AV Conduction Research Articles

Acute effects of right ventricular pacing on cardiac haemodynamics and transvalvular impedance

To assess the acute side-effects of right ventricular (RV) stimulation applied in apex and mid-septum, in order to establish the optimal lead location in clinical practice. During pacemaker implantation, the ventricular lead was temporarily fixed in the apex and then moved to mid-septum. In both positions, surface and endocardial electrograms and transvalvular impedance (32 cases), left ventricular (LV) pressure (23), and transthoracic echocardiography (10) were acquired with intrinsic activity and VDD pacing. A larger increase in QRS duration was noticed with apical than septal pacing (65±25 vs. 45±29 ms; P<10(-4)). The proportion of cases where RV stimulation affected the transvalvular impedance waveform was higher with apical lead location (56% vs. 20%; P<0.02). VDD pacing at either site reduced the maximum dP/dt by 6% with respect to intrinsic AV conduction (IAVC; P<0.005). The maximum pressure drop taking place in 100 ms was reduced by 6 and 8%, respectively, with apical and septal pacing (P<0.01 vs. IAVC). Apical VDD decreased mitral annulus velocity in early diastole (E') from 7.5±1.4 to 5.9±0.9 cm/s (P<0.02) and prolonged the E-wave deceleration time (DT) from 156±33 to 199±54 ms (P<0.02), while septal pacing induced non-significant modifications in E' and DT. Ventricular stimulation acutely impairs LV systolic and diastolic performance, independent of the pacing site. Septal lead location preserves RV contraction mechanics and reduces the electrical interventricular delay.

Pacemaker dependency after transcatheter aortic valve implantation with the self-expanding Medtronic CoreValve System

To determine pacemaker (PM) dependency at follow-up visit in patients who underwent new permanent pacemaker implantation (PPI) following transcatheter aortic valve implantation (TAVI). Single center prospective observational study including 167 patients without previous PM implantation who underwent TAVI with the self-expanding Medtronic CoreValve System (MCS) between November 2005 and February 2011. PM dependency was defined by the presence of a high degree atrioventricular block (HDAVB; second [AV2] and third degree [AV3B]), or a slow (<30 bpm) or absent ventricular escape rhythm during follow-up PM interrogation. A total of 36 patients (21.6%) received a new PM following TAVI. The indication for PM was AV2B (n=2, 5.6%), AV3B (n=28, 77.8%), postoperative symptomatic bradycardia (n=3, 8.3%), brady-tachy syndrome (n=1, 2.8%), atrial fibrilation with slow response (n=1, 2.8%) and left bundle branch block (n=1, 2.8%). Long term follow-up was complete for all patients and ranged from 1 to 40 months (median (IQR): 11.5 (5.0-18.0 months). Of those patients with a HDAVB, 16 out of the 30 patients (53.3%) were PM independent at follow-up visit (complete or partial resolution of the AV conduction abnormality). Overall, 20 out of the 36 patients (55.6%) who received a new PM following TAVI were PM independent at follow-up. Partial and even complete resolution of peri-operative AV conduction abnormalities after MCS valve implantation occurred in more than half of the patients.

Letter to the Editor in response to the Ukena et al. article regarding the effects of renal denervation on HR and AV conduction

Letter to the Editor in response to the Ukena et al. article regarding the effects of renal denervation on HR and AV conduction

Deep sedation and atrioventricular nodal reentry tachycardia ablation.

Cardiac ablation is an invasive procedure requiring conscious and deep sedation for immobility and analgesia. AVNRT ablation generates acute pain during the radiofrequency application. Although the success rate is high, the procedure is uncomfortable for patients who must remain motionless. Sedation in EP lab is needed for several purposes such as providing anaesthesia and airway management for cardio version during EP study and induction of atrial fibrillation, pain management, and haemodynamic monitoring. The best anaesthetic agent should not alter Electrophysiological properties including SA node, AV node functions, conduction velocities, and refractoriness. Most anaesthetic agents have not been studied in the context of EPS and most of our data were based on animal and laboratory experiments. A few investigators reported that anesthetic agents have no significant clinical effects on conduction system (1, 2). There are some reports concerning non-inducibility of AVNRT after intravenous sedation in pediatrics (3). Fazelifar et al. investigated inducibility of AVNRT and electrophysiological properties after deep sedation (4). Anesthesia with benzodiazepines and opiates used in a repeated bolus fashion can easily be provided without influencing accurate EP testing and/or arrhythmia induction. There are no known specific side-effects of benzodiazepines on cardiac conduction (1). Propofol and benzodiazepine may change heart rate via baroreflex regulatory mechanisms (5, 6). The authors demonstrated that AVNRT induction is not related to anesthetic agents and it could be performed safely in all patients who undergo slow pathway induction. Induction and ablation of reentrant arrhythmias such as AVNRT can be performed safely after deep sedation. Ablation after sedation in other supra-ventricular tachy-arrhythmias requires another well-designed randomized trial.

