

Patterns of left atrial (far‐field signals) or coronary sinus (CS) muscle (near‐field) have been defined in CS recordings. The purpose of this study was to define the activation patterns from the coronary sinus in patients with anterior and posterior type of atrioventricular nodal reentrant tachycardia (AVNRT) circuits.Methods and Results: This retrospective study involved a total of 149 patients with 155 episodes of AVNRT which were divided into 3 patterns. In the anterior pattern (123 tachycardias), the atrial deflection from the His bundle electrogram preceded that from the proximal CS electrogram. In the posterior pattern (23 tachycardias), the proximal CS electrogram (CSp) was recorded earlier than the His bundle atrial electrogram. In the left atrial pattern (9 tachycardias), activation of distal CS sites preceded both proximal CS and atrial activation from the His bundle electrogram. A decapolar catheter with a 5‐mm interelectrode distance was used for CS recording. The CS electrograms were analyzed to determine the total signal duration as well as the duration of the initial component. An initial slow wave was defined as a duration exceeding 10 ms. 1) The duration of the initial component in patients with the anterior pattern was longer than in those with the posterior pattern in CSp (7.3 ± 3.1 ms vs. 4.5 ± 2.0 ms), CS7‐8 (7.4 ± 2.9 ms vs. 3.8 ± 1.5 ms), CS5‐6 (7.3 ms ± 3.3 ms vs. 4.4 ms ± 2.5 ms) and CS3‐4 (6.7 ms ± 2.4 ms vs. 4.5 ms ± 2.0 ms) (p < 0.01). 2) Similarly the total electrogram duration in the CS was longer in patients with an anterior compared to a posterior pattern in CSp (38.3 ms ± 10.1 ms vs. 26.8 ± 6.1 ms), CS7‐8 (31.8 ms ±6.6 ms vs. 27.2 ms ± 6.0 ms), CS5‐6 (31.3 ms ± 6.8 ms vs. 26.5 ms ± 4.9 ms), and CS3‐4 (30.0 ms ± 6.3 ms vs. 25.0 ms ± 5.1 ms) (p < 0.01). 3) The percentage of tachycardias showing an initial slow wave followed by rapid activation was higher for anterior pattern patients compared with posterior pattern patients in CSp (62% vs. 13%), CS7‐8 (79% vs. 4%), CS5‐6 (72% vs. 4%), CS3‐4 (54% vs. 9%) and distal CS (47% vs. 0%) (p < 0.01).Conclusions: The pattern of an initial slow wave followed by a rapid wave in the CS was characteristic of an anterior AVNRT circuit and is explained by the initial involvement of far field left atrial components. In contrast, the predominant early rapid waves in the posterior AVNRT circuit are compatible with early CS activation from the right atrium.

Supraventricular Tachycardia Originating From the Posterior Atrioventricular Node in the Univentricular Heart With Single Atrium

Supraventricular tachycardia (SVT) was observed in a 13-year-old male patient with complex clinical features that included univentricular heart with single atrium, pulmonary atresia, and polysplenia syndrome. During electrophysiologic study, atrial burst stimuli reproducibly induced and terminated the SVT, while the occurrence of ventriculoatrial block did not interrupt the SVT. His bundle electrograms (HBEs) were recognized both in the anterior and posterior regions on the common atrioventricular (AV) valve annulus. The posterior His bundle activation was progressively delayed along with the shortening of atrial pacing cycle length until it finally lagged behind local ventricular activation. Thus, antegrade AV conduction was solely via the anterior AV node. In contrast, during the SVT, the earliest activation was observed in the posterior HBE. These observations suggested that the posterior AV node serves as an origin of the SVT and that two AV nodes were linked together possibly through a sling at the infra-Hisian level. Radiofrequency catheter ablation applied to the posterior HBE eliminated the SVT.

