Reduction of right ventricular pacing in patients with dual-chamber ICDs

BACKGROUND: Unnecessary right ventricular (RV) pacing in patients with implantable cardioverter defibrillators (ICD) may adversely affect heart failure morbidity and total mortality. Inhibition of Unnecessary RV Pacing with AV Search Hysteresis in ICDs (INTRINSIC RV) is a prospective, multicenter, randomized trial evaluating outcomes in ICD recipients programmed to single-chamber pacing (VVI) versus dual-chamber (DDDR) pacing with AV search hysteresis (AVSH). METHODS: Patients underwent ICD implant (for standard indications). The ICD was programmed to DDDR with AVSH regardless of any need for pacing. Rate-adaptive pacing was set at 60-130 ppm with dynamic AV delay from 200 to 90 ms. AVSH was programmed to search every 32 intervals and extend the AV delay by 50%. One week post-implant patients with ICDs were interrogated to assess the percentage of RV pacing with the expectation that most would have <20% RV pacing and would be randomized into INTRINSIC RV. Early analysis showed that targets for randomization were not met. AVSH parameters were modified under a protocol amendment to increase AV delay extension to 100%. We report findings related to this programming change based upon analyses of (nonrandomized) data pre- and post-amendment. RESULTS: Twenty-one percent of patients (n = 314) were enrolled pre-amendment and 79% (n = 1,216) were enrolled post-amendment. The mean percentage of RV pacing at the 1-week visit was 41.4 +/- 29.6% pre-amendment and 14.7 +/- 22.6% post-amendment (P < 0.0001). The proportion of patients eligible for randomization (RV pacing <20% at the 1-week visit) was 31.2% pre-amendment and 76.8% post-amendment (P < 0.0001). CONCLUSION: AVSH can dramatically reduce the percentage of RV pacing among ICD recipients.     

双腔起搏器房室间期自动搜索功能对右心室起搏比例影响的临床研究

目的比较植入双腔起搏器患者房室（AV）间期自动搜索功能（Search AV）打开与固定长AV间期起搏,对右心室起搏比例的影响。方法入选60例病态窦房结综合征或间歇性Ⅱ度或Ⅲ度AV传导阻滞患者,均安装双腔起搏器。程控首先关闭Search AV功能,固定长AV间期（起搏房室间期220ms,感知房室间期200ms）起搏3个月,后程控打开Search AV 3个月,自身对照,比较其心房起搏比例、心室起搏比例及高频心房事件次数。再根据患者是否1：1房室传导分为2个亚组,自身对照分别比较其心房起搏比例、心室起搏比例及高频心房时间次数。结果58倒患者完成随访,固定长AV间期起搏时比Search AV（＋）自动搜索功能打开时的心室起搏比例、高频心房事件次数都高,分别为（70．5±12．4）％vs（22．4±8．3）％,（86±16）次VS（31±11）次（P=0．007,P=0．006）;而心房起搏比例二者差异无统计学意义。在1：1房室传导组（33例）及非1：1房室传导组（25例）两亚组比较中,均得出相同结果。结论Search AV功能可以减少不必要的右心室起搏,减少高频心房事件。     

