Right Ventricular Electrogram Research Articles

Characteristics and Clinical Value of Electroanatomic Voltage Mapping in Cardiac Amyloidosis

BackgroundCardiac amyloidoses (CAs) are an increasingly recognised group of infiltrative cardiomyopathies associated with high risk of adverse cardiac events. We sought to characterise the characteristics and clinical value of right ventricular (RV) electroanatomic voltage mapping (EVM) in CA. MethodsFifteen consecutive patients undergoing endomyocardial biopsy (EMB) for suspected CA (median age 75 years, 1st-3rd quartiles 64-78 years], 67% male) were enrolled in an observational prospective study. Each patient underwent RV high-density EVM using a multipolar catheter and EMB. The primary outcome was death or heart failure hospitalisation at 1-year follow-up. We recorded electrographic features at EMB sampling sites and electroanatomic data in the overall RV, and explored their correlations with histopathologic findings and primary outcomes events. ResultsA final EMB-proven diagnosis of immunoglobulin light chain or transthyretin CA was formulated in 6 and 9 patients, respectively. Electrogram amplitudes in the bipolar and unipolar configurations averaged 1.55 ± 0.44 mV and 5.14 ± 1.50 mV, respectively, in the overall RV, with lower values in AL CA patients. We found a significant inverse correlation between both bipolar and unipolar electrogram amplitude and amyloid burden according to EMB (P = 0.001 and P = 0.025, respectively). At 1-year follow-up, 7 patients (47%) experienced a primary outcome event; the extent of bipolar dense scar area at RV EVM was an independent predictor of primary outcome events at multivariable analysis (odds ratio 2.40; P = 0.037). ConclusionsIn CA, electrogram amplitudes are around the lower limit of normal yet disproportionately low compared with the increased wall thickness. Out data suggest that RV electrogram amplitude may be a quantitative marker of amyloid burden, and that RV EVM may have prognostic value.

High rate pacing guided by short-term variability of repolarization prevents imminent ventricular arrhythmias autonomically by an ICD

Abstract Background The anesthetized, chronic complete atrioventricular block (CAVB) dog model allows reproducible inducibility of Torsade de Pointes (TdP) arrhythmias due to ventricular remodeling and after a challenge with an IKr-blocker. High rate pacing (HRP) prevents ventricular arrhythmias, but has long-term detrimental effects on cardiac function when applied continuously. Temporal dispersion of repolarization, quantified as short-term variability (STV), increases prior to ventricular arrhythmias and has been proposed as a marker to guide HRP. Purpose A proof-of-principle study to show STV determined automatically and in real-time by an ICD can guide HRP to prevent imminent ventricular arrhythmias. Methods Eight CAVB dogs were implanted with an ICD (Medtronic, lead in the right ventricular (RV) apex), with software to automatically determine STV online (STV-ICD). STV was determined from the activation recovery interval (ARI) of 31 consecutive beats with the formula: STV = Σ|ARI(n+1) − ARI(n)|/(N*√2). The CAVB dogs were challenged twice with dofetilide (0.025 mg/kg i.v. in 5 minutes or until the first TdP). In the first experiment, the individual STV-ICD threshold was determined prior to the first arrhythmic event and programmed into the ICD. In a serial experiment, HRP was initiated automatically once the STV-ICD threshold was reached, by gradually increasing the heart rate to 100 bpm. Occurrence of TdPs was monitored for 10 minutes from the start of dofetilide infusion in both experiments. During HRP, STV was measured offline from RV electrograms (EGM) and left ventricular (LV) monophasic action potential durations (MAPD) (STV-offline). Results During the inducibility experiment, 8/8 dogs had repetitive TdPs and STV-ICD increased from 0.96±0.42 to 2.10±1.26 ms* (*p<0.05). During the prevention experiment, all dogs reached the STV threshold. HRP decreased STV-offline from 2.02±1.12 to 0.78±0.28 ms*, which was accompanied by prevention of TdPs in 7/8 dogs* (Figure 1). Conclusion Temporal dispersion of repolarization, quantified as STV, can guide HRP automatically by an ICD to prevent ventricular arrhythmias. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Dutch Heart Foundation Public Private Partnership