Coronary Sinus Activation Pattern in Patients with Atrioventricular Nodal Reentrant Tachycardia

Patterns of left atrial (far-field signals) or coronary sinus (CS) muscle (near-field) have been defined in CS recordings. The purpose of this study was to define the activation patterns from the coronary sinus in patients with anterior and posterior type of atrioventricular nodal reentrant tachycardia (AVNRT) circuits. Methods and Results: This retrospective study involved a total of 149 patients with 155 episodes of AVNRT which were divided into 3 patterns. In the anterior pattern (123 tachycardias), the atrial deflection from the His bundle electrogram preceded that from the proximal CS electrogram. In the posterior pattern (23 tachycardias), the proximal CS electrogram (CSp) was recorded earlier than the His bundle atrial electrogram. In the left atrial pattern (9 tachycardias), activation of distal CS sites preceded both proximal CS and atrial activation from the His bundle electrogram. A decapolar catheter with a 5-mm interelectrode distance was used for CS recording. The CS electrograms were analyzed to determine the total signal duration as well as the duration of the initial component. An initial slow wave was defined as a duration exceeding 10 ms. 1) The duration of the initial component in patients with the anterior pattern was longer than in those with the posterior pattern in CSp (7.3 ± 3.1 ms vs. 4.5 ± 2.0 ms), CS7-8 (7.4 ± 2.9 ms vs. 3.8 ± 1.5 ms), CS5-6 (7.3 ms ± 3.3 ms vs. 4.4 ms ± 2.5 ms) and CS3-4 (6.7 ms ± 2.4 ms vs. 4.5 ms ± 2.0 ms) (p < 0.01). 2) Similarly the total electrogram duration in the CS was longer in patients with an anterior compared to a posterior pattern in CSp (38.3 ms ± 10.1 ms vs. 26.8 ± 6.1 ms), CS7-8 (31.8 ms ±6.6 ms vs. 27.2 ms ± 6.0 ms), CS5-6 (31.3 ms ± 6.8 ms vs. 26.5 ms ± 4.9 ms), and CS3-4 (30.0 ms ± 6.3 ms vs. 25.0 ms ± 5.1 ms) (p < 0.01). 3) The percentage of tachycardias showing an initial slow wave followed by rapid activation was higher for anterior pattern patients compared with posterior pattern patients in CSp (62% vs. 13%), CS7-8 (79% vs. 4%), CS5-6 (72% vs. 4%), CS3-4 (54% vs. 9%) and distal CS (47% vs. 0%) (p < 0.01). Conclusions: The pattern of an initial slow wave followed by a rapid wave in the CS was characteristic of an anterior AVNRT circuit and is explained by the initial involvement of far field left atrial components. In contrast, the predominant early rapid waves in the posterior AVNRT circuit are compatible with early CS activation from the right atrium.

Endocardial Electrograms From the Right Ventricular Outflow Tract After Induced Ventricular Fibrillation in Patients With Brugada Syndrome

The pathogenesis of Brugada syndrome (BS) is reported to be phase 2 reentry resulting from shortening of the action potential duration at the epicardial site of the right ventricular outflow tract (RVOT). However, several reports have shown a high incidence of ventricular late potentials (LPs) and a high rate of induction of ventricular fibrillation (VF) by programmed ventricular stimulation (PVS) among patients with BS. The aim of this study was to investigate the role of slow conduction for the initiation of VF by PVS in these patients. Endocardial mapping of the RVOT was conducted in 17 patients in whom VF was induced by PVS from the RV apex or RVOT; 11 patients had a positive LP. In 10 patients, RV mapping showed that low-amplitude fragmented and delayed potentials (DPs) were recorded at the RVOT below the pulmonary valve (PV) or between the PV and His bundle electrogram recording site. Electrograms recorded after PVS showed a high incidence of fractionated and disorganized DPs that lead to VF. Slow conduction at the RVOT may contribute to the induction of VF by PVS. However, the role of slow conduction in spontaneous VF remains controversial.

Radiofrequency catheter ablation of an orthodromic tachycardia in a patient with single ventricle

Radiofrequency catheter ablation of a recurrent orthodromic tachycardia was performed in a 10-year-old child with single ventricle and bidirectional Glenn procedure before a Fontan operation. Identification of a His bundle electrogram was achieved at the postero-inferior atrioventricular (AV) groove by the inferior vena cava route, and electrophysiological demonstration of a concealed accessory pathway-mediated tachycardia was possible when a ventricular extrastimuli given during the His bundle refractoriness showed advancement of the atrium. A single energy application during tachycardia in the right antero-superior region of the AV groove resulted in the definitive interruption of the accessory pathway.

