Left Ventricular Endocardial Activation Research Articles

Left ventricular endocardial activation maps during right ventricular pacing in pediatric patients.

Cardiac pacing from right ventricular (RV) sites may cause electromechanical ventricular dyssynchrony. Invasive and noninvasive mapping studies showed left ventricular (LV) activation sequence in adults. Aim of this study was to seek out the LV endocardial activation (LVEA) in pediatric patients who underwent RV pacing. Single-center, prospective study conducted on pediatric patients who underwent left sided catheter ablation of accessory pathways with the Carto Univu mapping system. After successful ablation procedures, LVEA was recorded by the ablation catheter during sinus rhythm (SR) and during para-hisian (PHP), midseptum (MSP), and apical (RVAP) pacing. Seventeen patients, 13 males, aged 12 (10-15) years, registered LV activation maps and times (LVAT). SR showed significantly shorter LVAT than during pacing. LVAT of PHP was shorter than MSP, while there were not significant differences among PHP and MSP versus RVAP. In SR initial LV endocardial activation occurred in two midseptum sites, inferior-posterior and superior-anterior. During PHP, initial activation occurred at parahisian basal septum, rapidly followed by midseptum as in SR. During MSP and RVAP initial activation occurred at midseptum and apex, respectively. From all initial sites, the excitation spreads toward the base of the lateral LV free wall. A mild linear correlation was found between QRS duration and LVAT for MSP and for PHP. In pediatric patients LVEA maps during RV pacing showed that the shortest LVAT was obtained with PHP. The LV activation pattern seemed similar in sinus rhythm, PHP and MSP, from midseptum to LV lateral base.

Correlation Between Functional Substrate Mapping and Cardiac Computed Tomography–Derived Wall Thinning for Ventricular Tachycardia Ablation

BackgroundFunctional substrate mapping during baseline rhythm can identify arrhythmogenic tissue during ventricular tachycardia (VT) ablation. Wall thinning and wall thickness channels (WTCs) derived from computed tomography angiography have been shown to correlate with low voltage and VT isthmuses. The correlation between functional substrate mapping, wall thinning, and WTCs in patients with infarct- or non–infarct-related cardiomyopathies (ICM and NICM, respectively) has not been previously described. ObjectivesThe purpose of this study was to correlate cardiac CTA-derived myocardial wall thinning with functional VT substrate mapping using isochronal late activation mapping. MethodsIn 34 patients with ICM or NICM undergoing VT ablation who had a preprocedure computed tomography angiography, myocardial wall thinning was segmented in layers of 1 to 5 mm. Areas of wall thinning and WTCs were then spatially correlated with deceleration zones (DZs) from registered left ventricular endocardial isochronal late activation maps. ResultsIn 21 ICM patients and 13 NICM patients, ICM patients had greater surfaces areas of wall thinning (P < 0.001). In ICM patients, 94.1% of primary DZs were located on areas of wall thinning, compared to 20% of DZs in NICM patients overall but 50% if there was any wall thinning present. Fifty-nine percent of DZs in ICM patients and 56% of DZs in NICM patients were located near WTCs. The positive predictive value for WTC in localizing DZs was 22.5% and 37.8% in ICM and NICM patients, respectively. ConclusionsWall thinning is highly sensitive for functional substrate in ICM patients. WTCs had modest sensitivity for functional substrate but low positive predictive value for identifying DZs in ICM and NICM patients. These findings suggest that wall thinning may facilitate more efficient mapping in ICM patients, but WTCs are insufficient to localize wavefront discontinuities.

During Early VF in Rabbit Hearts, His Bundle Pacing is Less Effective Than Working Myocardial Pacing in Modulating Left Ventricular Activation Rates.

The potential of pacing and capturing the His-Purkinje system (HPS) to synchronize VF wavefronts is not known even though the HPS is thought to be electrically linked during VF. In this study the effect of selective His Bundle (HB) pacing was compared with nearby working myocardial (WM) pacing on the left ventricular (LV) endocardial activation rates. Rabbit hearts (n = 9) were explanted and Langendorff perfused. Electrodes directly on the HB were identified and paced subsequently using an electrode array. The WM was paced through a silver wire inserted in the right ventricular septal wall. After VF was induced, the HB was paced at rates faster than the intrinsic HB activation rate (n = 18 episodes) and also at rates faster than the LV activation rate (n = 16). A basket array inserted in the LV was used to record electrograms before and during each pacing episode. Activation rates at five LV electrodes each from the earliest and latest activating sinus rhythm regions were analyzed before and during pacing. Both HB and WM pacing reduced LV activation rates during pacing, but WM pacing was more effective (p < 0.005). WM pacing events were more effective (p < 0.05) in reducing LV activation rates than HB pacingin episodes which were faster than LV activation rates. This study provides evidence that during early VF in rabbit hearts, the HPS cannot be driven to effectively modulate the LV activation rates.