Beat-to-beat variations in activation-recovery interval derived from the right ventricular electrogram can monitor arrhythmic risk under anesthetic and awake conditions in the canine chronic atrioventricular block model

In the chronic atrioventricular block (CAVB) dog model, beat-to-beat variation of repolarization in the left ventricle (LV) quantified as short-term variability of the left monophasic action potential duration (STVLVMAPD) increases abruptly upon challenge with a proarrhythmic drug. This increase occurs before the first ectopic beat (EB), specifically in subjects who demonstrate subsequent repetitive torsades de pointes arrhythmias (TdP). The purpose of this study was to demonstrate that STV is feasible to monitor arrhythmic risk through use of the intracardiac electrogram (EGM) derived from the right ventricular (RV) lead from pacemakers or implantable cardioverter-defibrillators. In 30 anaesthetized, inducible (≥3 TdP) CAVB dogs, STV between LV and RV monophasic action potential duration (STVLVMAPD and STVRVMAPD) was compared. In prospectively enrolled CAVB dogs, STV of the activation-recovery interval (ARI) derived from the RV EGM (STVRVARI) was measured before and after a challenge with dofetilide under anesthesia (2a; n = 10) and cisapride under awake conditions (2b; n = 8). Both STVLVMAPD and STVRVMAPD increased before the first EB (1.29 ± 0.58 ms to 3.05 ± 1.70 ms and 1.11 ± 0.53 ms to 2.18 ± 1.43 ms, respectively; P = 0.001). STVRVARI increased from 2.82 ± 0.33 ms to 3.77 ± 0.69 ms (P = .001). Inducible subjects (4/8) showed an increase in STVRVARI from 2.65 ± 0.55 ms to 3.45 ± 0.33 ms (in the first hour; P = .02) and 4.20 ± 1.33 ms (before the first EB; P = .04). Behavior of STV from the RV and LV is comparable. STVRVARI increases significantly before the occurrence of an arrhythmia in awake and anaesthetized conditions. This finding can be integrated into devices to monitor arrhythmic risk.

The concept of triple wavefront fusion during biventricular pacing: Using the EGM to produce the best acute hemodynamic improvement in CRT.

Previous reports suggest that biventricular pacing (BiVp) fused with intrinsic conduction (BiVp-fusion, triple wavefront fusion) is associated with improved resynchronization compared to pure-BiVp in cardiac resynchronization therapy (CRT). This study aimed to assess the association between acute hemodynamic benefit of CRT and signs of BiVp-fusion by using a novel electrogram (EGM)-based method. In 17 patients undergoing CRT implantation, 28 combinations of atrioventricular (AV) and interventricular (VV) delays were applied while invasively measuring acute hemodynamic response based on maximum rate of left ventricular (LV) pressure rise (LV dP/dtmax ) to assess optimal BiVp settings. BiVp-fusion was noted if farfield signal (caused by first intrinsic ventricular depolarization) was seen prior to right ventricular (RV) pacing (RVp) artifact on integrated bipolar RV EGM, or QRS morphology changed compared to pure-BiVp (short AV-delay) as seen on electrocardiogram (ECG). Mean optimal RVp timing was at 98 ± 17% of intrinsic right atrial (RA)-RVfarfield (interval from right atrial pace or sense to RV farfield signal) interval, while preactivating the LV at 50 ± 11% of RA-RVsense (interval from right atrial pace or sense to RV sense interval) interval. BiVp-fusion was noted in 16 of 17 (94%) patients on ECG during optimal BiVp. Eight of these patients showed intrinsic farfield signal prior to RVp artifact on RV EGM. In the remaining eight, the RVp was paced just within the RA-RVfarfield interval with a mean of 25 ± 14 ms prior to the onset; therefore, the intrinsic farfield was masked. Optimal hemodynamic BiVp facilitates triple wavefront fusion, by pacing the RV around the onset of intrinsic farfield signal on RV EGM, while preactivating the LV. Aiming at BiVp-fusion could be a target for noninvasive EGM-based CRT device setting optimization.