Reduction of RV pacing by continuous optimization of the AV interval

BACKGROUND: In patients requiring permanent pacing, preservation of intrinsic ventricular activation is preferred whenever possible. The Search AV+ (SAV+) algorithm in Medtronic EnPulsetrade mark dual-chamber pacemakers can increase atrioventricular (AV) intervals to 320 ms in patients with intact or intermittent AV conduction. This prospective, multicenter study compared the percentage of ventricular pacing with and without AV interval extension. METHODS: Among 197 patients enrolled in the study, the percentage of ventricular-paced beats was evaluated via device diagnostics at the 1-month follow-up. Patient cohorts were defined by clinician assessment of conduction via a 1:1 AV conduction test at the 2-week follow-up. The observed percentage of ventricular pacing with SAV + ON and the predicted percentage of ventricular pacing with SAV + OFF were determined from the SAV + histogram data for the period between the 2-week and 1-month follow-up visits. RESULTS: Of 197 patients, 110 (55.8%) had intact 1:1 AV conduction, of which 109 had 1-month data. SAV + remained ON in 99/109 patients; 10 patients had intrinsic A-V conduction intervals beyond SAV + nominal and therefore SAV + disabled. The mean percentage of ventricular pacing in the 109 patients was SAV+ ON = 23.1% (median 3.7%) versus SAV + OFF = 97.2% (median 99.7%). In 87 patients without 1:1 AV conduction, SAV + was programmed OFF in 6, automatically disabled in 52, and remained ON in 29. In 8 of these patients, 80-100% reduction in ventricular pacing was observed with SAV + ON. CONCLUSION: The Search AV+ algorithm in the EnPulse pacemaker effectively promotes intrinsic ventricular activation and substantially reduces unnecessary ventricular pacing.     

Comparison of two strategies to reduce ventricular pacing in pacemaker patients

Background: Managed Ventricular Pacing (MVP) and Search AV+ (SAV+) are two pacing algorithms designed to reduce ventricular pacing. MVP promotes conduction by operating in AAI/R mode with backup ventricular pacing during atrioventricular block (AVB). SAV+ operates in DDD/R mode with a nominal AV extension of 290 ms during atrial sensing and 320 ms during atrial pacing. The reduction in ventricular pacing was compared with these two algorithms in pacemaker patients.
Methods: The EnRhythm and EnPulse clinical studies assessed the percentage of ventricular pacing (%VP) after 1 month. Each patient's AVB status was assigned using the following hierarchical categories: persistent third-degree AVB (p3AVB), episodic third-degree AVB (e3AVB), second-degree AVB (2AVB), first-degree AVB (1AVB), and no AVB (nAVB). The%VP was tabulated for each AVB status category.
Results: Data were available from 322 patients of whom 129 received DDD(R) pacing with the MVP algorithm activated and 193 patients with DDD(R) pacing and the SAV+ function activated, each for a month period. MVP resulted in a significantly lower median%VP than SAV+ in all AVB categories except for p3AVB: nAVB (0.3 vs 2.9, P < 0.0001), 1AVB (0.9% vs 80.6%, P < 0.0001), 2AVB (37.6 vs 99.3, P< 0.002), e3AVB (1.2 vs 42.2, P = 0.02), p3AVB (98.9 vs 100, P = 1.00).
Conclusion: MVP resulted in a greater reduction in%VP than SAV+ across all patient groups except persistent third-degree AV block. The greatest reduction in%VP was observed in patients with mildly impaired AV conduction.     

Minimizing ventricular pacing by a novel atrioventricular (AV) delay hysteresis algorithm in patients with intact or compromised intrinsic AV conduction and different atrial and ventricular lead locations

Abstract

Purpose. To investigate if an advanced AV search hysteresis (AVSH) algorithm, Ventricular Intrinsic Preference (VIP^?), reduces the incidence of ventricular pacing (VP) in sinus node dysfunction (SND) with both intact and compromised AV conduction and with intermittent AV block regardless of the lead positions in the right atria and the ventricle.

Methods. Patients were classified as having intact AV (AVi) conduction if the PR interval was ≤ 210 ms on ECG and 1:1 AV conduction during atrial pacing up to 120 bpm with PR interval ≤ 350 ms. Otherwise the AV conduction was classified as compromised (AVc). Both AVi and AVc patients were randomized to VIP ON or OFF. VIP performed an intrinsic AV conduction search every 30 s for three consecutive atrial cycles with the extension of the sensed and paced AV (SAV/PAV) delays from basic values of 150/200 ms to 300/350 ms. Extended AV intervals were allowed for three cycles when VP occurred before returning to basic AV delays. The primary end-point was %VP at 12 months.

