Electrocardiographic imaging (ECGI), a novel diagnostic modality used for mapping of focal left ventricular tachycardia in a young athlete

We report the first clinical application of electrocardiographic imaging (ECGI), a new, noninvasive imaging modality for arrhythmias, in an athlete with focal ventricular tachycardia (VT) originating from a left ventricular (LV) diverticulum. A reconstructed map of the epicardial activation sequence during a single premature ventricular complex (PVC) of an identical QRS morphology to the clinical VT, generated from 224-electrode body surface ECGs and a chest CT (ECGI), localized the PVC to the site of the diverticulum. This correlated with subsequent maps obtained using standard techniques. We describe the first case that used ECGI to guide diagnosis and therapy of a clinical tachyarrhythmia.     

Endocardial, intramural, and epicardial activation patterns during sustained monomorphic ventricular tachycardia in late canine myocardial infarction

Thirteen dogs in whom at least one morphologically distinct sustained ventricular tachycardia (VT) could be reproducibly initiated by programmed cardiac stimulation 18 +/- 3 days following experimental myocardial infarction were placed on total cardiopulmonary bypass for detailed study of the endocardial and epicardial activation during VT under hemodynamically stable conditions. Thirteen morphologically distinct monomorphic VTs were investigated by simultaneous epicardial, endocardial, and intramural bipolar recordings. Local electrograms were used to generate computer-assisted isochronous-activation sequence maps. A complete reentry circuit could be mapped on the epicardial surface in 4 animals and on the endocardial surface in one other animal. In the remaining 8 animals, there was a gap period lasting 43-62 msec in the cardiac cycle during which no endocardial or epicardial activity was observed. In 6 of the 8 animals, bipolar intramural recordings from sites closely associated with regions of endocardial and epicardial conduction block showed intramural activity progressing slowly during the gap period. In these 6 animals, a reentry circuit could be completed by incorporating the local electrograms recorded from the intramural sites. VT could be reproducibly terminated by selectively rendering only these intramural sites refractory by critically timed extrastimuli that failed to result in global ventricular capture. VT could be terminated by epicardial cooling in 2 of the 4 animals with epicardial reentry. By contrast, epicardial cryoablation did not effect intramural reentry and failed to interrupt VT. In this study, intramural pathways constituted an integral part of the reentry circuit in a large proportion of the VTs.     

Noninvasive electrocardiogram imaging of substrate and intramural ventricular tachycardia in infarcted hearts

OBJECTIVES: The goal of this study was to experimentally evaluate a novel noninvasive electrocardiographic imaging modality during intramural reentrant ventricular tachycardia (VT). BACKGROUND: Myocardial infarction and subsequent remodeling produce abnormal electrophysiologic substrates capable of initiating and maintaining reentrant arrhythmias. Existing noninvasive electrocardiographic methods cannot characterize abnormal electrophysiologic substrates in the heart or the details of associated arrhythmias. A noninvasive method with such capabilities is needed to identify patients at risk of arrhythmias and to guide and evaluate therapy. METHODS: A dog heart with a four-day-old infarction was suspended in a human shaped torso-tank. Measured body surface potentials were used to noninvasively compute epicardial potentials, electrograms and isochrones. Accuracy of reconstruction was evaluated by direct comparison to measured data. Reconstructions were performed during right atrial pacing and nine cycles of VT. RESULTS: Noninvasively reconstructed potential maps, electrograms and isochrones identified: 1) the location of electrophysiologically abnormal infarct substrate; 2) the epicardial activation sequences during the VTs; 3) the locations of epicardial breakthrough sites; and 4) electrophysiologic evidence for activation of the Purkinje system and septum during the reentrant beats. CONCLUSIONS: Electrocardiographic imaging can noninvasively reconstruct electrophysiologic information on the epicardium during VT with intramural reentry, provide information about the location of the intramural components of reentry and image abnormal electrophysiologic substrates associated with infarction.     