Alternans of the Ventricular Electrogram in Patients with an Implanted Cardioverter-Defibrillator

The occurrence and significance of alternans of the ventricular electrogram (VEGM) in patients with an implanted cardioverter-defibrillator (ICD) has been rarely reported. This report describes our observations of VEGM alternans documented in nine patients with an ICD (seven new cases and two previously published cases for comparison). We found seven new cases of near-field VEGM alternans and added two of our previously reported examples. Catecholaminergic polymorphic ventricular tachycardia (CPVT) was diagnosed in one patient based on ICD recordings. Alternans occurred during ventricular tachycardia (VT) in eight patients. A fast sinus tachycardia could not be ruled out in one patient. Stable cycle length alternans was found in five patients. QRS alternans of the left ventricular (LV) electrogram (EGM) was recorded in all five patients who had a device for cardiac resynchronization therapy capable of sensing by the LV channel. These five cases exhibited corresponding alternans of the right ventricular (RV) EGM in three cases, none in one patient, and a questionable recording in another. Alternans of the far-field (FF) VEGM occurred simultaneously with RV EGM alternans in all four patients whose device provided an FF tracing. Ventricular alternans may be more common than realized in ICD patients with VT. The correlation of VEGM alternans with the surface electrocardiogram remains unknown. Although QRS alternans itself as an electrical pattern is generally benign, its cause may not be, as illustrated in our patient with CPVT. Furthermore, associated cycle length alternans or undersensing of the smaller alternans component may complicate ICD therapy.

Longitudinal Changes in Intracardiac Repolarization Lability in Heart Failure Patients with Implantable Cardioverter-Defibrillator

Background: While it is known that elevated baseline intracardiac repolarization lability is associated with the risk of fast ventricular tachycardia (FVT) /ventricular fibrillation (VF) in heart failure (HF), the effect of its longitudinal changes on the risk of FVT/VF is unknown. Methods: Near-field (NF) right ventricular (RV) intracardiac electrograms (EGMs) were recorded every 3-6 months at rest in 248 patients with structural heart disease, systolic HF (mean age 61.2613.3; 185[75%] male; 162[65.3%] ischemic cardiomyopathy) and implanted cardioverter-defibrillator (ICD) or cardiac resynchronization therapy defibrillator (CRT-D) [201 (81%) primary prevention]. Intracardiac beat-to-beat QT variability index (QTVINF) was measured on NF RV EGM. During the first study phase (median 18 months), participants made on average 2.4 visits. Then remote follow-up was continued for an additional median period of 3 years. Results: Average QTVINF did not change during the first year after ICD implantation (-0.34260.603 at baseline vs. -0.26260.552 at 6 months vs. -0.33460.603 at 12 months); however, it decreased thereafter (-0.51060.603 at 18 months; P50.042). Adjusted populationaveraged GEE model showed that the odds of developing FVT/VF increased by 75% for each 1 unit increase in QTVINF. (OR 1.75 [95%CI 1.05-2.92]; P50.031). However, individual patient-specific QTVINF trends (increasing, decreasing, flat) varied from patient to patient. For a given patient, the odds of developing FVT/VF were not associated with increasing or decreasing QTVINF over time (OR 1.27; [95%CI 0.05-30.10]; P5 0.881). Figure 1A,B shows population-averaged longitudinal trends in patients with and without FVT/VF. Figure 1C,D shows patient-specific longitudinal trends. Conclusion: While on average the odds of FVT/VF increased with an increase in QTVINF, patient-specific longitudinal trends in QTVINF did not affect the odds of FVT/VF.