Comparing Non-invasive Inverse Electrocardiography With Invasive Endocardial and Epicardial Electroanatomical Mapping During Sinus Rhythm.

This study presents a novel non-invasive equivalent dipole layer (EDL) based inverse electrocardiography (iECG) technique which estimates both endocardial and epicardial ventricular activation sequences. We aimed to quantitatively compare our iECG approach with invasive electro-anatomical mapping (EAM) during sinus rhythm with the objective of enabling functional substrate imaging and sudden cardiac death risk stratification in patients with cardiomyopathy. Thirteen patients (77% males, 48 ± 20 years old) referred for endocardial and epicardial EAM underwent 67-electrode body surface potential mapping and CT imaging. The EDL-based iECG approach was improved by mimicking the effects of the His-Purkinje system on ventricular activation. EAM local activation timing (LAT) maps were compared with iECG-LAT maps using absolute differences and Pearson’s correlation coefficient, reported as mean ± standard deviation [95% confidence interval]. The correlation coefficient between iECG-LAT maps and EAM was 0.54 ± 0.19 [0.49–0.59] for epicardial activation, 0.50 ± 0.27 [0.41–0.58] for right ventricular endocardial activation and 0.44 ± 0.29 [0.32–0.56] for left ventricular endocardial activation. The absolute difference in timing between iECG maps and EAM was 17.4 ± 7.2 ms for epicardial maps, 19.5 ± 7.7 ms for right ventricular endocardial maps, 27.9 ± 8.7 ms for left ventricular endocardial maps. The absolute distance between right ventricular endocardial breakthrough sites was 30 ± 16 mm and 31 ± 17 mm for the left ventricle. The absolute distance for latest epicardial activation was median 12.8 [IQR: 2.9–29.3] mm. This first in-human quantitative comparison of iECG and invasive LAT-maps on both the endocardial and epicardial surface during sinus rhythm showed improved agreement, although with considerable absolute difference and moderate correlation coefficient. Non-invasive iECG requires further refinements to facilitate clinical implementation and risk stratification.

Effect of selective His bundle pacing on ventricular fibrillation activation rates in rabbit hearts

Background/significanceThe His‐Purkinje system is electrically active and influences activation patterns and rates during ventricular fibrillation (VF). Purkinje system is involved in maintaining VF and may contribute to defibrillation shock failure. This study investigates if the His‐Purkinje system could be paced to modulate rate or patterns of activation during VF.MethodSeven New Zealand rabbit hearts were explanted and perfused in a Langendorff setup. The His bundle (HB) was accessed from the right atrial septal wall by opening the right atrium. An 8×8 Ag/AgCL electrode array was placed by the anterior vertex of Koch's triangle. The HB was identified using a custom real‐time stimulation‐recording and signal processing system. The system used spatial derivatives to identify electrodes specifically over the HB. A separate silver wire was inserted in the ventricular myocardium (VM) of the right septal wall to stimulate the VM and detect ventricular cycle lengths. A 64‐channel basket catheter (Orion catheter, Boston Scientific Inc) was inserted through an opening made in left atrium through the mitral valve and into the left ventricle. VF was induced by 50 Hz pacing on the left ventricular free wall. During VF, the HB was paced at 80 and 95% of intrinsic HB cycle lengths. Both the HB and VM were paced at 80 and 95% of the intrinsic VM cycle lengths. Both HB and VM were stimulated during VF at 10× the amplitude of the diastolic stimulation threshold. While the VM and HB were being stimulated, left ventricular endocardial activations were recorded from the basket catheter electrodes.The left ventricular endocardial recordings were analyzed using a custom graphical user interface developed in MATLAB (Mathworks, Inc., MA, USA). Broken channels or channels not in contact with the endocardial wall were excluded from the analysis.ResultsData from 2 out of 7 animals were excluded from analysis as pacing at electrodes with HB potentials did not lead to capture of the HB. HB pacing at 80% or 95% of HB CL did not affect the VF. In 4 animals, when the HB was paced at 95% of VM cycle lengths, the left ventricular endocardial activation rate was higher than when VM was paced at 95% of VM cycle lengths. In 3 animals, when HB was paced at 80% of VM cycle length, the left ventricular endocardial activation rate was higher than when the VM was paced at 80% of VM cycle length.Conclusion and discussionHB paced at 80 or 95% of HB cycle length did not affect the underlying VF. HB paced at 80% or 95% of VM cycle length affected the underlying VF activation rate more than when VM was paced at 80% or 95% VM CL. The increase in ventricular activation rate suggests ventricular tissue is activated at the Purkinje endpoints of the His‐Purkinje system as a result of His bundle pacing.Support or Funding InformationNational Institutes of Health award number R01HL128752 to Dr. Derek DosdallThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Localization of Activation Origin on Patient-Specific Endocardial Surface by the Equivalent Double Layer (EDL) Source Model With Sparse Bayesian Learning.