462 Simvastatin in the Setting of INOS Deletion Improves Survival in Mice With Ventricular Hypertrophy Secondary to Calcineurin Overexpression

Overexpression of calcineurin (CN) causes cardiac hypertrophy and arrhythmic deaths secondary to either heart block or ventricular tachyarrhythmias (VT). Statins have been reported to prevent the development of left ventricular hypertrophy (LVH) in some experimental models and in patients with heart disease. We have previously reported that simvastatin prevented VT associated with CN overexpression but did not improve survival or modify the magnitude of LVH. Inducible nitric acid (NO) synthase (INOS) has been implicated in cardiac injury. Here, we tested the hypothesis that simvastatin would improve survival in transgenic mice with CN overexpression and INOS deletion. Double recombinant mice with CN overexpression and INOS deletion were treated daily with 2mg/kg simvastatin (n=10) or placebo (n=11) up to 270 days of age. ECGs were monitored for 5 minutes every 10 days commencing at age 35 days. Heart rate, P-R interval, AV block and spontaneous VT were compared between groups at ages 46 and 126 days. Heart weight, heart septum thickness and left ventricle wall thickness were compared between groups at death. Survival was also compared between the two groups. Simvastatin did not significantly reduce cardiac mass or dimensions. Simvastatin improved survival in the INOS-CN mice (Figure) and increased resting heart rate. Simvastatin did not modify AV conduction or magnitude of heart block but tended to reduce ventricular arrhythmia frequency. Tabled 1View Large Image Figure ViewerDownload (PPT) Simvastatin treatment improved survival in double recombinant INOS deletion x CN mice in the absence of structural remodeling. The mechanism(s) of improved survival will require further study.

900 A Prospective Canadian Multi-Center Randomized Parallel Study on Spontaneous Atrioventricular Conduction Preservation

Limiting unnecessary ventricular pacing (VP) in patients (pts) who receive a dual-chamber (DDD) pacemaker (PM) appears desirable. Programming long AV delays have serious limitations in that respect: long PR intervals may be suboptimal to preserve AV synchrony, and often times % of VP >10% are observed despite all the efforts to minimize VP. On the other hand, despite the fact that AAI pacing has been superior to DDD with long AV delay, it is seldom used because of the fear of AV conduction problems. The SafeR™ mode by Sorin is one of the available algorithmS that aim to minimize unnecessary VP while decreasing the associated risk of AAI pacing. The CAN-SAVE R study is a Canadian multi-center randomized study that compares the efficacy the SafeR™ mode with DDD pacing with a long AV delay in a large population of pts not presenting with permanent high degree AV Block (AVB). Its objectives are three-fold: to compare the % of VP, atrial fibrillation (AF)(primary endpoint) and the impact on LV and LA remodeling at 3 years (by echo). 373 patients from10 centers in Canada were randomized by July 2nd 2009: 63% males, mean age= 71±10 years, LVEF= 50±5%, LAVol= 24±3mL. Pacing indications were Sinus Node dysfunction (SND) (47%), AV block (24%), SND + AV block (14%) and other (mainly syncope: 15%). By July 31st 2012, 330 patients are expected to have completed their 3-year follow-up (89%). This is more than the 270 pts needed to achieve the primary endpoint (at 0.8 power). The data should be available for analysis in early September 2012, in time for presentation at CCC in October. Tabled 1

Pseudo-atrial flutter

A 63-year-old man undergoing treatment for Parkinson's disease and with no history of cardiac disease showed a newly emergent arrhythmia during a follow-up visit. The 12-lead ECG suggested atrial flutter with a cycle length of 180ms (330 cycles/min or 5.5Hz) pattern in all the leads. With an intrinsic ventricular rate of 86bpm, the initial machine-based assessment was atrial flutter with 4:1 AV conduction. Multiple ECGs were recorded and a closer scrutiny of the serially recorded digital ECG waveforms manually helped in ruling out the arrhythmia and diagnosing it as a Parkinson's tremor-induced artifact.

Can AV Node Ablation Help Save AV Conduction?

Can AV Node Ablation Help Save AV Conduction?