Cardiac-Directed Expression of Adenylyl Cyclase VI Facilitates Atrioventricular Nodal Conduction

The purpose of this study was to test the hypothesis that cardiac-directed expression of adenylyl cyclase VI (AC(VI)) facilitates atrioventricular (AV) nodal conduction. Cardiac-directed expression of AC(VI), unlike other strategies to increase cyclic adenosine monophosphate generation, reduces mortality in murine cardiomyopathy. Recent reports suggest that AC(VI) expression may also protect against lethal bradycardia. We performed immunofluorescence staining for AC(VI) in the AV node of transgenic mice. We then performed electrophysiologic studies (EPSs) using a 1.7-F octapolar catheter at the AV junction in 11 transgenic AC(VI) mice and 14 control mice. Immunofluorescence staining revealed increased AC(VI) expression in the AV node of transgenic mice versus controls. During EPS, AV intervals approximated PR intervals (R2 = 0.99) and related linearly to atrial-to-His intervals (R2 = 0.98; both p < 0.0001). Thus, we studied AV intervals to avoid electrocardiogram pacing artifacts and inconsistent inscription of His bundle electrograms. At baseline, AC(VI) mice had shorter AV intervals (47 +/- 9 ms) than controls (57 +/- 11 ms; p = 0.02), despite similar sinus rates. In pacing, AV intervals were shorter in AC(VI) mice than controls for a wide cycle-length range (p < 0.01). The AC(VI) mice also had shorter AV Wenckebach cycle lengths (AC(VI): 114 +/- 12 ms; control: 131 +/- 28 ms; p = 0.05) and ventriculo-atrial effective refractory periods (AC(VI): 97 +/- 21 ms; control: 127 +/- 15 ms; p = 0.05). We observed no differences between groups in sinus node function, and ventricular arrhythmias were not inducible. Cardiac-directed expression of AC(VI) facilitates AV nodal conduction without altering sinus node function. These results suggest the need to define a role for AC(VI) gene transfer in treating diseases of AV conduction.

Successful Elimination of Concealed Accessory Pathway‐Mediated Tachycardia by Ablation of AV Nodal Slow Pathway

We report a case of atrioventricular reentrant tachycardia (AVRT) using a concealed para-Hisian accessory pathway for retrograde conduction, which also required anterograde conduction over the AV nodal slow pathway to maintain the tachycardia. The shortest VA interval during AVRT (70 ms) was noted at a site with His bundle electrogram amplitude of 0.25 mV. The AVRT was cured by radiofrequency ablation of the AV nodal slow pathway without affecting accessory pathway conduction. The patient has not reported any sustained palpitations at 2 years after ablation while receiving no medications. The case presented in this report illustrates a para-Hisian AVRT that was successfully eliminated by an unconventional approach of ablation of the atrial inputs to the AV nodal slow pathway.

Cryoablation of a Nodoventricular Mahaim Fiber

An 11-year old female presented with paroxysmal tachycardia and was diagnosed with a Mahaim fiber during electrophysiologic study. A preexcited tachycardia and the typical variety of AV nodal reentry tachycardia were induced at different times. During preexcited tachycardia, the His bundle electrogram followed the ventricular electrogram, and, introduction of atrial premature beats at different coupling intervals, advanced the peri-AV nodal atrial tissue, with no change in the ventricular cycle length, leading to a diagnosis of an antidromic tachycardia due to a nodoventricular fiber. Cryoablation at a mid-septal location under three-dimensional guidance successfully eliminated both tachycardias without detrimental effects to the AV node.