Results. Among 389 patients, 30.1% had intact and 69.9% had compromised AV conduction. The mean %VP at 12 months was 9.6% by VIP compared to 51.8% with standard AV settings in patients with AVi (P < 0.0001) and 28.0% versus 78.9% (P < 0.0001) with AVc. With VIP, excessive %VP among most used lead positions was not seen. Conversely, when VIP was off %VP was low only in patients who had leads in the RA septal–RV septal position (23.0%).

Conclusions. VIP feature reduces VP both in patients with SND and with intermittent heart block regardless of the lead positions in the right atria and the ventricle.     

Increasing left ventricular pacing output decreases interventricular conduction time in patients with biventricular pacing systems

OBJECTIVE: To evaluate the effect of increasing LV pacing output on interventricular timing in patients with biventricular pacing systems. BACKGROUND: Clinical improvement with biventricular pacing is likely related to reduction in ventricular dysynchrony in patients with cardiomyopathy. We hypothesized that increasing left ventricular pacing output would reduce interventricular conduction time and could affect ventricular synchrony. METHODS: Forty-two sequential patients with biventricular pacing systems that permitted independent LV pacing were selected at the time of routine device interrogation. The interval between LV pacing stimulus and onset of the RV electrogram was measured during LV pacing at capture threshold and at maximum pacing output for each patient. RESULTS: The average time from LV pacing stimulus to right ventricular electrogram onset was 142.5 +/- 32.5 ms (range 90-230 ms) at threshold and 132.3 +/- 30.4 ms (range 90-220 ms) at maximum pacing output, with a mean decrease in conduction time of 10.2 +/- 10.9 ms (range 0-45 ms). There was significantly greater interventricular conduction shortening with increased pacing output in patients with ischemic cardiomyopathy compared to others (14.9 +/- 11.9 ms vs 4.0 +/- 4.6 ms; P < 0.01). CONCLUSIONS: Conduction time from LV to RV shortens as LV pacing output is increased. This effect is seen to a greater degree in patients with ischemic cardiomyopathy, possibly related to the presence of myocardial scar near the pacing electrode. Further investigation is needed to assess the clinical outcomes related to this new method for optimizing resynchronization therapy.     

Hemodynamically optimized temporary cardiac pacing after surgery for congenital heart defects

Disturbance of normal AV synchrony and dyssynchronous ventricular contraction may be deleterious in patients with otherwise compromised hemodynamics. This study evaluated the effect of hemodynamically optimized temporary dual chamber pacing in patients after surgery for congenital heart disease. Pacing was performed in 23 children aged 5 days to 7.7 years (median 7.3 months) with various postoperative dysrhythmias, low cardiac output, and/or high inotropic support and optimized to achieve the highest systolic and mean arterial pressures. The following four pacing modes were used: (1) AV synchronous or AV sequential pacing with individually optimized AV delay in 11 patients with first- to third-degree AV block; (2) AV sequential pacing using transesophageal atrial pacing in combination with a temporary DDD pacemaker for atrial tracking and ventricular pacing in three patients with third-degree AV block and junctional ectopic tachycardia, respectively, who had poor signal and exit block on atrial epicardial pacing wires; (3) R wave synchronized atrial pacing in eight patients with junctional ectopic tachycardia and impaired antegrade AV conduction precluding the use of atrial overdrive pacing; (4) Atrio-biventricular sequential pacing in two patients. Pressures measured during optimized pacing were compared to baseline values at underlying rhythm (13 patients with first-degree AV block or junctional ectopic tachycardia) or during pacing modes commonly used in the given clinical situation: AAI pacing (1 patient with slow junctional rhythm and first-degree AV block during atrial pacing), VVI pacing (2 patients with third-degree AV block and exit block and poor sensing on epicardial atrial pacing wires) and dual-chamber pacing with AV delays set to 100 ms (atrial tracking) or 150 ms (AV sequential pacing) in 7 patients with second- to third-degree AV block and functional atrial pacing wires. Optimized pacing led to a significant increase in arterial systolic (mean) pressure from 71.5 +/- 12.5 (52.3 +/- 9.0) to 80.5 +/- 12.2 (59.7 +/- 9.1) mmHg (P < 0.001 for both) and a decrease in central venous (left atrial) pressure from 12.3 +/- 3.4 (10.5 +/- 3.2) to 11.0 +/- 3.0 (9.2 +/- 2.7) mmHg (P < 0.001 and < 0.005, respectively). In conclusion, several techniques of individually optimized temporary dual chamber pacing leading to optimal AV synchrony and/or synchronous ventricular contraction were successfully used to improve hemodynamics in patients with heart failure and selected dysrhythmias after congenital heart surgery.     