Cardiovascular Effects and Safety of Fingolimod in Clinical Practice (P04.138)

Objective: To describe the cardiovascular safety and tolerability of fingolimod in a clinical/academic practice. Background Fingolimod is approved by the FDA for relapsing multiple sclerosis (RRMS). Bradycardia and slowing of AV conduction were observed with fingolimod initiation in clinical trials. Screening electrocardiogram (EKG) and a first dose observation (FDO) period is recommended in all patients starting this medication. Design/Methods: Patients starting fingolimod from December 2010 to August 2011 were identified through the electronic medical record database. Demographics, cardiovascular history, screening EKG, cardiology consultation notes, FDO experience and 3 month follow-up data were retrieved and tabulated. Results: A total of 318 patients were identified. A history of hypertension was present in 30 (9.4%) of patients and a history of cardiac disease was present in 8 (2.5%) patients. Betablockers, calcium channel blockers, and digoxin were used by 3.7%, 2.8%, and 0.6% of patients respectively. Pretreatment EKG studies were available in 300 (94.3%) patients and were abnormal in 80 (25.2%) cases. Cardiology consultation was requested in 33 (10.4%) patients and use of fingolimod was cleared for all. During FDO mean heart rate change was -11.5 bpm (p Conclusions: Screening EKG showed abnormalities in a quarter of patients starting fingolimod, and identified patients at risk for symptomatic bradycardia. Fingolimod was well tolerated and no severe or serious cardiovascular adverse effects were encountered during FDO. Disclosure: Dr. Bermel has received personal compensation for activities with Astellas, Biogen Idec, Novartis, and Teva Neuroscience as a consultant and/or speaker. Dr. Ontaneda has nothing to disclose. Dr. Hara-Cleaver has received personal compensation for activities with Biogen Idec, Novartis, Serono, Inc., and TEVA Neuroscience as a consultant. Dr. Rudick has received personal compensation for activities with Biogen Idec, Genzyme, and Wyeth/Pfizer. Dr. Rudick has received research support from Biogen Idec through the Cleveland Clinic. Dr. Cohen has received personal compensation for activities with Biogen Idec, Eli Lilly & Company, Novartis, and Vaccinex. Dr. Cohen has received research support for activities with Biogen Idec, BioMS, Genzyme Corporation, Novartis, Synthon, and Teva Neuroscience.

Cryoablation for AVNRT: Importance of Ablation Endpoint Criteria

For ablation of atrioventricular nodal reentrant tachycardia (AVNRT), cryoablation has been shown to be a safe alternative to radiofrequency ablation. However, previous studies have shown a higher recurrence rate with cryoablation compared to radiofrequency ablation. This study reviewed our experience using cryoablation for typical AVNRT using stringent endpoint criteria for slow pathway ablation, yet preserving the desirable safety profile of cryoablation. Seventy-five consecutive cases of typical AVNRT underwent cryoablation. Ablation of the AV nodal slow pathway was performed with the goal of eliminating tachycardia, AH jump, and retrograde atrial echo beats. The primary efficacy endpoint was freedom of recurrent supraventricular tachycardia at follow-up. Analysis of AVN characteristics, number of lesions, and complications was performed. Seventy-two (96%) patients met the primary efficacy endpoint over an average follow-up of 34.6 (12.6-68.3) months. In patients who had complete elimination of the slow pathway, there were no recurrences. The presence of an AH jump with a single retrograde echo was highly associated with a recurrence (P = 0.0001). There were no complications, including AV conduction block. The efficacy of cryoablation for management of AVNRT can be comparable to radiofrequency energy if the suggested endpoint of elimination of tachycardia, AH jump with retrograde atrial beats, is met. Prior studies evaluating cryoablation in this setting did not require this endpoint, which could have contributed to the relatively higher rate of late recurrences.

P-wave locking in the postventricular atrial refractory period of cardiac resynchronization devices

Electrical desynchronization in cardiac resynchronization therapy (CRT) occurs when sinus P waves are continually locked in the postventricular atrial refractory period (PVARP). This process is characterized by sequences of a P wave as an atrial event in the PVARP followed by a conducted and sensed ventricular event. Such sequences are more common in patients with a prolonged PR interval, often initiated by premature ventricular complexes (PVC) and terminated by PVCs or slowing of the sinus rate. Specific algorithms automatically identify a recurring pattern of P wave locking in the PVARP, whereupon they shorten the PVARP temporarily until atrial tracking is restored with the programmed sensed AV interval. The Biotronik family of Lumax CRT devices use an AV control window which is not an algorithm that "unlocks" P waves trapped in the PVARP. Rather, it prevents P waves from becoming trapped in the PVARP. A ventricular sensed event occurring within the AV control interval does not start a PVARP so that P wave locking cannot occur when the AV conduction time is shorter than the AV control interval.