Identifying the Fast and Slow AV Nodal Pathway Conduction Times Using the AH and VA Intervals Recorded in the his Bundle Electrogram

Identifying the Fast and Slow AV Nodal Pathway Conduction Times Using the AH and VA Intervals Recorded in the his Bundle Electrogram

“V‐H‐A Pattern” as a Criterion for the Differential Diagnosis of Atypical AV Nodal Reentrant Tachycardia from AV Reciprocating Tachycardia

During ventricular extrastimulation, His bundle potential (H) following ventricular (V) and followed by atrial potentials (A), i.e., V-H-A, is observed in the His bundle electrogram when ventriculo-atrial (VA) conduction occurs via the normal conduction system. We examined the diagnostic value of V-H-A for atypical form of atrioventricular nodal reentrant tachycardia (AVNRT), which showed the earliest atrial activation site at the posterior paraseptal region during the tachycardia. We prospectively examined the response of VA conduction to ventricular extrastimulation during basic drive pacing performed during sinus rhythm in 16 patients with atypical AVNRT masquerading atrioventricular reciprocating tachycardia (AVRT) utilizing a posterior paraseptal accessory pathway and 21 with AVRT utilizing a posterior paraseptal accessory pathway. Long RP' tachycardia with RP'/RR > 0.5 was excluded. The incidences of V-H-A and dual AV nodal physiology (DP) were compared between atypical AVNRT and AVRT. V-H-A was demonstrated in all the 16 patients (100%) in atypical AVNRT and in only 1 of the 21 (5%) in AVRT (P < 0.001). DP was demonstrated in 10 patients (63%) in atypical AVNRT and in 4 (19%) in AVRT (P < 0.05). The sensitivity of V-H-A for atypical AVNRT was higher than that of DP (P < 0.05). Positive and negative predictive values were 94% and 100%, respectively, for V-H-A and 71% and 74%, respectively, for DP. The appearance of V-H-A during ventricular extrastimulation is a simple criterion for differentiating atypical AVNRT masquerading AVRT from AVRT utilizing a posterior paraseptal accessory pathway.

Experimental Model of Inappropriate Sinus Tachycardia: Initiation and Ablation

The purpose of the present study was to develop an experimental model of inappropriate sinus tachycardia (IST) by injecting a catecholamine into a fat pad containing autonomic ganglia (AG) innervating the sinus node (SN). Initial protocols in 3 groups of pentobarbital anesthetized dogs consisted of (1) slowing the heart rate (HR) by electrical stimulation of AG in the fat pad; (2) the effect of intravenous injection of epinephrine (0.1-0.3 mg) on the HR and systolic blood pressure (BP); (3) the response of SN rate to intravenously injected isoproterenol (1 microgm/kg). These studies established a reference for the response to epinephrine injection (mean dose 0.2 +/- 0.9 mg, n = 14) into the fat pad at the base of the right superior pulmonary vein (RSPV). ECG leads, right atrial and His bundle electrograms, BP and core body temperature were continuously monitored. Epinephrine, injected into the fat pad, caused a significant increase in heart rate (HR, average: 211 +/- 11/min, p < 0.05 compared to control) but little change in systolic BP, 149 +/- 10 mmHg, p = NS (Group I, N = 8). The tachycardia lasted >30 minutes. Ice mapping and P wave morphology showed the tachycardia origin in the SN in 6/8 and in the crista terminalis (CT) in 2. Injection of 0.4 cc of formaldehyde into the FP restored HR (159 +/- 16) toward baseline (154 +/- 18). In Group II (N = 6), the same regimen induced a significant increase in both HR and systolic BP (194 +/- 17/min and 230 +/- 24 mmHg, respectively) compared to control values (143 +/- 23/min, 162 +/- 24 mmHg) which lasted for > 30 minutes. Ice mapping and P wave morphology showed that the pacemaker was in the SN (1), overlying the CT (2), or atrioventricular junction (2). Formaldehyde (0.4 cc) injected into the FP restored both HR and systolic BP toward baseline values (148 +/- 29/min and 152 +/- 24 mmHg, p = NS) and prevented, slowing of the HR by electrical stimulation of the AG; moreover, the same dose of epinephrine injected intravenously increased HR and SBP but only for 2-5 minutes; Isoproterenol (1 microg/kg) injected intravenously induced essentially the same increase in sinus rate after AG ablation as in the control state (194 +/- 15/min vs 193 +/- 23/min, p = NS). Experimental IST is mainly localized in the SN or CT. Ablation of the AG terminates IST without impairing the SN response to an adrenergic challenge.