Ablation treatment of ventricular arrhythmias can be facilitated by pre-procedure planning aided by electrocardiographic inverse solution, which can help to localize the origin of arrhythmia. Our aim was to improve localization accuracy of the inverse solution for activation originating on the left-ventricular endocardial surface, by using a sparse Bayesian learning (SBL). The inverse problem of electrocardiography was solved by reconstructing endocardial potentials from time integrals of body-surface electrocardiograms and from patient-specific geometry of the heart and torso for three patients with structurally normal ventricular myocardium, who underwent endocardial catheter mapping that included pace mapping. Complementary simulations using dipole sources in patient-specific geometry were also performed. The proposed method is using sparse property of the equivalent-double-layer (EDL) model of cardiac sources; it employs the SBL and makes use of the spatio-temporal features of the cardiac action potentials. The mean localization error of the proposed method for pooled pacing sites ( n=52) was significantly smaller ( p=0.0039) than that achieved for the same patients in the study of Erem etal. Simulation experiments localized the source dipoles ( n=48) from forward-simulated potentials with the error of 9.4 ± 4.5mm (mean ± SD). The results of our clinical and simulation experiments demonstrate that localization of left-ventricular endocardial activation by means of the Bayesian approach, based on sparse representation of sources by EDL, is feasible and accurate. The proposed approach to localizing endocardial sources may have important applications in pre-procedure assessment of arrhythmias and in guiding their ablation treatment.

Does cardiac resynchronization therapy benefit patients with right bundle branch block: cardiac resynchronization therapy has a role in patients with right bundle branch block.

Does cardiac resynchronization therapy benefit patients with right bundle branch block: cardiac resynchronization therapy has a role in patients with right bundle branch block.

Long-Duration Ventricular Fibrillation Exhibits 2 Distinct Organized States

Previous studies showed that endocardial activation during long-duration ventricular fibrillation (VF) exhibits organized activity. We identified and quantified the different types of organized activity. Two 64-electrode basket catheters were inserted, respectively, into the left ventricle and right ventricle of dogs to record endocardial activation from the endocardium during 7 minutes of VF (controls, n=6). The study was repeated with the K(ATP) channel opener pinacidil (n=6) and the calcium channel blocker flunarizine (n=6). After 2 minutes of VF without drugs, 2 highly organized left ventricular endocardial activation patterns were observed: (1) ventricular electric synchrony pattern, in which endocardial activation arose focally and either had a propagation sequence similar to sinus rhythm or arose near papillary muscles, and (2) stable pattern, in which activation was regular and repeatable, sometimes forming a stable re-entrant circuit around the left ventricular apex. Between 3 and 7 minutes of VF, the percent of time ventricular electric synchrony was present was control=25%, flunarizine=24% (P=0.44), and pinacidil=0.1% (P<0.001) and the percent of time stable pattern was present was control=71%, flunarizine=48% (P<0.001), and pinacidil=56% (P<0.001). The remainder of the time, nonstable re-entrant activation with little repeatability was present. After 3 minutes, VF exhibits 2 highly organized endocardial activation patterns 96% of the time, one potentially arising focally in the Purkinje system that was prevented with a K(ATP) channel opener but not a calcium channel blocker and the other potentially arising from a stable re-entrant circuit near the apical left ventricular endocardium.