Longitudinal changes in intracardiac repolarization lability in patients with implantable cardioverter-defibrillator

Background: While it is known that elevated baseline intracardiac repolarization lability is associated with the risk of fast ventricular tachycardia (FVT)/ventricular fibrillation (VF), the effect of its longitudinal changes on the risk of FVT/VF is unknown.Methods and Results: Near-field (NF) right ventricular (RV) intracardiac electrograms (EGMs) were recorded every 3–6 months at rest in 248 patients with structural heart disease [mean age 61.2 ± 13.3; 185(75%) male; 162(65.3%) ischemic cardiomyopathy] and implanted cardioverter-defibrillator (ICD) or cardiac resynchronization therapy defibrillator (CRT-D) [201 (81%) primary prevention]. Intracardiac beat-to-beat QT variability index (QTVINF) was measured on NF RV EGM. During the first study phase (median 18 months), participants made on average 2.4 visits. Then remote follow-up was continued for an additional median period of 3 years. Average QTVINF did not change during the first year after ICD implantation (−0.342 ± 0.603 at baseline vs. −0.262 ± 0.552 at 6 months vs. −0.334 ± 0.603 at 12 months); however, it decreased thereafter (−0.510 ± 0.603 at 18 months; P = 0.042). Adjusted population-averaged GEE model showed that the odds of developing FVT/VF increased by 75% for each 1 unit increase in QTVINF. (OR 1.75 [95%CI 1.05–2.92]; P = 0.031). However, individual patient–specific QTVINF trends (increasing, decreasing, flat) varied from patient to patient. For a given patient, the odds of developing FVT/VF were not associated with increasing or decreasing QTVINF over time [OR 1.27; (95%CI 0.05–30.10); P = 0.881].Conclusion: While on average the odds of FVT/VF increased with an increase in QTVINF, patient-specific longitudinal trends in QTVINF did not affect the odds of FVT/VF.

Right Ventricular Pacing and Sensing Function in High Posterior Septal and Apical Lead Placement in Cardiac Resynchronization Therapy

BackgroundThe conventional right ventricular (RV) lead position in cardiac resynchronization therapy pacemakers (CRT-P) is the RV apex (RV-A). Little is known about electrophysiological stability and associated complications of pacing leads in RV high posterior septal (RV-HS) position in CRT-P. MethodsTwo hundred and thirty-five consecutive CRT-P patients were included from 1999-2010. Pacing thresholds at 0.5ms and 2.5V, sensing electrograms and lead impedances were measured at implant and repeated 1,3,6,12,18 and 24months after CRT-P. Electrophysiological measurements of leads located in RV-A and RV-HS were analyzed retrospectively. Bipolar RV leads were used, including high impedance leads, passive fixation and active fixation. ResultsRV pacing leads were implanted in RV-A (n=79) and RV-HS (n=156). Average RV pacing thresholds from CRT implant procedure to 24-month follow-up at 0.5ms were 0.77±0.69V in RV-A and 0.71±0.35V in RV-HS (P=0.31), and at 2.5V were 0.06±0.08ms in RV-A and 0.07±0.05ms in RV-HS (P=0.12). Average RV electrogram amplitudes from baseline to 24months after CRT were 15.3±6.9mV in RV-A and 12.1±6.0mV in RV-HS (P=0.55). Average RV impedances during follow-up were 850±286Ω in RV-A and 618±147Ω in RV-HS (P=0.57). Similar RV lead revisions between RV-A and RV-HS were observed after 2-year follow-up (P=0.55). ConclusionsThe RV-HS lead position demonstrated stable and acceptable long-term pacing and sensing function, with rates of complications comparable to conventional RV-A lead position in CRT. The RV-HS lead position is feasible in CRT-P.

