Microvolt T-Wave Alternans During Atrial and Ventricular Pacing

Introduction: Assessment of microvolt T-wave alternans (MTWA) by the spectral analysis (SA) method requires the heart rate to be stable within a certain range. This can be achieved by ventricular pacing (VP). We compared MTWA during short-term VP versus atrial pacing (AP).
Methods: Patients presenting for evaluation of risk of sudden cardiac death underwent an invasive electrophysiologic study. The concordance of results of MTWA-VP with MTWA-AP was evaluated, as well as the specificity, sensitivity, negative, and positive predictive values of MTWA-VP versus MTWA-AP. The maximum recorded amplitude of MTWA (MValt) in concordant positive results, as well as noise levels in all, were compared in both pacing modes.
Results: We studied 42 consecutive patients, of whom 31 completed both tests (32 by AP, 40 by VP). Compared to AP, VP—MTWA SA had a sensitivity of 93%, specificity of 71%, negative predictive value of 92%, and positive predictive value of 72%. The results were concordant in 25 patients (80%, κ= 0.62, P < 0.001). The noise level was significantly higher during VP than AP (1.4 ± 0.8 vs 1± 0.8, P< 0.01), and there was a trend toward a higher amplitude of TWA by VP (10.7 ± 5.3 vs 7.8 ± 3.9, P = 0.058).
Conclusions: MTWA SA is more likely to be completed during VP than AP. Overall there was concordance between both tests. VP generates higher amplitudes and noise, and a higher percentage of nonnegative results.     

Atrial Electromechanical Sequence and Contraction Synchrony during Single- and Multisite Atrial Pacing in Patients with Brady-Tachycardia Syndrome

Objectives: Investigation of which atrial pacing modality provides atrial synchrony and the most physiological atrial contraction pattern in patients with brady-tachycardia syndrome.
Methods: Fifteen healthy subjects and 57 patients with sinus node dysfunction, atrial fibrillation recurrences, and prolonged P-wave on the electrocardiogram treated with multisite atrial (MSA) pacing were studied. One atrial lead was implanted in the coronary sinus (CS) ostium area, the other at the right atrial appendage (RAA): RAA+CS group (28 patients), or Bachmann's bundle (BB) region: BB+CS group (29). Sinus rhythm (SR) and CS, RAA, BB, RAA+CS, and BB+CS pacing modalities were evaluated. Electromechanical delay (EMD) in atrial walls was assessed by tissue Doppler echocardiography. Interatrial (ΔinterA), intra-right (ΔRA), and intra-left (ΔLA) atrial dyssynchrony were calculated.
Results: During SR, in the study group versus controls, important ΔinterA: 55 ± 23 versus 22 ± 11 ms (P < 0.01) and ΔLA: 47 ± 21 versus 21 ± 6 ms (P < 0.001) were present. Single-site BB and both MSA pacing modes restored ΔinterA and ΔLA (ΔinterA: 24 ± 16, 20 ± 13 and 14 ± 9 ms, ΔLA: 28 ± 18, 28 ± 13 and 20 ± 10 ms during BB, RAA+CS and BB+CS pacing, respectively). CS pacing prolonged lateral RA EMD, while RAA pacing LA walls EMD, which resulted in ΔinterA persistence. CS pacing induced ΔRA (50 ± 23 vs 16 ± 8 ms, P < 0.0001 vs controls). Atrial contraction sequence during BB pacing resembled that observed in controls.
Conclusions: (1) Single-site BB and both MSA pacing modes restored atrial synchrony. (2) Single-site RAA and CS ostium pacing retained interatrial dyssynchrony; moreover, CS pacing created RA dyssynchrony. (3) Single-site BB pacing provided physiological atrial contraction sequence.     