Create an engineered conduction tissue by seeding cardiac progenitor cells on gelatin foam

CompleteAV conduction block is typically treated by implanting an electronicpacemaker device; however, long‐term pacing therapy in pediatricpatients has significant complications. In this study, an engineered conduction tissue seeded with cardiac progenitor cells were implanted in rat hearts to create an alternative AV conduction pathway. The engineered conduction tissue was created by seeding cardiac progenitor cells on gelatin foam and exhibited sustained electrical coupling through persistent expression and function of gap junction proteins and pacemaker genes. Cardiac progenitor cells in the constructs were shown to survive in the hearts and the coupling of grafted cells with host cardiomyocytes was shown. Our experiments suggest the possibility that engineered tissue constructs can function as an electrical conduit and, ultimately, may offer a substitute treatment to conventional pacing therapy.

Effect of a Pacing Mode Preserving Spontaneous AV Conduction on Ventricular Pacing Burden and Atrial Arrhythmias

Using dual-chamber pacemakers with new algorithms: Manage Ventricular Pacing (MVP™), minimizes unnecessary ventricular pacing (VP). This function operates in AAI/R mode with backup VP during AV block. The aim of "Generation MVP" study was to assess the VP burden and atrial arrhythmias (AA) burden according to indication of pacing and MVP™ function programming of AdaptaDR implantable pacemaker (Medtronic Inc., Minneapolis, MN, USA). The multicenter observational "Generation MVP" study included 220 patients aged 75.9 ± 11 years (men = 52%) implanted for sinus node dysfunction (SND; n = 115) or atrio-ventricular block (AVB; n = 105). Programming MVP function has been left to the physician's discretion. Percentage of VP and AA burden (percentage of time spent in AA) stored in memories were assessed at 2 and 10 months. 220 patients were followed at 2 months (174 MVP [On], 46 MVP [off]) and at 10 months (165 MVP [On], 55 MVP [off]). Median percentage of VP is significantly lower when MVP is programmed [On] versus [off] at 2 and 10 months follow-up for SND and AVB indications of pacing (P < 0.001). Finally, programming MVP function is performed at middle term (10 months) for 84% of patients with SND and 65% of patients with AVB: median percentage of VP is as low as 0.6% for patients with SND and 12% for patients with AVB versus 95% for SND and 99% for AVB when MVP function is programmed [off](P < 0.001). Median AA burden was significantly lower when MVP function was programmed [On] versus [off] at 2 months (8.7% vs 28%; P < 0.001) and 10 months (1% vs 22%; P < 0.001). In this study programming MVP function decreases percentage of VP at 2 and 10 months for patients paced for SND or AVB. Moreover median AA burden is reduced when MVP function was programmed [On] vs [off] at two follow-ups.

Reappraisal of the Traditional Wenckebach Phenomenon with a Modified Ladder Diagram

Understanding of the traditional Wenckebach phenomenon is enhanced by using a modified ladder diagram where AV conduction in any cycle is represented by a slanted line in the AV bar together with similar AV conduction lines of all the preceding cycles. The diagram facilitates calculation of the duration of RR intervals (equal to the basic PP or sinus interval minus the PR or AV increment applied to this particular cycle) and the duration of the pause (equal to 2 × PP or sinus interval minus the sum of all the increments applied to the AV delay). The modified Wenckebach diagram should help students understand the mysterious clustering of QRS complexes or "paradoxical" increase of the ventricular rate that occurs during a Wenckebach sequence.