Differential Entrainment Distinguishes Atrioventricular Nodal Reentry Tachycardia from Atrioventricular Reentrant Tachycardia

Entrainment from the right ventricular (RV) apex and the base has been used to distinguish atrioventricular reentrant tachycardia (AVRT) from atrioventricular nodal reentry tachycardia (AVNRT). The difference in the entrainment response from the RV apex in comparison with the RV base has not been tested. Fifty-nine consecutive patients referred for ablation of supraventricular tachycardia (SVT) were included. Entrainment of SVT was performed from the RV apex and base, pacing at 10-40-ms faster than the tachycardia cycle length. SA interval was calculated from stimulus to earliest atrial electrogram. Ventricle to atrium (VA) interval was measured from the RV electrogram (apex and base) to the earliest atrial electrogram during tachycardia. The SA-VA interval from apex and base was measured and the difference between them was calculated. Thirty-six AVNRT and 23 AVRT patients were enrolled. Mean age was 44 ± 12 years; 52% were male. The [SA-VA]apex-[SA-VA]base was demonstrable in 84.7% of patients and measured -9.4 ± 6.6 in AVNRT and 10 ± 11.3 in AVRT, P < 0.001. The difference was negative for all AVNRT cases and positive for all septal accessory pathways (APs). The difference between entrainment from the apex and base is readily performed and is diagnostic for all AVNRTs and septal APs.

Timing of the Left Ventricular Electrogram and Acute Hemodynamic Changes During Implant of Cardiac Resynchronization Therapy Devices

To examine the relationship between timing of the left ventricular (LV) electrogram (EGM) and its acute hemodynamic effect on instantaneous change in LV pressure (LVdP/dt(MAX)). In 30 patients (mean = age 67 +/- 7.9 years) who underwent implant of cardiac resynchronization therapy systems, the right ventricular (RV) lead was implanted at the RV apex (n = 23) or RV septum (n = 7). The LV lead was placed in a posterior (n = 14) or posterolateral (n = 16) coronary sinus tributary. QRS duration, interval from Q wave to intrinsic deflection of the LV EGM (Q-LV), and interval between intrinsic deflection of RV EGM and LV EGM (RV-LV interval) were measured. The measurements were correlated with the hemodynamic effects of optimized biventricular (BiV) stimulation, using the Pearson correlation coefficient. The mean LVdP/dt(MAX) at baseline was 734 +/- 180 mmHg/s, and increased to 905 +/- 165 mmHg/s during simultaneous BiV pacing, and to 933 +/- 172 mmHg/s after V-V interval optimization. The Pearson correlation coefficient R between QRS duration, the Q-LV interval, and the RV-LV interval at the respective LVdP/dt(MAX) was 0.291 (P = 0.66), 0.348 (P = 0.030), and 0.340 (P = 0.033). Similar significant correlations were observed between the acute hemodynamic effect of optimized BiV stimulation and the Q-LV and the RV-LV intervals. However, individual measurements showed an 80-ms cut-off for the Q-LV interval, beyond which the increase in LVdP/dt(MAX) was <10%.

Morphology of the RV Electrogram during LV Pacing is Related to the Hemodynamic Effect in Cardiac Resynchronization Therapy