Rate Augmentation and Atrial Arrhythmias in DDDR Pacing

SPENCER, W.H., ET AL.: Rate Augmentation and Atrial Arrhythmias in DDDR Pacing. Dual chamber, rate-modulated pacemakers provide the capability of augmenting the heart rate of patients with chronotropic incompetence but also may cause atrial arrhythmias because of high rate, competitive atrial pacing. We studied ten patients with two consecutive 24-hour Holter monitors during which they were alternately programmed to either DDD or DDDR pacing in random order. Maximum heart rates (max HR) were measured at every 15-minute interval during each 24-hour period. DDDR pacing showed rate augmentation, 80 ± 7 average max HR when compared with DDD pacing, average max HR 76 ± 5. These results were even more striking when waking hours (7 am to 10 pm) were compared: average max HR 86 ± 7 DDDR versus 78 ± 4 average max HR DDD. Several patients showed marked rate augmentation. Seven of ten patients preferred DDDR pacing over DDD pacing. In the entire population, DDDR pacing did not result in an increased number of atrial arrhythmias (1.25 atrial events 124 hour) when compared to DDD pacing (1.75 atrial events/ 24 hour). We conclude that DDDR pacing provides heart rate augmentation during daily life in a clinical population while not resulting in a significant increase in atrial arrhythmias. (PACE, Vol. 13, December, Part 11, 1990)     

Physiologic Pacing for Atrial Fibrillation Prevention in Sinus Node Disease: Long-Term Results

Background: Physiologic pacing has been demonstrated to be effective in preventing atrial fibrillation recurrences in patients with sinus bradycardia. Aim of the study was to evaluate long-term incidence of atrial fibrillation in a large population of patients affected by sinus node disease receiving physiologic pacing. Furthermore, predictors of arrhythmia recurrence and effect of pacing mode were investigated.
Population: Four hundred twenty-five patients (220 Male, 77 ± 9 years) were retrospectively analyzed: implanted system was AAI in 20.5% and DDD in 79.5%. Thirty-four percent had atrial fibrillation before implant.
Results: Follow-up lasted on average 51 ± 36 months (median 42, range 1 month–18 years). Sixty-six percent were on antiarrhythmic drug therapy. After 5 years, 89% survived, 74.5% had at least one episode of atrial fibrillation, 39.9% were submitted to electrical cardioversion, 67.2% were hospitalized because of cardiac causes, 33.3% developed permanent atrial fibrillation. Primary conduction system disease and valvular heart disease were independent predictors for atrial fibrillation recurrence. Preimplant atrial fibrillation predicted arrhythmia recurrence during the follow-up, but it did not predict development of permanent atrial fibrillation. AAI pacing, when compared with DDD, was associated to a lower rate of atrial fibrillation recurrences (AAI 28.7%, DDD 53.3%, P < 0.001).
Conclusion: In spite of expected benefits of physiologic pacing, the development of atrial fibrillation and permanent atrial fibrillation were quite common. The additional benefits of multifunction pacemakers designed to prevent and treat atrial fibrillation should be evaluated in controlled studies.     

Incidence of Atrial Fibrillation in Patients with Different Mode of Pacing. Long-term Follow-up

We evaluated the incidence of atrial fibrillation in 189 patients (92males, 97females, mean age 75 ± 12yrs, range 41–100yrs) with pacemaker, during a mean follow-up of 5.5yrs (range 1–24yrs). The indications for implant were: complete AV block (115pts), second degree Möbilz 2 AV block (51pts). bifascicular block (5pts). sick sinus syndrome (14pts), symptomatic bradycardia (4pts). The mode of stimulation considered were VVI (105pt), VVI rate responsive (21pts), single lead VDD (43pts), DDD (20pts). The occurrence of retrograde VA conduction in patients with VVI or VVI rate responsive pacing was also evaluated. Atrial fibrillation occurred in 40 pts (21%). The highest incidence was evidenced in patients with sick sinus syndrome (9pts, 64%), and in patients with VVI stimulation (28pts, 27%). On the contrary, the lowest incidence was found in single lead VDD stimulation (4pts, 9%). The patients with dual chamber pacing showed a relatively high incidence of the arrhythmia (5pts, 25%). Atrial fibrillation occurred in 9 out of 32 patients with retrograde VA conduction, and in 22 out of 94 patients without retrograde conduction (28% versus 23%, p=NS). In conclusion, it is confirmed that patients with sick sinus syndrome are at high risk for atrial fibrillation. Single lead VDD stimulation seems to be the better mode of pacing in preventing atrial fibrillation, while dual chamber pacing showed minor efficacy. The presence of retrograde VA conduction could not predict the occurrence of the arrhythmia.     