An Optimized AV Delay Algorithm for Patients with Intermittent Atrioventricular Conduction

Detection and promotion of an intermittent atrioventricular (A V) conduction is the objective of an AV delay hysteresis algorithm in dual chamber pacemaker (DDDj pacing. The AV delay following an atrial event is automatically extended by a programmable interval (AV hysteresis interval) if the previous cycle showed spontaneous AV conduction, i.e., a ventricular event was detected within the previous AV delay. An automatic search mode scans for spontaneous ventricular events during the hysteresis interval: a single AV delay extension (equal to the programmed AV delay hysteresis) will occur after a successive, programmable number of AV cycles with ventricular pacing. If a spontaneous AV conduction is present, the AV delay will remain extended by the hysteresis interval. Our first results in 17 patients with intermittent AV block disclosed a satisfactorily working algorithm with effective reduction of ventricular stimuli. In relation to the underlying conduction disturbance and pacemaker settings, the majority of our patients showed a reduction of ventricular pacing events up to 90% without any adverse hemodynamic or electrophysiological changes. Based on clinical (promotion of a physiological activation and contraction sequence) and technical (reduction of power consumption) advantages, the AV hysteresis principle could be of incremental value for future dual chamber pacing in patients with intermittent complete heart block.     

Linking as the Cause of Unnecessary Right Ventricular Pacing

Background: The current report describes a manifestation of linking phenomenon in DDD pacemaker recipients: impairment of atrioventricular (AV) conduction and ensuing unnecessary right ventricular (RV) pacing. Methods: Three patients with second‐degree AV block and sudden impairment of native AV conduction following pacemaker implantation are presented. Loss of native AV conduction was considered functional and related to repetitive retrograde invasion of ventricular depolarization to the AV junction that was “linked” to ventricular pacing triggered by nonconducted P‐waves. Conclusion: This case series demonstrates that linking phenomenon should be considered in analysis of pacemaker behavior, and that retrograde concealment can be responsible for unnecessary RV pacing. (PACE 2010; 1359–1363)     

Evaluation of atrial conduction time at various sites of right atrial pacing and influence on atrioventricular delay optimization by surface electrocardiography

Cardiac function and electrical stability may be improved by programming of optimal AV delay in DDD pacing. This study tested the hypothesis if the global atrial conduction time at various pacing sites can be derived from the surface ECG to achieve an optimal electromechanical timing of the left heart. Data were obtained from 60 patients following dual chamber pacemaker implantation. Right atrial septal pacing was associated with significantly shorter atrial conduction time (P < 0.0005) and P wave duration (P < 0.005), compared to standard right atrial pacing sites at the right atrial appendage or at the right free wall. The last two pacing sites showed no significant difference. In a group of 31 patients with AV block, optimal AV delay was achieved by programming a delay of 100 ms from the end of the paced P wave to peak/nadir of the paced ventricular complex. Optimization of AV delay resulted in a relative increase of echocardiographic stroke volume (SV) (10.9 +/- 13.7%; 95% CI: 5.9-15.9%) when compared to nominal AV delay (170 ms). Optimized AV delay was highly variable (range 130-250 ms; mean 180 +/- 35 ms). The hemodynamic response was characterized by a weak significant relationship between SV increase and optimized AV delay (R2 = 0.196, R = 0.443, P = 0.047). The study validated that septal pacing is advantageous for atrial synchronization compared to conventional right atrial pacing. Tailoring the AV delay with respect to the surface ECG improved systolic function significantly and was superior to nominal AV delay settings in the majority of patients.     