Transmural temporospatial left ventricular activation during pacing from different sites: potential implications for optimal pacing

AIMS: Previous studies showed that right ventricular (RV) endocardial pacing can be deleterious even in individuals with initially normal left ventricular (LV) function. The mechanism(s) by which RV endocardial pacing may cause LV dysfunction is unknown. This study compares the temporospatial LV transmyocardial activation profiles during sinus rhythm with normal His/Purkinje conduction vs. currently utilized and proposed cardiac pacing sites. METHODS AND RESULTS: Mongrel dogs were instrumented with transmural electrodes that tracked transmyocardial activation sequences at five sites in the LV. Pacing/recording catheters were positioned in the RV apex and on the RV and LV sides of the ventricular septum. An epicardial pacing electrode was also sewn to the mid-lateral LV epicardium. Electrograms were recorded during sinus rhythm and pacing from the RV endocardium, LV septum, LV epicardium and during biventricular pacing. Compared to normal sinus/His/Purkinje rhythm (NSR), RV endocardial pacing significantly (P < 0.05) prolonged transmural activation (NSR endocardium 6.1 +/- 1 ms vs. RV endocardium 23.0 +/- 2.6 ms). The highly ordered temporospatial pattern of transmural activation during sinus rhythm was replaced with dispersion and intermingling of endo-, mid-, and epicardial activation. LV epicardial and biventricular pacing did not correct these abnormalities. Only LV septal pacing achieved the transmural and transseptal activation sequences similar to sinus rhythm. CONCLUSION: Clinically utilized pacing modalities, including biventricular pacing, cause abnormal transmyocardial activation. LV septal pacing results in transmyocardial activation patterns that closely resemble those seen in sinus rhythm.     

伴右心室出口的左心室起源缺血性室性心动过速的标测和消融

目的折返性的缺血性室性心动过速（VT）绝大多数发生于左心室并表现为右束支阻滞（RBBB）图形。本文报道1组VT折返环位于左心室但出口在右心室且表现为左束支阻滞（LBBB）的病例。方法32例因陈旧性心肌梗死伴VT而接受电生理检查和射频消融的患者,其中4例临床有LBBB形态的VT。使用非接触等电位和虚拟单极标测判断VT起源,结合舒张中期电位（MDP）和拖带标测确定折返关键通路和消融靶点。用盐水冲洗电极导管在折返环的关键峡部行线性消融。结果全部32例患者中,4例临床有LBBB型VT者均成功被诱发,其中1例有两种LBBB型VT,1例同时有RBBB型VT但周长与LBBB型相同;另有1例共有6种形态的VT,包括RBBB和LBBB型。在右心室内的非接触式等电位标测可迅速确定VT在右心室的传出部位,该处的虚拟单极标测显示rS型提示左心室起源。3例在左心室成功拖带并消融成功,靶点均紧邻左心室间隔,其中1例位于下壁,1例在前壁,1例两种LBBB型VT分别在前壁和下壁间隔旁消融成功。随访1～4．2年,未服抗心律失常药无VT发作。而1例诱发出6种单形（包括RBBB和LBBB型）VT患者因巨大室壁瘤及心功能障碍不能耐受而中途放弃消融。结论紧邻室间隔的前壁和下壁心肌梗死后的左心室起源VT可能因在右心室有出口而表现为LBBB型,需要在标测和消融时予以注意。     

Body surface mapping of ectopic left ventricular activation. QRS spectrum in patients with prior myocardial infarction.

To improve electrocardiographic localization of the site of origin of ectopic left ventricular (LV) impulse formation in the heart with prior myocardial infarction, 62-lead body surface QRS integral maps were studied during LV pacing at a total of 221 endocardial sites in 14 patients with previous anterior (AMI), inferior (IMI), lateral (LMI), or anterior and inferior (AMI/IMI) myocardial infarction. The anatomic location of each pacing site was computed using digitized biplane fluoroscopic images and plotted on standardized LV endocardial polar projections. A data base of characteristic AMI and IMI mean QRS integral maps was developed after visually selecting subgroups with nearly identical QRS integral morphology from the ectopic activation sequences produced at 110 sites in eight patients with AMI and at 66 sites in four patients with IMI. Intrasubgroup pattern uniformity and intersubgroup pattern variability were statistically verified. The endocardial pacing site locations belonging to each AMI and IMI subgroup were depicted as segments on the respective LV polar projections. In patients with AMI, a total of 18 typical mean QRS integral patterns were obtained, whereas 22 different mean total QRS integral patterns showing more substantial intersubgroup variation were acquired in patients with IMI. Posterolateral regions exhibited a relatively low electrocardiographic sensitivity (six AMI and five IMI patterns) as compared with anteroseptal regions (12 AMI and 17 IMI patterns). Total QRS integral patterns obtained at 24 sites in one patient with LMI were largely compatible with the IMI mean total QRS integral patterns, whereas the majority of total QRS integral patterns acquired at 21 sites in one patient with AMI/IMI corresponded with the AMI mean total QRS integral patterns. The results show that total body surface QRS integral maps generated during LV pacing in patients with prior myocardial infarction cluster by pattern and that each QRS integral pattern is related to a circumscribed endocardial segment of ectopic impulse formation. The relation between a given QRS integral pattern and the position and size of the corresponding paced segment is dependent on infarct location. The present infarct-specific data base of characteristic total body surface QRS integral patterns provides a clinical tool to obtain detailed electrocardiographic localization of ventricular arrhythmias in patients with previous myocardial infarction.     