DDD Pacing: An Effective Treatment Modality for Recurrent Atrial Arrhythmias

We performed atrial EP studies (atrial substrate evaluation) on 10 patients. These patients had evidence of paroxysmal, sustained, recurrent atrial arrhythmias (7 men and 3 women with a mean age of 64 ± 15 years). All patients combined a brady-tachy syndrome; 7 patients had a sick sinus syndrome (SSS) and 3 patients a typical vagally induced atrial arrhythmia. No anti-arrhythmic drug was allowed in 3 patients with SSS, 1 drug failed in 4 patients and the combination of 2 drugs failed in 3 patients during the first to eighth years prior to pacemaker implantation. Atrial substrate evaluation was feasible in all these patients off anti-arrhythmic therapy and showed important abnormalities of atrial loco-regional conduction parameters and long refractory periods (RP). The remarkable point was, in 7 patients, a paradoxical improvement in intra-atrial conduction delay at rapid pacing rate. The DDD pacing mode was chosen in all patients. No technical problem occurred during implantation. Atrial pacing rate was programmed to be slightly higher than the mean diurnal heart rate calculated on Holter monitoring. After implantation, the mean follow-up period was 18 ± 25 months with an average of one Holter every 4 months during the first 2 years. The 7 patients who improved intra-atrial conduction at rapid pacing rate were controlled without drugs, 2 patients were controlled with 1 drug, and 1 patient with 2 drugs. Atrial pacing in the DDD mode in a selected group of patients prevents paroxysmal and drug-resistant atrial arrhythmias. Atrial substrate evaluation is a sensitive tool for assuring the long-term benefit of atrial pacing. In this subset of patients, maintenance of AV synchrony by DDD pacing is preferable to catheter ablation of the His bundle.     

Long-Term Effects of Dynamic Atrial Overdrive Pacing on Sleep-Related Breathing Disorders in Pacemaker or Cardioverter Defibrillator Recipients

Introduction: Sleep-related breathing disorders occur in 20–30% of Europeans and North Americans, including 10% of sleep apnea syndrome (SAS). A preliminary study suggested that atrial overdrive pacing with a fixed heart rate might alleviate SAS. However, it is not known whether dynamic atrial overdrive pacing alleviates SAS.
Methods: Patients with indications for a dual chamber pacemaker or implantable cardioverter-defibrillator (ICD) were screened for SAS using the Pittsburgh Sleep Quality Index (PSQI) questionnaire. If PSQI was >5, cardio-respiratory polygraphy was performed before and 4 and 7 months after device implantation. Patients were randomized to algorithm ON–OFF (group A) or OFF–ON (group B) and the apnea-hypopnea index (AHI) was measured.
Results: Out of 105 consecutive patients, 46 (44%) had a positive PSQI. This analysis included 12 patients (mean age = 61 ± 10 years, body mass index 28.9 ± 6.5 kg/m², left ventricular ejection fraction = 38.3 ± 13.6%; 10 men). All patients suffered from obstructive or mixed SAS. There were no significant differences in PSQI or AHI between baseline and follow-up or between the two study groups. Therefore, the study was terminated ahead of schedule.
Conclusions: The prevalence of obstructive or mixed SAS was high in pacemaker or ICD recipients and reduced left ventricular ejection fraction. In these patients, long-term dynamic atrial overdrive pacing using did not improve PSQI or SAS. Therefore, patients with relevant obstructive or mixed SAS should not be offered atrial pacing therapy.     