Alternating Ventricular Preexcitation

A 45-year-old woman diagnosed with Wolff-Parkinson-White syndrome preferred treatment with propafenone rather than catheter ablation. A 12-lead electrocardiogram (Fig. 1) after the drug administration showed sinus arrhythmia; alternating ventricular preexcitation; and alternating T wave inversion in the inferior leads during normal AV conduction. Fig. 1 Ventricular preexcitation may disappear because of decreased conduction delay over the AV node, relative to the accessory pathway; this was similar to that observed on vagal tone withdrawal. However, loss of ventricular preexcitation associated with decreased sinus cycle length was observed, which excluded the first possibility as a mechanism for intermittent preexcitation. The other mechanisms include prolongation of the refractory period (RP) of the accessory pathway (AP) due to increased vagal tone1) and linking. Linking is defined as repetitive conduction over 1 of 2 potential pathways, with persistent conduction block in the other pathway maintained by concealed retrograde conduction.2),3) However, the alternating preexcitation cannot be attributed to linking and was most probably caused by prolongation of the antegrade RP of the AP by propafenone greater than sinus cycle length (Fig. 2). Fig. 2 Intermittent ventricular preexcitation is associated with a long antegrade RP of the AP and a prolonged preexcited RR interval during atrial fibrillation.4) Twave inversion in the inferior leads occurs because of the memory effect.5) Alternating ventricular preexcitation is a rare electrocardiographic phenomenon associated with RP of the AP greater than the length of the sinus cycle.

Assessment of the effects of changes in body temperature on cardiac electrophysiology in anaesthetised guinea pigs

IntroductionAnaesthetised guinea pigs are commonly used within Safety Pharmacology to evaluate drug effects on cardiac electrophysiology. However, anesthesia compromises the ability to thermoregulate, which can be further challenged when more invasive surgery is required. As anaesthetised animals are often used when screening for cardiotoxicity, thereby influencing go/no–go decisions, we wanted to quantify the impact of small temperature changes on the recorded electrophysiological parameters. MethodsMale guinea pigs were anaesthetised by pentobarbital, placed on a pre-heated table and a rectal thermistor inserted for monitoring of body temperature. After intubation animals were vagotomised and β-blocked, and lead II ECG needle electrodes attached. Following thoracotomy an atrial pacing electrode was attached and a suction MAP electrode positioned on the ventricular epicardium. In control animals temperature was kept constant (38.1±0.1°C) over the duration of the experiment. Animals in one group were slowly warmed to 41.9°C by a heating plate and a heating lamp, and in another group slowly cooled to 34.4°C by turning off all heating equipment. MAP duration at 90% repolarisation (MAPD90), AV conduction, ECG and body temperature were recorded during cardiac pacing every 5min up to 50min. ResultsNo time-dependent changes were seen in the control group. In contrast, a linear correlation was found between changes in body temperature and MAPD90, AV conduction, QTc and QRS intervals. For each degree temperature fell below 38°C MAPD90 was prolonged by 6.1ms, and for each degree above 38°C MAPD90 was shortened by 5.3ms. Corresponding changes were seen for QTc interval and AV conduction time, while effects on the QRS interval were smaller. DiscussionThe data highlights the importance of carefully controlling body temperature when performing electrophysiological recordings in laboratory animals. A change by a single degree can affect electrophysiological parameters by 5–10%, thus increasing the risk for a false positive or negative interpretation of cardiotoxicity.

The study of the relation between different end points of slow atrioventricular nodal pathway ablation and clinical efficiency in patients with atrioventricular nodal reentrant tachycardia (slow-fast kind)

ObjectiveThe study of the Relation between different end points of slow atrioventricular nodal pathway ablation and clinical efficiency in patients with atrioventricular nodal reentrant tachycardia.Methods350 patients with atrioventricular nodal re-entrant...

The advanced experience in combining Biv-pacing with AVN-first for improving efficiency from CRT

Background and objectivesCardiac resynchronisation therapy (CRT) is now an established non-pharmacologic therapy for advanced congestive heart failure (CHF) with electromechanical delay. However, lack of a favourable response in about 1/3...

Clinical efficacy of intervention therapy in patients with acute myocardial infarction complicating complete atrioventricular block

ObjectiveThe aim of this study was to investigate the efficacy of intervention therapy in patients with acute myocardial infarction (AMI) complicating complete atrioventricular block (CAVB).MethodsData from 80 consecutive patients with...

AV Dissociation, an Inevitable Response

The independent activation of the atria and ventricles, AV dissociation, is a common phenomenon that occurs during a wide variety of electrophysiologic circumstances. The clinical significance of AV dissociation is often misunderstood. This article examines the basis and clinical implications of AV dissociation. AV dissociation is often an obligatory, secondary phenomenon, and should not be construed as the primary disorder; it may be due to either the AV conduction system being completely blocked (3° AV block) or the P wave and the QRS complex being generated from separate sources (usually, the AV junction or ventricle) but occurring close together during the physiologic refractory period of each other. The latter may happen in junctional or ventricular arrhythmias including escape or accelerated rhythm, tachycardia, or premature beats. The crucial clinical point is not the AV dissociation itself, but that an underlying triggering primary disorder is present and should be identified.