Cardiac Electrophysiological Activation Pattern Estimation From Images Using a Patient-Specific Database of Synthetic Image Sequences

While abnormal patterns of cardiac electrophysiological activation are at the origin of important cardiovascular diseases (e.g., arrhythmia, asynchrony), the only clinically available method to observe detailed left ventricular endocardial surface activation pattern is through invasive catheter mapping. However, this electrophysiological activation controls the onset of the mechanical contraction; therefore, important information about the electrophysiology could be deduced from the detailed observation of the resulting motion patterns. In this paper, we present the study of this inverse cardiac electrokinematic relationship. The objective is to predict the activation pattern knowing the cardiac motion from the analysis of cardiac image sequences. To achieve this, we propose to create a rich patient-specific database of synthetic time series of the cardiac images using simulations of a personalized cardiac electromechanical model, in order to study this complex relationship between electrical activity and kinematic patterns in the context of this specific patient. We use this database to train a machine-learning algorithm which estimates the depolarization times of each cardiac segment from global and regional kinematic descriptors based on displacements or strains and their derivatives. Finally, we use this learning to estimate the patient’s electrical activation times using the acquired clinical images. Experiments on the inverse electrokinematic learning are demonstrated on synthetic sequences and are evaluated on clinical data with promising results. The error calculated between our prediction and the invasive intracardiac mapping ground truth is relatively small (around 10 ms for ischemic patients and 20 ms for nonischemic patient). This approach suggests the possibility of noninvasive electrophysiological pattern estimation using cardiac motion imaging.

Excitation of the Intrinsic Conduction System Through His and Interventricular Septal Pacing

Direct His bundle pacing results in rapid synchronous ventricular activation. However, clinical experiences with such pacing have been associated with long procedure times and compromised pacing and sensing performance. We evaluated myocardial activation sequences (AS) for pacing of the His bundle and peri-His region and assessed acute pacing performance using custom-designed plunge electrodes. Unipolar pacing was performed in isolated swine hearts (n = 10) using four quadripolar stimulation/sensing electrodes implanted into the interventricular septum and equally spaced between the membranous septum and the coronary sinus ostium (zones 1-4, respectively; electrode depth (ED) 1 = most distal, ED 4 = most proximal). Optimal pacing sites were defined as: pacing thresholds < or = 1.5 V, a P-R ratio of < or = 0.5, and > or = 50% occurrence of an intrinsic midseptal left ventricular (LV) endocardial electrical breakout (BO) and activation pattern. Pacing thresholds improved with greater depth of electrode location within the septum (ED 1: 1.51 +/- 0.8 V vs ED 4: 5.2 +/- 3.8 V, P < 0.001), as did the P-R ratio (0.34 +/- 0.6 vs 0.78 +/- 1.0, P < 0.05). His potentials were only observed in zone 1 and 2 electrodes (0.12 and 0.02 mV, respectively). Only electrodes in zones 1 and 2 produced LV endocardial electrical BOs in the midseptal region that demonstrated an intrinsic-like endocardial AS. Depth 1 and 2 electrodes (11.75 and 8.75 mm, respectively) in zone 1 satisfied all three optimal pacing site requirements. This study has shown that LV activation patterns similar to sinus rhythm may be achieved without direct activation of the His bundle, while maintaining acceptable pacing and sensing performance. These data indicate that pacing systems designed to stimulate the tissues below the point at which the His bundle penetrates the central fibrous body may provide improved system efficiency and LV performance in comparison to both direct His bundle pacing and traditional pacing sites.

Tailoring cardiac resynchronization therapy using interventricular asynchrony. Validation of a simple model