Automatic Beat‐to‐Beat Left Heart AV Normalization:

Programming the right heart AV interval to a normal value may cause a nonphysiological left heart AV due to interatrial and interventricular conduction delays, thus affecting cardiac performance. Since AV normalization at rest and exercise may be invalidated by pacing or sensing (mode) changes, the aim of this study was to (1) study the feasibility of a mode independent pacemaker (PM) algorithm for automatic beat-to-beat left AV normalization, (2) establish normal values for the time between mitral flow A wave (Af) and ventricular activation (Va), the AfVa interval, the mechanical surrogate of left AV, and (C) determine the range of values of the interatrial electromechanical delays (IAEMDs) and the effect of RA pacing. To pace with the proper right AV, the previously reported RV-paced interventricular electromechanical delay and the interatrial electromechanical delay, either P-sensed (IAEMDs) or atrial-paced (IAEMDp) are required inputs. Data were collected during diagnostic echo Doppler studies in 84 subjects divided in three groups: (1) control with narrow QRS and no structural heart disease (n = 33, age 50 +/- 21 years, 42% men); (2) patients in sinus rhythm with diverse cardiac pathologies except LBBB (n = 39, age 69 +/- 14 years, 56% men), and (3) DDD-paced patients (n = 12, mean age 71 +/- 6 years). Normal values of AfVa were established from the control group, while IAEMDs and IAEMDp and active atrial flow time (A-peak), in all subjects. The algorithm was tested by computer simulation under all possible modes with the following calculation: RAV = N + IAEMD - IVD, where RAV is the right AV, N is the desired normal AfVa value, IAEMD is either P-sensed or A-paced, and IVD is close to zero for intrinsic narrow QRS and biventricular pacing, or 79 ms for RV pacing. The results demonstrated (1) Normal (controls) AfVa: 85 +/- 15 ms (range 52-110 ms); (2) IAEMDs (All): 84 +/- 16 ms; (3) atrial pacing prolonged IAEMDs by 57 +/- 18 ms (from 93 +/- 15 to 150 +/- 25 ms, P < 0.0001); and (4) Computer simulation of rate and mode changes validated the normalization algorithm. An automatic, beat-to-beat left AV normalization algorithm to preserve a normal AfVa without a hemodynamic sensor is feasible. The normal value of AfVa is 85 +/- 15 ms.     

Activation sequence modification during cardiac resynchronization by manipulation of left ventricular epicardial pacing stimulus strength

BACKGROUND: Success of cardiac resynchronization therapy (CRT) depends on altering electrical ventricular activation (VA) to achieve mechanical benefit. That increases in stimulus strength (SS) can affect VA has been demonstrated previously in cardiomyopathy patients undergoing ablation. OBJECTIVE: To determine whether increasing SS can alter VA during CRT. METHODS: In 71 patients with CRT devices, left ventricle (LV) pacing was performed at escalating SS. Timing from pacing stimulus to right ventricular (RV) electrogram, ECG morphology, and maximal QRS duration on 12 lead ECG were recorded. RESULTS: Demographics: Baseline QRS duration 153 +/- 25 ms, ischemic cardiomyopathy 48%, ejection fraction 24%+/- 7%. With increased SS, conduction time from LV to right ventricle (RV) decreased from 125 +/- 56 ms to 111 +/- 59 ms (P = 0.006). QRS duration decreased from 212 +/- 46 ms to 194 +/- 42 ms (P = 0.0002). A marked change in QRS morphology occurred in 11/71 patients (15%). The RV ring was the anode in 6, while the RV coil was the anode in 5. Sites with change in QRS morphology showed decrease in conduction time from LV to RV from 110 +/- 60 ms to 64 +/- 68 ms (P = 0.04). Twelve patients (16%) had diaphragmatic stimulation with increased SS. CONCLUSIONS: Increasing LV SS reduces QRS duration and conduction time from LV to RV. Recognition of significant QRS morphology change is likely clinically important during LV threshold programming to avoid unintended VA change.     