Biventricular (BiV) pacing and left ventricular (LV) pacing both improve LV function in patients with heart failure and LV dyssynchrony. We studied the hemodynamic effect of the atrioventricular (AV) interval and the associated changes in the right ventricular (RV) electrogram (EGM) during LV pacing and compared this with the hemodynamic effect of optimized sequential BiV pacing. In 16 patients with New York Heart Association (NYHA) class II to IV, sinus rhythm with normal AV conduction, left bundle branch block (LBBB), QRS > 130 ms, and optimal medical therapy, the changes in RV EGM during LV pacing with varying AV intervals were studied. The hemodynamic effect associated with these changes was evaluated by invasive measurement of LVdP/dt(max) and compared with the result of optimized sequential BiV pacing in the same patient. All patients showed electrocardiographic fusion during LV pacing. The morphology of the RV EGM showed changes in the RV activation that indicated a shift in the extent of fusion from LV pacing. These changes were associated with significant changes in LVdP/dt(max). Baseline LV dP/dt(max) was 734 +/- 177 mmHg/s, which increased to 927 +/- 202 mmHg/s (P<0.0001) with optimized LV pacing and to 920 +/- 209 mmHg/s (P<0.0001) with optimized sequential BiV pacing. The RV EGM is a proper indicator for intrinsic activation over the right bundle during LV pacing and reveals the transition to fusion in the RV EGM that is associated with a decrease in LVdP/dt(max). The hemodynamic effect of optimized LV pacing is equal to optimized sequential BiV pacing.

620 Optimized LV pacing by fusion with intrinsic right bundle activation compared to biventricular pacing and the effect on the right ventricular electrogram

Background In patients with normal atrioventricular (AV) conduction left ventricular (LV) pacing is superior to biventricular (BiV) pacing, due to intrinsic conduction over the right bundle branch during LV pacing. Aim of the study To investigate the hemodynamic effect of LV pacing and its association with the right ventricular (RV) electrogram (EGM) as an indicator of ventricular fusion. Methods A BiV pacing system was implanted in 13 patients (8 males, age 66.8±10.2 years) with heart failure NYHA class III-IV, ejection fraction 21.1± 5.6% and sinus rhythm with normal AV conduction. The hemodynamic effect of LV, BiV simultaneous and (BiVsim) optimized V-V interval (BiV opt) pacing was evaluated by invasive measurement of LV dP/dt max with different AV intervals. A 12 lead ECG and the RV EGM obtained by pacemaker telemetry were recorded to evaluate fusion. Results The RV EGM showed a dominant R wave with AV intervals starting 30 ms below the intrinsic PR time (RV R-wave), changing to a configuration with a dominant S wave at short AV delays where no fusion is present (RV S-wave). In between an intermediate RV EGM morphology is recorded (RV-inter). LV dP/dtmax for baseline was 756±167, LV (RV R-wave) 936±209, LV (RV inter) 856±193, LV (RV S-wave) 787±176, BiV sim 896±217 and BiVopt 936±216 mmHg/s. Conclusion LV pacing with the optimal AV interval (LV opt) is superior to BiV (p=0.04) and equal to BiVopt pacing. A change in the RV EGM from a prominent R wave to an intermediate morphology during LV pacing is associated with a significant decrease in LV dP/dtmax (p=0.0022). The change in the RV EGM indicates a shift in the extent of fusion from LV pacing.

CHARACTERISTICS OF RIGHT VENTRICULAR ACTIVATION DETECTED BY BODY SURFACE POTENTIAL MAPPING AMONG POSTOPERATIVE TETRALOGY OF FALLOT PATIENTS WITH AND WITHOUT ARRHYTHMIA

In order to study myocardial activation, 15 patients with repaired Tetralogy of Fallot had body surface potential maps (BSPM) (180 electrode array). All had ambulatory EKG (H), exercise EKG (Ex) and intracardiac electrophysiology (EP). Advanced right bundle branch block (RBBB) was present in 12/15; partial RBBB in 1/15; no RBBB in 2/15. BSPM characteristics of advanced RBBB were lack of right ventricular (RV) breakthrough (12/12); low left ventricular peak to peak voltage (PPV)(1202 ± 544 UV); high RV PPV (3194 ± 1064);high T wave PPV (1549 ± 626) (consistent with “propagation” of repolarization); all significantly different from a normal population previously studied. Although advanced RBBB was “central” in 8/12 and “peripheral” in 4/12 by EP, no difference in RV activation was detected by BSPM among these two groups. Multiple RV activation centers (MC) were seen in 5/12; 5/5 having either sustained ventricular tachycardia (VT) during EP (3/5) or frequent premature ventricular contractions (PVC) on H or Ex (4/5). Without MC 1/7 had VT; 1/7 had PVC's (p< .01). Patients with MC had fractionation of intracardiac RV electrogram in 4/4 having EP mapping near the His bundle, (1/7 without MC) (p < .01). An anterior superior activation front was recognized in 8/12 with advanced RBBB, appearing 0-18 ms after initial RV activation, consistent with cell-cell propagation across the superior ventricular septum. We conclude: Within the spectrum of advanced RBBB, BSPM may show abnormalities of impulse propagation in the RV associated with ventricular arrhythmia.