Para-Hisian pacing: Useful clinical technique to differentiate retrograde conduction between accessory atrioventricular pathways and atrioventricular nodal pathways

Para-Hisian pacing is a useful tool to differentiate between retrograde conduction over an accessory pathway and retrograde conduction over the fast or slow atrioventricular (AV) nodal pathways. 1-3 Para-Hisian pacing uses right ventricular (RV) pacing close to the His bundle or proximal right bundle branch (RBB). As the position of the ventricular pacing catheter changes subtly during respiration (or by changing pacing output), the pacing stimulus changes capture among (1) basal anteroseptal RV plus His bundle or proximal RBB (His bundle-RBB capture); (2) capture of basal anteroseptal RV alone; and (3) His bundle-RBB capture alone. These changes in pacing capture result in abrupt changes in the timing of His bundle activation relative to the timing of ventricular activation. The presence or absence of a change in atrial activation sequence, stimulus-atrial (SA) intervals, and His bundle-atrial (HA) interval identifies whether retrograde conduction is dependent on ventricular activation (retrograde conduction over an accessory pathway) or His bundle activation (retrograde conduction over the AV node) or both (accessory pathway and AV node; Figures 1 and 2). The loss of His bundle-RBB capture is usually identified by the widening of the QRS complex, indicating that some of the ventricular myocardium (farthest from the RV basal septal pacing site) is activated by the His-Purkinje system during both RV and His bundle-RBB capture. Our preferred approach is to position the RV pacing catheter toward the RV outflow tract, 1‐2 cm superior to the His bundle catheter. While pacing at moderate output (5‐10 mA and 2 ms pulse width), the RV catheter is slowly withdrawn toward the His bundle catheter (proximal RBB) until intermittent His bundle-RBB capture occurs because of changes in catheter position during respiration. As the pacing catheter is moved closer to the His bundle, the ventricular potential in the His bundle electrogram becomes earlier and the retrograde His bundle potential becomes later, providing greater separation between the local ventricular and His bundle potentials. The use of closely spaced electrodes (1 mm edge-to-edge) on the His bundle catheter shortens the duration of the local ventricular potential in the His bundle electrogram, preventing the masking of the His bundle potential by the local ventricular potential. Closely spaced electrodes on the pacing catheter may provide a smaller pacing field, facilitating intermittent loss of His bundle-RBB capture with small changes in catheter position during respiration. A deflectable RV pacing catheter is positioned more easily for para-Hisian pacing and subsequent positioning of the pacing catheter close to the location of an accessory pathway (Figure 3A). In patients with proximal RBB block (such as resulting from previous ablation), His bundle-RBB capture requires pacing proximal to the RBB block site and may not be achieved from the RV. Other approaches include changing pacing output to achieve intermittent His bundle-RBB capture and use of the distal electrodes on the His bundle catheter for pacing. 4

Cryoablation of paraHissian pathways in children

Introduction: Radiofrequency catheter ablation of paraHissian pathways raises concern for AV node injury. CryoAblation is advocated as a safe alternative for ablations near the AV node. Purpose: To assess the efficacy and incidence of AV node injury during CryoAblation of paraHissian pathways. Methods: We performed a retrospective review of all CryoAblations at our institution. Demographics, SVT mechanism, ablation data, complications and outcome were recorded. Results: A total of 37 patients underwent CryoAblation for SVT, of which 5 (see table) had a paraHissian pathway. The average age was 11.6 1.8 years. All demonstrated a His bundle electrogram at the site of successful ablation. All were acutely successful and no cases were terminated prematurely due to proximity to the AV node. Two of 5 had recurrence of preexcitation, but only one had recurrence of SVT. None are on antiarrhythmic medications. Mean follow-up was 8.3 6.5 months. Transient AV node injury occurred in 2 patients with complete recovery of AV node function immediately upon termination of Cryo. In patient #1, AV node injury was evidenced by maximal preexcitation at the onset of a CryoMapping (-30°C). In patient #4, loss of preexcitation and AV block occurred at the onset of a CryoAblation (-70°C). There was no permanent AV node injury. Permanent RBBB occurred in patient #4. Conclusions: CryoAblation provides an effective means for ablation of paraHissian pathways with the ability to ensure AV node conduction remains intact. The reassurance of maintenance of AV node conduction allows for perseverance in ablations near the AV node with the use of CryoAblation.