Heart Rate Turbulence after Ventricular Pacing Trains During Programmed Ventricular Stimulation

Background: This study tested the hypothesis that heart rate turbulence (HRT) following ventricular pacing trains depends on train cycle length, presence of retrograde ventriculoatrial (VA) conduction, and left ventricular (LV) function.
Methods: We analyzed digital recordings of programmed ventricular stimulation (PVS) performed in 82 patients (57 men) referred for electrophysiologic studies of ventricular arrhythmias, whose mean age was 64 ± 12 years and LV ejection fraction (EF) was 47 ± 15%. Profiles of sinus RR intervals after all available 8-beat ventricular pacing trains (600-and 400-ms) were averaged. Heart rate turbulence slope (HRTS) was analyzed as the maximum positive slope of a regression line through a sequence of 2–5 (HRTS2 - HRTS5) consecutive RR intervals within the first 5 RR intervals after the pacing train.
Results: Dynamics of RR intervals had biphasic and monophasic patterns, in patients with and without VA conduction, respectively. Sinus nodal response was less prominent after 600-ms than 400-ms pacing trains. After 400-ms pacing trains, HRTS was significantly shallower in patients with LVEF ≤40% than in those with LVEF >40%. HRTS4 was the best discriminator between the two groups (6.8 ± 8.6 ms/RR vs 19.6 ± 26.0 ms/RR, P = 0.017).
Conclusion: In patients with VA conduction, HRT after ventricular pacing trains reflects a combination of vagal withdrawal due to transient hypotension and suppression of sinus node automaticity. Attenuation of vagal modulation was detected in patients with LV dysfunction during standard PVS.     

Organized incessant atrial arrhythmias in the setting of severe, isolated biatrial scarring

Introduction: Diffuse transmural fibrosis and scarring limited to the area without atrial dilation or significant structural heart or other systemic disease has not been reported. We present three cases of a syndrome characterized by refractory organized atrial arrhythmias, diffuse atrial scarring with electrical silence, and mechanical paralysis in the absence of atrial dilation or any systemic or neurodegenerative disorders.
Methods: Patients referred for electrophysiology study of atrial arrhythmias were included. Electroanatomic mapping with the Carto system (Biosense Webster, Diamond Bar, CA, USA) and magnetic resonance imaging ( MRI) with scar sequencing were performed.
Results: There was no family or personal history of cardiac, muscular, or developmental diseases. All patients had organized atrial arrhythmias. Echocardiograms showed atrial standstill with normal atrial and ventricular dimensions. No other structural abnormalities were noted. Carto mapping revealed severe biatrial diffuse scarring. The left atrial (LA) was less affected than the right atrial (RA). MRI findings confirmed biatrial scarring. During tachycardia, islands of dissociated electrical activity could be seen in the right atria. Entrainment mapping was not performed in the atria as high-output pacing could not capture the atria. Coronary sinus entrainment demonstrated the coronary sinus (CS) not to be critical to the tachycardia. Ablation was targeted toward channels of low voltage but was not successful in any cases. All required atrioventricular (AV) nodal ablation with pacing.
Conclusion: An association between biatrial cardiomyopathy and scarring with normal atrial dimensions has been described. Since severe scarring has not been reported with organized arrhythmias this may represent a new syndrome.     

Long-term Survival of VDD Pacing

All patients with VDD systems implanted at a tertiary pacing center were identified from a computer database and data collected on pacing indications, follow-up duration, rate response, reasons for programming changes, and implant P wave amplitudes. Results: 366 implants were identified for which complete data were available for 335 leads implanted in 316 patients. The mean follow-up period was 24.1 months, and age at implant was 73.5 ± 11.8 years. During follow-up, 19 patients died (6%) and 62 (19.6%) were followed elsewhere. Indications for pacing were complete heart block, 56.6%; intermittent AV block, 21.8%; postablation complete heart block, 5.4%; 2:1 AV block, 13%; and others, 3.2%. Two groups: no mode change (NMC, n = 280) and mode change (MC, n = 36) were identified. Reasons for reprogramming in the MC group were as follows: atrial sensing, 11; AF/atrial flutter, 18; chronotropic incompetence, 3; and others 4. Significantly more MC patients had rate response programmed ON (44.4% vs 22.1%, P < 0.05). No significant differences between the two groups were found in other variables, including male gender (55.5% vs 54.6%), length of follow-up (27.1 ± 17.8 vs 23.8 ± 20.6 months), age at last follow-up (72 ± 12.3 vs 75.9 ± 11.9years), and P wave amplitude (1.7 ± 0.9 vs 1.8 ± 0.9mV). Conclusion: Reprogramming of VDD systems is infrequent. When necessary, it is usually prompted by atrial arrhythmias or failure of atrial sensing. When adequate atrial chronotropy has been verified, VDD is an acceptable alternative to DDD pacing and survives well over the long term.     