Hemodynamic effect of the ventricular pacing site in fetal lambs with complete atrioventricular block

Complete atrioventricular (AV) block in hydrops fetalis is associated with high mortality. Fetal ventricular pacing to restore ventricular rate can be an effective procedure, however, no fetal data has shown an appropriate epicardial ventricular pacing site. To evaluate the hemodynamic effect of right and left ventricular pacing in fetal lambs with complete AV block, a fetal complete AV block model was created. Aortic pressure, central venous pressure, and QRS duration were measured, and right and left ventricular output was estimated in seven fetal lambs. The uterus was opened under maternal anesthesia, and under local anesthesia, catheters were inserted into the fetal superior vena cava and ascending aorta through a neck incision. Pacing leads were then sutured onto the fetal right and left ventricular epicardium via a midline thoracotomy. Complete AV block was created by cryoablation of the AV node. Ventricular output was estimated using echocardiography by a transuterine approach. Fetal hemodynamics were observed before AV block creation (control), and after complete AV block creation with the right and left ventricular pacing set at 150/min. The right ventricular output was 320 +/- 66 mL/kg per minute at control, decreased to 243 +/- 65 mL/kg per minute during right ventricular pacing (P < 0.05), and was 254 +/- 61 mL/kg per minute during left ventricular pacing. The left ventricular output was 224 +/- 98 mL/kg per minute at control, 176 +/- 77 mL/kg minute during right ventricular pacing, and 178 +/- 67 mL/kg per minute during left ventricular pacing. Biventricular (combined ventricular) output was 544 +/- 134 mL/kg per minute at control, 419 +/- 114 mL/kg per minute during right ventricular pacing, and 432 +/- 100 mL/kg minute during left ventricular pacing. Systolic aortic pressure was 62.2 +/- 8.7 mmHg at control, 55.2 +/- 9.5 mmHg during right ventricular pacing, and 53.4 +/- 9.1 mmHg during left ventricular pacing. Central venous pressure (CVP) was 2.6 +/- 0.5 mmHg at control, 4.0 +/- 2.7 mmHg during right ventricular pacing, and 4.4 +/- 2.5 mmHg during left ventricular pacing. The QRS duration was 51 +/- 54 ms at control, but lengthened to 87 +/- 19 ms during right ventricular pacing and to 78 +/- 21 ms during left ventricular pacing (P < 0.05). In conclusion, the right ventricular output decreased during right ventricular pacing in fetal lambs with complete AV block, while it was preserved during the left ventricular pacing. Left ventricular pacing might be superior for treating hydropic fetuses with complete AV block.     

Adverse effects of long-term right ventricular apical pacing and identification of patients at risk of atrial fibrillation and heart failure

In patients needing a pacemaker (PM) for bradycardia indications, the amount of right ventricular (RV) apical pacing has been correlated with atrial fibrillation (AFib) and heart failure (HF) in both DDD and VVI mode. RV pacing was linked with left ventricular (LV) dyssynchrony in almost 50% of patients with PM implantation and atrioventricular (AV) node ablation for AFib. In patients with normal systolic function needing a PM, apical RV pacing resulted in LV ejection fraction (LVEF) reduction. These negative effects were prevented by cardiac resynchronization therapy (CRT). Algorithms favoring physiological AV conduction are possible useful tools able to maintain both atrial and ventricular support and limit RV pacing. However, when chronic RV pacing cannot be avoided, it appears necessary to reconsider the cut-off value of basic LVEF for CRT. In HF patients, RV pacing can induce greater LV dyssynchrony, enhanced by underlying conduction diseases. In this context, a more deleterious effect of RV pacing in implantable cardioverter-defibrillator (ICD) patients with low LVEF can be expected. In some major ICD trials, DDD mode was correlated with increased mortality/HF. This negative impact was attributed to unnecessary RV pacing >40-50%, virtually absent in VVI-40 mode. However, some data suggest that avoiding RV pacing may also not be the best option for patients requiring an ICD. In patients with impaired LV function, AV synchrony should therefore be ensured. The best pacing mode in ICD patients with HF should be defined on an individual basis.     