An acute model for spontaneous, sustained atrial fibrillation arising from the pulmonary vein-atrial junction

High frequency stimulation of autonomic ganglia (AG) on the atrium near the pulmonary veins (PV) can convert delivered atrial extrastimuli into paroxysmal atrial fibrillation (AF). In order to induce spontaneous sustained AF we injected parasympathomimetics (PSPMs) into the AG located at the PVs. Methods: In 12 Na-pentobarbital anesthetized dogs, a right thoracotomy was performed and an electrode catheter was apposed to the right superior (RS) PV. After a pericardiotomy, a 26-gauge needle with a polyethylene tube attached was inserted into the fat pad (FP) containing AG on the atrium adjacent to the RSPV. The cannula was held in place by tissue glue. ECG leads, right atrial and His bundle electrograms (EGs) and blood pressure were continuously monitored. The 12 dogs were divided into 2 groups. In each group we measured average cycle lengths (CL) and durations of induced AF in the baseline state due to rapid atrial pacing. Acetylcholine (Ach, 1-100mM, Group I) or carbachol (CARB, 1-10mM, Group II) was injected (0.5cc) into the FP at the base of the RSPV. The former is hydrolyzed cholinesterases, whereas the latter is not. Results: Table 1 details the significant increase in the duration of the spontaneous (4) and induced (8) AF after the PSPM were injected into the FP. Furthermore, CARB injection significantly increased both the shortest EG CL at the PV-A junctions and duration of AF compared to control, p 0.05. In 3 cases of CARB injection, AF was sustained for more that 1 hour. CONCLUSIONS: Injection of Ach and CARB into the FP/AG at the base of the RSPV results in a spontaneous or induced sustained AF showing marked shortening of the refractory period of the PV or atrial electrograms adjacent to the injected FP. EGs with the shortest CL were found at the PV-atrial junctions suggesting that local AG hyperactivity can incite focal “drivers” for the induction of AF.

Identification of preferential sites of parasympathetic input to the atrioventricular node in man

Objectives The effects of subthreshold stimulation performed at various sites in the perinodal and posteroseptal space on atrioventricular (AV) nodal conduction were investigated. Background The identification of specific or preferential sites of parasympathetic innervation to the AV node is suggested by observations made in both the animal and clinical laboratories. Pathologic studies of the parasympathetic innervation to the AV node show it is made up of serpiginous fibers traveling at highly specific sites within the myocardium endocardially towards the compact AV node. Methods We utilized endocardial subthreshold stimulation to selectively identify and characterize AV nodal inputs. Fourteen patients (age: 56 ± 4 years) undergoing electrophysiologic testing with or without radiofrequency ablation for supraventricular tachycardia were studied. A steerable quadripolar catheter was positioned in 3 to 9 locations in the region between the site recording the His bundle electrogram and the coronary sinus (CS) os under flouroscopic and electroanatomic guidance. We mapped anterosuperior sites at or near sites with His potential recordings, and up to 2 mm inferior to the His bundle recording, posteroseptal sites included the CS os and sites along the posterior, superior, and inferior border of the CS. Atrial pacing was performed at a cycle length 50 ms longer than Wenckebach cycle length. Subthreshold stimulation was applied at a frequency of 10 Hz and 20 Hz delivered to the distal electrode pair. AH and HV intervals were recorded before and during subthreshold stimulation. AH prolongation was defined as a reproducible increase in AH interval by >10 ms from a stable baseline AH interval. Results Eight of 14 patients demonstrated prolongation of AV conduction at a mean of 1.75 ± 0.2 sites. Mean AH prolongation was 56.4 ± 13.0 ms (p = 0.02) from baseline. AH prolongation was achieved 15.4 ± 1.8 mm below the His bundle recording in 7 patients, at the site of the His bundle recording in 3 patients, and along the posterior CS os border in 3 patients. Conclusion Subthreshold stimulation prolongs AV nodal conduction only at specific sites within the triangle of Koch, suggesting discrete parasympathetic endocardial inputs into the AV nodal region.

Determination of repetitive slow pathway conduction for evaluation of the efficacy of radiofrequency ablation in AVNRT.