This study explores the use of interventricular asynchrony (interVA) for optimizing cardiac resynchronization therapy (CRT), an idea emerging from a simple pathway model of conduction in the ventricles. Measurements were performed in six dogs with chronic left bundle branch block (LBBB) and in 29 patients of the Pacing Therapies for Congestive Heart Failure (PATH-CHF)-I study. In the dogs, intraventricular asynchrony (intraVA) was determined using left ventricular (LV) endocardial activation maps. In dogs and patients, the maximum rate of rise of LV pressure (LV dP/dt(max)) and the pulse pressure (PP) and interVA [time delay between upslope of LV and right ventricular (RV) pressure curves] were measured during LV, RV, and biventricular (BiV) pacing with various atrioventricular (AV) delays. Measurements in the canine hearts supported the pathway model in that optimal resynchronization occurred at approximately 50% reduction of intraVA and at an interVA value halfway that during LBBB and LV pacing. In patients with significant hemodynamic response during pacing (n = 22), intrinsic interVA and interVA at peak improvement (interVA(p)) varied widely between patients (from -83 to -15 ms and from -42 to +31 ms, respectively). However, the model predicted individual interVA(p) accurately (SD of +/-6 ms and +/-12 ms for LV dP/dt(max) and PP, respectively). At equal interVA, LV and BiV pacing produced equal hemodynamic response, but in 11 of 22 responders, BiV pacing reduced interVA insufficiently to reach the maximum hemodynamic response. LV pacing at short AV delay proved to result in better hemodynamics than predicted by the model, indicating that additional factors determine hemodynamics during LV preexcitation. Guided by a simple pathway model, interVA measurements accurately predict optimal hemodynamic performance in individual CRT patients.

Right and Left Ventricular Activation Sequence in Patients with Heart Failure and Right Bundle Branch Block: A Detailed Analysis Using Three‐Dimensional Non‐Fluoroscopic Electroanatomic Mapping System

Three-dimensional mapping in RBBB and heart failure. Recently, right bundle branch block (RBBB) was proved to be an important predictor of mortality in heart failure (HF) patients as much as left bundle branch block (LBBB). We characterized endocardial right ventricular (RV) and left ventricular (LV) activation sequence in HF patients with RBBB using a three-dimensional non-fluoroscopic electroanatomic contact mapping system (3D-Map) in order to provide the electrophysiological background to understand whether these patients can benefit from cardiac resynchronization therapy (CRT). Using 3D-Map, RV and LV activation sequences were studied in 100 consecutive HF patients. Six of these patients presented with RBBB QRS morphology. The maps of these patients were analyzed and compared post hoc with those of the other 94 HF patients presenting with LBBB. Clinical and hemodynamic profile was significantly worse in RBBB group compared to LBBB. Patients with RBBB showed significantly longer time to RV breakthrough (P<0.001), longer activation times of RV anterior and lateral regions (P<0.001), and longer total RV endocardial activation time (P<0.02) compared to patients with LBBB. Time to LV breakthrough was significantly shorter in patients with RBBB (P<0.001), while total and regional LV endocardial activation times were not significantly different between the two groups. Degree of LV activation delay is similar between HF patients with LBBB and RBBB. Moreover, patients with RBBB have larger right-sided conduction delay compared to patients with LBBB. The assessment of these electrical abnormalities is important to understand the rationale for delivering CRT in HF patients with RBBB.

The spectrum of inter- and intraventricular conduction abnormalities in patients eligible for cardiac resynchronization therapy.

Although cardiac resynchronization therapy (CRT) has clearly demonstrated its clinical benefit in patients with congestive heart failure (CHF) and intraventricular conduction abnormalities, selection of eligible patients and/or optimal pacing site are still a matter of debate. The aim of the study was to analyze the spectrum of conduction abnormalities in CRT candidates. A total of 26 patients (mean age 62 +/- 9 years) with CHF and conduction disturbances (QRS > or = 130 ms) were studied. The underlying heart disease was dilated cardiomyopathy (DCM) (n = 12) or coronary artery disease (CAD) (n = 14). High density, left ventricular endocardial activation maps were constructed using an electroanatomic mapping system (CARTO). Based on endocardial activation patterns, left ventricular conduction abnormalities were classified as left bundle branch block (LBBB) (n = 9), nonspecific intraventricular conduction disturbances (n = 10), and the bifascicular block (n = 7). In DCM patients the endocardial activation sequences corresponded with a 12-lead ECG pattern with a homogeneous spread of activation wavefront and the latest activation laterally (LBBB) or anteriorly (bifascicular block), respectively. CAD patients presented with variable activation patterns that reflected the location of the postinfarct scar, and the 12-lead ECG was less predictive. Although there was a trend for longer QRS durations for DCM subjects (170 +/- 23 vs 156 +/- 23 ms, P = NS), left ventricular activation time was significantly longer in the CAD group (115 +/- 21 ms vs 134 +/- 23 ms, P < 0.05). CRT candidates represent a broad spectrum of conduction abnormality patterns with variable inter- and intraventricular activation delays. CAD subjects have more pronounced intraventricular conduction abnormality. The standard ECG is less reliable in the characterization of complex conduction abnormalities.