Reduction of right ventricular pacing with advanced atrioventricular search hysteresis: results of the PREVENT study

Background: Right ventricular pacing predisposes to the development of heart failure and atrial fibrillation. Automatic atrioventricular search hysteresis (AVSH) is a commonly used strategy to decrease the percentage of right ventricular pacing (%VP) in patients without permanent AV block, but the results have not been optimal. Methods: The randomized, crossover PREVENT study evaluated whether an enhanced AVSH with two new features can reduce %VP compared with standard AVSH. The new features are the repetitive hysteresis [switch from extended to basic AV delay after a consistent loss of intrinsic AV conduction (IAVC) lasting for six consecutive atrial cycles] and the scan hysteresis (periodic IAVC search extension over six consecutive atrial cycles). Both standard AVSH and enhanced AVSH performed a periodic IAVC search every 180 cardiac cycles and operated with a basic AV‐delay of 225 ms and a rate‐independent maximum AV‐delay of 300 ms for paced and sensed atrial events. Results: Among 178 patients, 53.4% had no evidence of AV block at enrollment and 46.6% had history of intermittent AV block. The median %VP was decreased by enhanced AVSH compared to standard AVSH (4.0% vs 5.5%, P < 0.001), particularly in patients with a history of AV block (21.4% vs 25.5%, P < 0.001). The primary study hypothesis that 25% of all patients would experience > 20% relative %VP reduction was not met as 46 (25.8%) patients (95% confidence interval, 20.5–31.8%) presented such relative reduction. Conclusion: The enhanced AVSH algorithm reduces %VP compared with standard AVSH in patients with intermittent AV block. (PACE 2011; 34:975–983)     

Preserving normal ventricular activation versus atrioventricular delay optimization during pacing: the role of intrinsic atrioventricular conduction and pacing rate

The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 +/- 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal AV delay in the DDD mode and comparison between AAI and DDD with optimal AV delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (ARI) was 282 +/- 68 ms for rate 70/min and 330 +/- 98 ms for rate 90/min (P < 0.01). The optimal AV delay was 159 +/- 22 ms. AV delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16% +/- 9%. At rate 70/min the patients with ARI < or = 270 ms had higher AFTVI in AAI than in DDD (0.214 +/- 0.05 m vs 0.196 +/- 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI (0.192 +/- 0.03 m vs 0.166 +/- 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 +/- 0.03 m vs 0.162 +/- 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 +/- 0.05 m vs 0.173 +/- 0.05 m, P < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 +/- 0.05 m vs 0.158 +/- 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate.     

Full Ventricular Capture Indicated by the QT Interval Function

The atrioventricular (AV) interval is critical in dual chamber (DDD) pacing in patients with hypertrophic obstructive cardiomyopathy (HOCM) to obtain full ventricular capture (FVC) with maximal reduction of the left ventricular (LV) outflow gradient and optimal LV diastolic filling. We studied the relationship of FVC, fusion, spontaneous AV conduction, and the QT interval. Methods: 11 patients with various cardiac diseases and stable AV conduction received a QT sensing Diamond (tm) Vitatron, DDD pacemaker. Software was downloaded into the pacemaker. In the DDD pacing mode, with the QT interval measured from the ventricular pacing stimulus to the end of the T wave, the AV interval was shortened from 400 ms, in 20-ms steps, to 90 ms. At 90 ms the stimulation rate was increased by 30 beats/mm and the AV interval was increased stepwise. FVC and fusion was examined on the surface ECG, Results: At 400 ms interval, spontaneous AV conduction inhibited the pacemaker. Shortening the AV interval resulted in pacing with a short QT interval. Further reduction of the AV interval resulted in a longer QT interval up to a point where the QT interval became stable. This point, the bending point in the plot of measured QT interval versus shortened AV intervals, coincided with the point of FVC. The relation of the QT-AV interval plot and the point of fusion was comparable when lengthening the AV interval at a 30 beats/mm faster stimulation rate. Conclusion: The bending point in the QT interval versus AV interval plots showed a good correlation with the FVC and fusion points observed on ECG. The results suggest that automatic discrimination between fusion and full capture using QT interval measurements may be feasible.     