Comparison of Resting Hemodynamic Indices and Exercise Performance During Atrial Synchronized and Asynchronous Ventricular Pacing

Resting hemodynamic indices and exercise tolerance were measured during atrial synchronized (VAT) and asynchronous ventricular pacing (VOO) in 35 patients with implanted pacemakers which could be externally programmed to function in either pacing mode. Cardiac output and mean systemic arterial pressure were significantly greater during VAT pacing (VAT: 4.5 ± 1.21 /min, 115 ± 28 mmHg; VOO: 3.7 ± 0.8 1/min 105 ± 25 mmHg respectively), although there was no difference in pulmonary artery end-diastolic pressure. Maximal exercise performance was assessed using the Bruce protocol in both pacing modes. Neither the patient nor the supervising physician was aware of the preselected pacing mode; a second physician monitored the electrocardiogram and blood pressure but influenced the point of exercise termination only if a potentially dangerous arrhythmia or hypotension occured. Blood pressure responses were superior and atrial rates lower during VAT pacing, In all but five patients, exercise tolerance was improved by VAT pacing. This amounted to 33 percent or more in 23/35 patients. This improvement was shown to be maintained in the 20 patients who had repeat exercise tests several weeks later. Ventricular arrhythmias, hypotension, and lightheadedness frequently complicated exercise during asynchronous pacing but occurred rarely with atrial synchronized pacing. Resting hemodynamic indices did not predict the extent of improvement gained by physiological pacing.     

The Induction of Atrial Flutter and Fibrillation and the Termination of Atrial Flutter by Esophageal Pacing

In patients with Wolff-Parkinson-White syndrome (WPW), it is important to assess the ventricular response during atrial flutter or fibrillation since conduction across the accessory pathway during these atrial rhythms may cause hemodynamic impairment or life-threatening ventricular arrhythmias. We have recently reported the effective use of an esophageal electrode in pacing the atrium. In this study we praspectively assessed the ability to induce atrial flutter and fibrillation by esophageal pacing in 23 patients with WPW or other electrophysiological abnormalities. An esophageal bipolar electrode with 29 mm interelectrode distance was positioned in the esophagus to record the most rapid and largest esophageal electrogram (mean distance of 36.6 ± 2.9 cm (SD) from the nares). Pacing was performed at cycle lengths of 40–340 ms (mean 166 ± 72), pulse durations of 7.0–9.9 ms, and currents of 10–25 mA. Atrial flutter alone was induced in 6 patients, fibrillation alone in 11 patients, and both arrhythmias in 5 patients, In one patient neither flutter nor fibrillation was induced by esophugeal pacing, and fibrillation was induced only with difficulty using intracavitary pacing. Of the 11 patients with flutter, the arrhythmia was terminated in 8 by esophageal pacing at cycle lengths of 160–220 ms fmean 176 ± 18 ms). All patients tolerated the procedure well with only mild to moderate discomfort. Therefore, esophageal pacing appears to offer an effective, well tolerated method of initiating atrial fibrillation and flutter and terminating atrial flutter and offers a potentially useful noninvasive method of following patients serially.     

Impact of Temporary Interruption of Right Ventricular Pacing for Heart Block on Left Ventricular Function and Dyssynchrony