Frequency of ventricular late potentials and fractionated right ventricular electrograms after operative repair of tetralogy of Fallot

This study was conducted to assess the incidence of abnormalities of ventricular depolarization in sinus rhythm after repair of tetralogy of Fallot and their relation to spontaneous ventricular arrhythmias. Forty-four patients were studied, 10 before surgery (mean age 6.9 years) and 34 after repair (mean age 8.1 years, mean age at surgery 6.5 years, mean interval between surgery and evaluation 11 months). Evaluation was performed by means of body surface and intracavitary signal-averaging techniques, by recording local right ventricular (RV) electrograms at several sites and by 24-hour Holter monitoring (n = 28). No electrophysiologic abnormality was observed in children before surgery. Ventricular late potentials were detected in 18 patients (53%) after repair. Body surface detection of ventricular late potentials was frequently masked by the postoperative right bundle branch block pattern. Local RV electrograms were fractionated in 11 cases (32%) (mean duration 103 ± 33 ms), most often in the RV outflow tract (n = 9), but no relation was found between fragmentation of RV electrograms and the presence of ventricular late potentials. Spontaneous ventricular arrhythmias occurred in 12 children after repair (43%), but were complex in only 4 patients (14%). There was no correlation between spontaneous ventricular arrhythmias and the presence of ventricular late potentials, presence of fractionated RV electrograms, presence of a proximal right bundle branch block or postoperative hemodynamic status. In conclusion, ventricular late potentials and fractionated RV electrograms during sinus rhythm are common after repair of tetralogy of Fallot (71 % of the cases) but are absent before surgery. In this short-term postoperative study no relation was found between these electrophysiologic abnormalities and the occurrence of spontaneous ventricular arrhythmias, and long-term follow-up studies are needed to assess their prognostic significance.

Local abnormalities of right ventricular depolarization after repair of tetralogy of Fallot: A basis for ventricular arrhythmia

Ventricular arrhythmia is common after repair of tetralogy of Fallot (TF) and may cause sudden death. To explore the mechanisms, ambulatory electrocardiographic monitoring and electrophysiologic studies were undertaken, without the use of provocative tests, in 22 patients 5 to 24 years (mean 13) after repair. His-Purkinje and right ventricular (RV) apical activation times were measured to assess conduction. Endocardial mapping of the right ventricle was performed, with additional recordings from the left ventricle in 10 patients, to detect abnormalities of local depolarization and repolarization. Local RV electrograms were fractionated or delayed in 12 patients (55%) at 1 or more RV sites (septum in 7 patients, outflow in 7, free wall in 2 and apex 1 patient), reflecting disordered depolarization, but left ventricular recordings were normal in all. Ventricular arrhythmia out of hospital was more common (p < 0.05) and more severe (p < 0.01) in the patients with depolarization abnormalities than in those with normal electrographic findings. In contrast, there was no association between ventricular arrhythmia and conduction disturbances. Abnormalities of RV repolarization, consisting of low-frequency signals after the T wave, were observed in 17 patients (77%), but were not associated with arrhythmia. Thus, ventricular arrhythmia during daily life was associated with fractionated depolarization at multiple sites in the right ventricle. This suggests that there are widespread areas of RV myocardial damage that provide substrates for ventricular tachycardia.