The left ventricular apex is the optimal site for pediatric pacing: correlation with animal experience.

Pacing at the commonly used right ventricular (RV) apex results in impaired ventricular performance. Previous animal studies indicated that the left ventricular (LV) apex is a superior pacing site. The purpose of this study was to investigate in dogs whether this good performance is associated with a more synchronous electrical activation pattern of the LV and whether the LV apex is also a good pacing site in children. In 11 healthy dogs and 8 children undergoing cardiac surgery, dual chamber pacing was performed at the RV apex, LV apex and LV lateral free wall (LVFW). In dogs, a basket electrode was inserted into the LV to assess pattern and timing of LV endocardial activation. In the children, hemodynamic measurements were performed immediately after recovery from cardiopulmonary bypass. In dogs, LV apex pacing resulted in synchronous activation around the LV circumference whereas RV apex and LVFW pacing resulted in asynchrony of activation between the septum and LVFW. In both canine and children's hearts most hemodynamic variables remained at sinus rhythm level during LV apex pacing, but LVdPdtmax, stroke work (dogs), and pulse pressure (children) were reduced as compared with sinus rhythm during RV apex and LVFW pacing. LV apex pacing results in synchronous activation of the LV and is, in adult dogs and in children, associated with superior hemodynamic performance.

P2130 Electroanatomical mapping of left-ventricular endocardial activation and acute haemodynamic effect of left-ventricular stimulation in patients with dilated cardiomyopathy and left bundle branch block

P2130 Electroanatomical mapping of left-ventricular endocardial activation and acute haemodynamic effect of left-ventricular stimulation in patients with dilated cardiomyopathy and left bundle branch block

Quantitative Analysis of Left Ventricular Endocardial Activation During Progressive Ventricular Fibrillation

Quantitative Analysis of Left Ventricular Endocardial Activation During Progressive Ventricular Fibrillation

Quantitative analysis of left ventricular endocardial activation during progressive ventricular fibrillation

Quantitative analysis of left ventricular endocardial activation during progressive ventricular fibrillation

Endocardial mapping during sinus rhythm in patients with coronary artery disease and nonsustained ventricular tachycardia

Programmed stimulation in patients with nonsustained ventricular tachycardia (VT) and coronary artery disease (CAD) induces sustained VT in 30 to 50% of patients. The presence of inducible, sustained VT identifies patients at high risk for sudden death. This study sought to determine whether patients with nonsustained VT who have inducible, sustained VT would have differences of left ventricular endocardial activation and conduction compared with those of patients without inducible, sustained VT. Thirty-six patients with CAD referred for evaluation of nonsustained VT underwent programmed ventricular stimulation and catheter mapping of left ventricular endocardial activation. Using previously validated methods, electrograms were classified as normal, abnormal or fractionated based on measurement of local electrogram duration and amplitude. Programmed stimulation induced sustained, uniform VT in 16 of 36 patients (44%). Patients with inducible, sustained, uniform VT had significantly more sites with abnormal (48%) and fractionated (5.5%) electrograms than did those without inducible VT (35% abnormal and 0.4% fractionated; p = 0.05 and 0.01, respectively). Patients with inducible VT had a mean of 15% of mapped sites displaying late electrograms versus only 3% in those without inducible VT (p < 0.01). The duration of the longest local electrogram in patients with inducible, sustained, uniform VT was 128 ms compared with 100 ms in those without inducible VT (p < 0.001). Thus, patients with CAD presenting with nonsustained VT who have inducible, sustained, uniform VT have significantly greater degrees of local conduction slowing and delayed activation than do those without inducible, sustained, uniform VT. These observations support reentry as the mechanism of the induced arrhythmias in these patients.

Polymorphic ventricular tachycardia induced by programmed stimulation: Response to procainamide

Objectives. This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG).Background. Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia.Methods. Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs.Results. We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p < 0.008).Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm.Conclusions. The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the appllcation of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

Geometrically Accurate Transaortic Mapping of Left Ventricular Endocardial Activation During Surgery

Geometrically Accurate Transaortic Mapping of Left Ventricular Endocardial Activation During Surgery