Background: The increasing data suggest an association between chronic right ventricular (RV) and left ventricular (LV) dysfunction. We sought to determine the effect of temporary interruption of long-term RV pacing on LV function and mechanical dyssynchrony in children and young adults with complete heart block.
Methods: Twelve patients aged 20.0 ± 7.4 years with congenital heart block (group I) and six patients aged 22.7 ± 11.0 years with surgically acquired heart block (group II) with RV pacing were studied. The pacing rate was reduced to less than patient's intrinsic heart rate and maintained for 5 minutes. The LV ejection fraction (EF), three-dimensional systolic dyssynchrony index (SDI), two-dimensional global longitudinal strain and strain rate, and Doppler-derived isovolumic acceleration before and after interruption of RV pacing were compared.
Results: The LVEF and GLS increased while QRS duration decreased after the pacing interruption in both the groups (all P < 0.05). While SDI decreased in both groups I (6.8 ± 2.3%– 3.8 ± 0.8%, P = 0.001) and II (9.2 ± 4.1 %– 5.0 ± 1.6%, P = 0.032), it remained higher in group II than in group I (P = 0.046) after the pacing interruption. The prevalence of LV dyssynchrony (SDI > 4.7%) decreased in group I (83 %– 25%, P = 0.006) but not in group II (67 %– 50%, P = 0.50). The %increase in LVEF correlated positively with %reduction of LV SDI (r = 0.80, P = 0.001).
Conclusions: Temporary interruption of chronic RV pacing acutely improves LV dyssynchrony and systolic function in children and young adults, the magnitude of which is greater in patients with congenital than those with surgically acquired heart block. (PACE 2010; 41–48)     

Asymmetric dimethylarginine concentration and early recurrence of atrial fibrillation after electrical cardioversion

Background: The purpose of this study was to determine whether high asymmetric dimethylarginine (ADMA) levels could predict early recurrence of atrial fibrillation (AF) after successful electrical cardioversion (CV).
Methods : Seventy patients with persistent AF, but without known heart disease, who underwent elective electrical CV were enrolled. Blood samples for ADMA determination were drawn from all patients just before the CV.
Results : The study population comprised 64 patients (men 73%, age 62.56 ± 7.72 years, duration of AF 6.00 ± 1.90 months) in whom sinus rhythm was restored. After 1-month follow-up, 30 (47%) patients had recurrence of AF. The median ADMA concentration was significantly higher in patients with AF recurrence (1.93 μmol/L vs 1.43 μmol/L; P = 0.001). AF recurrence was associated with higher pre-CV ADMA levels (odds ratio [OR]= 4.20; 95% confidence interval [CI], 1.44–12.22; P = 0.001). On multivariate analysis, ADMA was the only independent predictor of arrhythmia recurrence (OR = 4.19; 95%CI, 1.12–15.77; P = 0.034).
Conclusion : Our data suggest that high levels of ADMA are associated with an increased risk of AF recurrence within 1 month after electrical CV, supporting the hypothesis that ADMA might participate in the process of atrial remodeling.     

Backup Right Ventricular Pacing with a 0.035" Guidewire during Implantation of Left Ventricular Leads

Introduction: During implantation of biventricular devices, manipulation of the guiding sheath during localization of the coronary sinus (CS) ostium may result in injury to the right bundle and complete heart block. A preventive measure is to implant the right ventricular (RV) lead first, though this may interfere with manipulation of the guiding sheath and dislodge the permanent lead . We tested the feasibility of backup pacing with a 0.035" guidewire, advanced through the guiding sheath during CS localization.
Methods: One hundred six consecutive patients (mean age = 70 ± 11 years, 81 men) undergoing biventricular device implantation were studied. A 0.035" guidewire with an uncoated tip was advanced into the right ventricle through the guiding sheath, and unipolar capture threshold, R-wave sensing amplitude, and pacing impedance were measured.
Results: RV pacing was successful in all patients. The mean capture threshold was 3.8 ± 2.1 V/0.5 ms, R-wave amplitude 5.4 ± 4.3 mV, and pacing impedance 226 ± 78 Ω. No arrhythmia was observed during the tests. Two patients developed complete heart block during the implant procedure and were successfully paced temporarily using the 0.035" guidewire.
Conclusion: Temporary RV pacing, using a 0.035" guidewire within the guiding sheath, is a simple, reliable, and safe method that allows backup pacing in case of traumatic complete heart block, developing during the implantation of biventricular devices.     