To determine whether the loss of repetitive slow pathway conduction identifies a successful radiofrequency ablation of atrioventricular nodal reentry tachycardia (AVNRT). Thirty nine consecutive patients undergoing ablation of AVNRT using the slow pathway approach were included. At baseline and after each radiofrequency application with an episode of junctional rhythm, repetitive slow pathway conduction was assessed as follows: Effective refractory period of the fast pathway was determined. The coupling interval of the first atrial extrastimulus (A2) was set at 30 ms below the effective refractory period of the fast pathway to ensure its conduction via the slow pathway. The second atrial extrastimulus (A3) was introduced at progressively longer coupling intervals starting from 200 ms until: (1) it propagated to the His bundle or (2) an anterogradely blocked AV nodal echo of A2 appeared before a conducted A3 depolarized the atrium in the His bundle electrogram. The response was termed repetitive slow pathway conduction if A3 was conducted with an AH > 200 ms. Application was considered successful if no AVNRT could be induced. Repetitive slow pathway conduction was present after 1 of 39 successful and after 34 of 40 ineffective applications (P < 0.0001). Repetitive slow pathway conduction identified a successful application with 97% sensitivity, 86% specificity, 86% positive predictive value, and 97% negative predictive value. The presence of repetitive slow pathway conduction identifies an unsuccessful application with a clinically meaningful negative predictive value.

Proarrhythmic Effects of Fluoroquinolone Antibacterial Agents: In Vivo Effects as Physiologic Substrate for Torsades

Drug-induced prolongation of the QT interval is often associated with the onset of Torsades de Pointes (TdP) resulting in a life-threatening ventricular arrhythmia. The potential of the proarrhythmic effects of the new fluoroquinolone antibacterial agents, levofloxacin and sparfloxacin, was examined in the chronic complete atrioventricular block dogs with stable idioventricular automaticity using Holter ECG monitoring in conscious state (Experiment 1). Next, to better analyze the mechanisms of the proarrhythmic property, the cardiovascular effects of these two drugs were compared in the halothane-anesthetized dogs under the monitoring of ECG, His bundle electrogram, systemic and left ventricular pressure, monophasic action potential, cardiac output, and effective refractory period (Experiment 2). In Experiment 1, oral administration of 6 mg/kg (n = 4) as well as 60 mg/kg (n = 4) of levofloxacin did not induce any ventricular premature depolarization. On the other hand, oral administration of 60 mg/kg of sparfloxacin (n = 4) induced TdP leading to ventricular fibrillation in all animals within 24 h, while 6 mg/kg of sparfloxacin (n = 4) did not induce any ventricular premature depolarization. In Experiment 2, intravenous administration of 0.3 mg/kg as well as 3.0 mg/kg of levofloxacin slightly increased cardiac output, but no significant changes were detected in the other parameters (n = 6). On the other hand, intravenous administration of 0.3 mg/kg of sparfloxacin prolonged the effective refractory period. Additional administration of 3.0 mg/kg of sparfloxacin decreased the heart rate and prolonged the effective refractory period and ventricular repolarization phase in a similar extent, but no significant changes were detected in the other parameters (n = 6). These results suggest that backward shift of the relative repolarization period in a cardiac cycle may be the mechanism responsible for the torsadegenic effect of sparfloxacin.

Transient entrainment of bundle-branch reentry by atrial and ventricular stimulation: elucidation of the tachycardia mechanism through analysis of the surface ECG.

Different responses to entrainment have been reported in relation to the pacing site of a variety of tachycardias. However, transient entrainment of bundle-branch reentrant tachycardia (BBRT) has not been investigated systematically. We attempted entrainment of 13 BBRTs in 9 patients by pacing first the right ventricle and then the right atrium. The initial pacing cycle length (CL) was 10 ms faster than the tachycardia CL. Subsequent pacing sequences were performed with 5- to 10-ms CL decrements until tachycardia termination or loss of postatropine 1:1 AV conduction. Both full ventricular-paced and AV-conducted QRS complex references were obtained during sinus rhythm pacing from the same sites and with similar CL as during entrainment. Transient entrainment was achieved by ventricular and atrial stimulation in 11 and 8 tachycardias, respectively. Constant fusion was always present during entrainment by ventricular stimulation. There was no change in the QRS complex (orthodromically concealed fusion) during entrainment by atrial stimulation in 6 of 6 tachycardias with left bundle-branch block morphology and in 1 of 2 tachycardias with right bundle-branch block morphology. BBRT, especially if it has a left bundle-branch block morphology, can be differentiated from other wide-QRS-complex tachycardia mechanisms through analysis of the ECGs recorded during tachycardia entrainment by atrial and ventricular stimulation. This diagnostic approach may be especially useful when it is difficult to record a stable or sufficiently sized His bundle electrogram or when spontaneous changes in the ventricular CL precede similar changes in the His bundle CL.