Reduction of right ventricular pacing in patients with sinus node dysfunction through programming a long atrioventricular delay along with the DDIR mode

Background  

Right ventricular (RV) pacing increases the incidence of atrial fibrillation (AF) and hospitalization rate for heart failure. Many patients with sinus node dysfunction (SND) are implanted with a DDDR pacemaker to ensure the treatment of slowly conducted atrial fibrillation and atrioventricular (AV) block. Many pacemakers are never reprogrammed after implantation. This study aims to evaluate the effectiveness of programming DDIR with a long AV delay in patients with SND and preserved AV conduction as a possible strategy to reduce RV pacing in comparison with a nominal DDDR setting including an AV search hysteresis.     

Continuously adjusting CRT therapy: clinical impact of adaptive cardiac resynchronization therapy

Cardiac resynchronization therapy (CRT) is a well-established therapy to reduce morbidity and mortality in patients with moderate and severe symptomatic congestive heart failure. Left ventricular (LV) pacing that fuses with intrinsic right ventricular (RV) conduction results in similar or even better cardiac performance compared to biventricular (Biv) pacing. Optimal programming of the atrio-ventricular (AV) and inter-ventricular (VV) delays is crucial to improve LV performance since suboptimal programming of AV and VV delays affect LV filling as well as cardiac output. CRT optimization using echocardiogram is resource-dependent and time consuming. Adaptive CRT (aCRT) algorithm provides a dynamic, automatic, ambulatory adjustment of CRT pacing configuration (Biv or LV pacing) and optimization of AV and VV delays. aCRT algorithm is safe and efficacious for CRT-indicated patients without permanent atrial fibrillation. It has been shown to improve CRT response and reduce morbidity and mortality for patients with normal AV conduction.     

Effects of AV Sequential Versus Asynchronous AV Pacing on Pulmonary Hemodynamics

We studied the effects of various pacing modes on cardiac hemodynamics and pulmonary gas alterations in chronic heart blocked dogs. Changing the pacing mode from an atrioventricular interval of 100 ms (AV100) to a ventriculo-atrial interval of 100 ms (VA100) caused a significant fall in left ventricular pressure (117.64 +/- 11.91 to 95.60 +/- 16.58 mmHg) and cardiac output from 2.18 +/- 0.24 to 1.46 +/- 0.20 L/min. Following the change in pacing mode from AV100 to VA100, there was an increase in the alveolar-arterial O2 gradient from 23.28 +/- 6.97 to 28.74 +/- 8.43 mmHg and a decrease in the arterial CO2 tension from 32.42 +/- 3.22 to 29.42 +/- 3.22 mmHg. There was also a decrease in arterial CO2 tension when the AV100 pacing mode was compared to asynchronous ventricular pacing (32.42 +/- 3.22 versus 30.56 +/- 2.82 mmHg). The minute volume of O2 also decreased when the pacing mode was changed from AV100 to asynchronous ventricular pacing (0.134 +/- 0.01 versus 0.126 +/- 0.01 L/min) and decreased further at VA100 to 0.114 +/- 0.01 L/min. Other significant changes were also observed: the percent of expired CO2 decreased when the pacing mode was changed from AV100 to VA100 (3.68 +/- 0.13 versus 3.37 +/- 0.26%) or to asynchronous ventricular pacing (3.40 +/- 0.31%). The end-expiratory O2 increased and CO2 decreased when the pacing mode was changed from AV100 to VA100. The breath-by-breath correlation of end-expiratory O2 and CO2 with left ventricular systolic pressure showed an almost immediate increase in O2 and reduction in CO2 concentration associated with decreasing systolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)