Dofetilide for Atrial Arrhythmias in Congenital Heart Disease: A Multicenter Study

Background: Very little is known about use of the class III antiarrhythmic dofetilide in patients with congenital heart disease (CHD).
Methods: A multicenter retrospective review of experience with dofetilide in CHD patients was undertaken.
Results: Twenty adults with CHD and refractory atrial arrhythmias were treated with dofetilide at four institutions over a 7-year period. Three (15%) experienced adverse effects during in-hospital initiation of dofetilide (two with torsade de pointes, one with excessive QTc prolongation) and were not continued on this therapy. The remaining 17 were discharged taking dofetilide, with either resolved or improved arrhythmia. One was lost to follow-up. Five subsequently discontinued dofetilide due to waning effectiveness, manifest by recurrence of their arrhythmias. Eleven (55%) remained on dofetilide at most recent visit, with a median follow-up of nearly 1 year. Seven of these 11, or 35% of the CHD patients originally started on dofetilide, experienced a complete resolution of their arrhythmia. The remaining four had breakthrough episodes of atrial arrhythmia, but remained on dofetilide. No patient experienced torsade de pointes after the in-hospital initiation period.
Conclusions: Used appropriately, dofetilide appears to be a viable adjunct to catheter-based ablation and alternative pharmacological approaches for the treatment of atrial arrhythmias in adult patients with congenital heart disease.     

The Effects of Rate-Adaptive Atrial Pacing Versus Ventricular Backup Pacing on Exercise Capacity in Patients with Left Ventricular Dysfunction

Background: Atrial rate-adaptive pacing may improve cardiopulmonary reserve in patients with left ventricular dysfunction.
Methods: A randomized, blinded, single-crossover design enrolled dual-chamber implantable defibrillator recipients without pacing indications and an ejection fraction ≤40% to undergo cardiopulmonary exercise treadmill stress testing in both atrial rate-adaptive pacing (AAIR) and ventricular demand pacing (VVI) pacing modes. The primary endpoint was change in peak oxygen consumption (VO₂). Secondary endpoints were changes in anaerobic threshold, perceived exertion, exercise duration, and peak blood pressure.
Results: Ten patients, nine males, eight with New York Heart Association class I, mean ejection fraction 24 ± 7%, were analyzed. Baseline VO₂ was 3.6 ± 0.5 mL/kg/min. Heart rate at peak exercise was significantly higher during AAIR versus VVI pacing (142 ± 18 vs 130 ± 23 bpm; P = 0.05). However, there was no difference in peak VO₂ (AAIR 23.7 ± 6.1 vs VVI 23.8 ± 6.3 mL/kg/min; P = 0.8), anaerobic threshold (AAIR 1.3 ± 0.3 vs VVI 1.2 ± 0.2 L/min; P = 0.11), rate of perceived exertion (AAIR 7.3 ± 1.5 vs VVI 7.8 ± 1.2; P = 0.46), exercise duration (AAIR 15 minutes, 46 seconds ± 2 minutes, 54 seconds vs VVI 16 minutes, 3 seconds ± 2 minutes, 48 seconds; P = 0.38), or peak systolic blood pressure (AAIR 155 ± 22 vs VVI 153 ± 21; P = 0.61) between the two pacing modes.
Conclusion: In this study, AAIR pacing did not improve peak VO_2, anaerobic threshold, rate of perceived exertion, or exercise duration compared to VVI backup pacing in patients with left ventricular dysfunction and no pacing indications.     

Feasibility Of Temporary Biventricular Pacing In Patients With Reduced Left Ventricular Function After Coronary Artery Bypass Grafting

Background and Methods: Biventricular pacing improves hemodynamics after weaning from cardiopulmonary bypass in patients with severely reduced left ventricular (LV) function undergoing coronary artery bypass grafting (CABG). We examined the feasibility of temporary biventricular pacing for 96 hours postoperatively. Unipolar epicardial wires were placed on the roof of the right atrium (RA), the right ventricular (RV) outflow tract, and the LV free lateral wall and connected to an external pacing device in 51 patients (mean LV ejection fraction 35 ± 4%). Pacing and sensing thresholds, lead survival and incidence of pacemaker dysfunction were determined.
Results: Atrial and RV pacing thresholds increased significantly by the 4th postoperative day, from 1.6 ± 0.2 to 2.5 ± 0.3 V at 0.5 ms (P = 0.03) at the RA, 1.4 ± 0.3 V to 2.7 ± 0.4 mV (P = 0.01) at the RV, and 1.9 ± 0.6 V to 2.9 ± 0.7 mV (P = 0.3) at the LV, while sensing thresholds decreased from 2.0 ± 0.2 to 1.7 ± 0.2 mV (P = 0.18) at the RA, 7.2 ± 0.8 to 5.1 ± 0.7 mV (P = 0.05) at the RV, and 9.4 ± 1.3 to 5.5 ± 1.1 mV (P = 0.02) at the LV. The cumulative overall incidence of lead failure was 24% by the 4th postoperative day, and was similar at the RV and LV. We observed no ventricular proarrhythmia due to pacing or temporary pacemaker malfunction.
Conclusions: Biventricular pacing after CABG using a standard external pacing system was feasible and safe.     