Hyperkalemia enhances the effect of adenosine on IK,ADO in rabbit isolated AV nodal myocytes and on AV nodal conduction in guinea pig isolated heart.

The atrioventricular (AV) node is insensitive to changes in extracellular potassium concentration, [K+]o, because of the absence of the inward rectifier potassium current (IK1). However, we propose that in the presence of adenosine, elevated [K+]o should increase the adenosine-activated inward rectifier potassium current (IK,ADO) in AV nodal myocytes and hence augment the negative dromotropic effect of the nucleoside. The effects of normal (4.8 mmol/L) and high (8.0 mmol/L) [K+]o on adenosine-induced changes in resting membrane potential (Vm), IK,ADO, and membrane resistance (Rm) in rabbit isolated AV nodal myocytes and in AV nodal conduction delay (atrium-to-His bundle, AH, interval) in guinea pig isolated hearts were determined with the use of whole-cell patch-clamp and His bundle electrogram techniques, respectively. High [K+]o alone did not significantly affect membrane current, Rm, or Vm in AV nodal myocytes. However, high [K+]o in the presence of adenosine (3 micromol/L) markedly increased Im (-0. 249+/-0.038 to -0.571+/-0.111 nA, P<0.05) at -100 mV and reduced Rm (151+/-21 to 77+/-8 MOmega, P<0.02). Adenosine still hyperpolarized Vm from -48+/-2 to -65+/-1 mV (P<0.001). High [K+]o alone did not significantly affect the AH interval in isolated hearts. However, high [K+]o markedly lengthened the AH interval prolongation caused by adenosine (4 micromol/L, 7.9+/-0.8 vs 22.1+/-3.0 ms, P<0.001). The potentiating effect of high [K+]o on adenosine-induced delay in AV nodal conduction was abolished by BaCl2 (100 micromol/L). By increasing IK,ADO and decreasing Rm of AV nodal myocytes, elevated [K+]o, augments the depressant effect of adenosine on AV nodal conduction.

The effect of intravenous procainamide on the HV interval at electrophysiologic study.

The His bundle electrogram recorded at electrophysiologic study clearly differentiates atrioventricular (AV) node disease from distal conduction system disease. The distal conduction system may be tested further by infusing procainamide (10-15 mg/kg) intravenously. High-grade distal AV block or prolongation of the HV interval <80 ms was defined as an abnormal response to this test. We retrospectively reviewed the medical records of 79 patients who underwent electrophysiologic study with intravenous procainamide. An abnormal response to procainamide was observed in only 3% of 37 patients with a normal baseline HV (</= ms), in 48% of 27 patients with mild HV prolongation (56 to 70 ms), and in all 15 patients with moderate HV prolongation (<70 ms) (P <0.0001 for the trend). Procainamide induced high-grade AV block in 4 of 28 patients (14%) studied for syncope and in 1 of 51 patients (2%) studied for ventricular tachycardia. Syncope as the indication for electrophysiologic study (P = 0.05) and left bundle branch block morphology (P = 0.03) were predictors of high-grade AV block; baseline HV and QTc intervals were significantly prolonged in patients who developed AV block with procainamide. We identified a strong linear correlation (R = 0.85) between post-drug and baseline HV intervals, with a regression slope of 1.17 +/- 0.09 and an intercept (+/- standard error) of 5.8 +/- 5.0 ms. This linear response to procainamide and published prospective studies support pacing syncope patients with baseline HV <70 ms. Therefore, procainamide infusion during the electrophysiologic study of patients with undifferentiated syncope should be reserved for those with mild HV prolongation from approximately 55 to 70 ms.