Atrial Arrhythmia Management with Sensor Controlled Atrial Refractory Period and Automatic Mode Switching in Patients with Minute Ventilation Sensing Dual Chamber Rate Adaptive Pacemakers

Although a long postventricular atrial refractory period fPVARP) may prevent the occurrence of pacemaker mediated tachycardias and inadvertent tracking of atrial arrhythmias in dual chamber (DDD) pacing, the maximum upper rate will necessarily be compromised. We tested the feasibility of using minute ventilation sensing in a dual chamber rate adaptive pacemaker (DDDR) to shorten the PVARP during exercise in 13 patients with bradycardias (resting PVARP = 463 ± 29 msec) to avoid premature upper rate behavior. Graded treadmill exercise tests in the DDD and DDDR modes at this PVARP resulted in maximum ventricular rates of 98 ± 8 and 142 ± 3 beats/min, respectively (P < 0.0001), due to chronotropic incompetence and upper rate limitation in the DDD mode, both circumvened with the use of sensor. In order to simulate atrial arrhythmias, chest wall stimulation was applied for 30 seconds at a rate of 250 beats/min at a mean unipolar atrial sensitivity of 0.82 mV. Irregular ventricular responses occurred in the DDD mode fthe rates at a PVARP of 280 and 463 ± 29 msec were, respectively 92 ± 5 and 66 ± 3 msec; P < 0.0001). In the DDDR mode at a PVARP of 463 ± 29 msec, regular ventricular pacing at 53 ± 2 beats/min occurred due to mode switching to VVIR mode in the presence of repetitive sensed atrial events within the PVARP. One patient developed spontaneous atrial fibrillation on follow-up, which was correctly identified by the pacemaker algorithm, resulting in mode switch from DDDR to regular VVIR pacing and preservation of rate response. In conclusion, sensor controlled PVARP allows a long PVARP to be used at rest without limiting the maximum rate during exercise. In addition, to offer protection against retrograde conduction, a long PVARP and mode switching also limit the rate during atrial arrhythmias and allow regular ventricular rate responses according to the physiological demands.     

Type II Atrial Flutter Interruption with Transesophageal Pacing: Use of Propafenone and Possible Change of the Substrate

Type II atrial flutter (AFII) is an arrhythmia which usually cannot be interrupted by atrial pacing: the underlying mechanism is considered to be a leading circle without an excitable gap. We investigated whether the administration of propafenone, an antiarrhythmic drug, which primarily decreases conduction velocity, has a beneficial effect on AFII interruption using transesophageal pacing. Twelve patients with an AFII were randomized into 2 groups in which pacing was performed without treatment (group A) or two hours after the administration of 600 mg of oral propafenone (group B). Sinus rhythm was attained in 0 of 6 patients in group A and in 4 of 6 patients in group B (P < 0.05). The baseline mean cycle length was the same in both groups (175 ± 7 (A) vs 168 ± 8 ms (B); it lengthened significantly after the administration of propafenone (219 ± 33 vs 168 ± 8 ms; P < 0.05). Propafenone did not significantly lengthen the cycle in the two patients in whom interruption of the arrhythmia was impossible. Our data show that propafenone has a facilitating effect on atrial pacing only when it significantly prolongs the cycle length of the arrhythmia, possible expression of a conversion of AFII into type I, with an anatomical substrate and an excitable gap allowing arrhythmia capture and interruption. In the two patients in whom sinus rhythm was not restored, the absence of a direct dependence of the cycle length on the change in conduction velocity induced by propafenone may be explained by the persistence of a functionally determined circuit, resistant to atrial pacing.