Transmural ventricular activation during consecutive cycles of sustained ventricular tachycardia associated with coronary artery disease

Although computerized mapping has enabled the intraoperative delineation of global ventricular activation from a single complex of ventricular tachycardia (VT), beat-to-beat reproducibility of isochronic maps has not been defined. To determine the reliability of single-beat analysis, epicardial and transmural ventricular electrograms during 6 consecutive VT cycles were analyzed in 10 patients during intraoperative mapping of sustained monomorphic VT. Bipolar electrograms were recorded simultaneously using sock and needle electrodes from up to 96 epicardial and 156 transmural sites. In each patient, at each electrode site, local activation time, electrogram duration and morphology were compared over 6 consecutive beats. A total of 9,816 electrograms were analyzed. For each patient, the isochronic activation map during VT was reproducible. Mean beat-to-beat variations in local epicardial and transmural activation times were only 1.7 +/- 1.7 and 2.04 +/- 1.9 ms, respectively (difference not significant). Moreover, electrogram duration did not vary significantly. Mean variations in epicardial and transmural electrogram durations were 2.1 +/- 1.8 and 1.4 +/- 1.9 ms, respectively (difference not significant). There were only 2 instances of 2:1 conduction failure; both occurred intramurally and adjacent to a site of VT origin. Thus, transmural ventricular activation during sustained monomorphic VT is reproducible regardless of electrode site or electrogram duration. These results demonstrate that analysis of a single beat of VT is a reliable and expedient method to delineate ventricular activation during intraoperative computerized mapping for the purpose of clinical decision-making in patients with sustained monomorphic VT.     

Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics

Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.     

Distribution of excitation frequencies on the epicardial and endocardial surfaces of fibrillating ventricular wall of the sheep heart

Tissue heterogeneities may play an important role in the mechanism of ventricular tachycardia (VT) and fibrillation (VF) and can lead to a complex spatial distribution of excitation frequencies. Here we used optical mapping and Fourier analysis to determine the distribution of excitation frequencies in >20 000 sites of fibrillating ventricular tissue. Our objective was to use such a distribution as a tool to quantify the degree of organization during VF. Fourteen episodes of VT/VF were induced via rapid pacing in 9 isolated, coronary perfused, and superfused sheep ventricular slabs (3x3 cm(2)). A dual-camera video-imaging system was used for simultaneous optical recordings from the entire epi- and endocardial surfaces. The local frequencies of excitation were determined at each pixel and displayed as dominant frequency (DF) maps. A typical DF map consisted of several (8.2+/-3.6) discrete areas (domains) with a uniform DF within each domain. The DFs in adjacent domains were often in 1:2, 3:4, or 4:5 ratios, which was shown to be a result of an intermittent Wenckebach-like conduction block at the domain boundaries. The domain patterns were relatively stable and could persist from several seconds to several minutes. The complexity in the organization of the domains, the number of domains, and the dispersion of frequencies increased with the rate of the arrhythmia. Domain patterns on the epicardial and endocardial surfaces were not correlated. Sustained epicardial or endocardial reentry was observed in only 3 episodes. Observed frequency patterns during VT/VF suggest that the underlying mechanism may be a sustained intramural reentrant source interacting with tissue heterogeneities.     

Left ventricular septal and apex pacing for optimal pump function in canine hearts

OBJECTIVES: The goal of this study was to test the hypothesis that left ventricular (LV) pump function is optimal when pacing is performed at the LV near the sites where the impulses exit the Purkinje system. BACKGROUND: Pacing at the conventional site, the right ventricular (RV) apex, adversely affects hemodynamics. During normal sinus rhythm (SR), electrical activation of the working myocardium starts at the LV septal endocardium and spreads from apex to base. METHODS: Experiments were conducted in anesthetized open-chest dogs with normal ventricular conduction to investigate hemodynamic effects of pacing at various epicardial LV sites, the RV apex, and combinations of these sites (n = 11) and of RV and LV septal pacing (n = 8). The LV septal endocardium was reached via the RV by puncturing through the septum with a barbed electrode. Left ventricular systolic (LVdP/dtpos and stroke work) and diastolic (LVdP/dtneg and Tau) function were assessed using pressure-volume relations (conductance catheter technique). RESULTS: Left ventricular systolic and diastolic function were highly dependent on the site of pacing, but not on QRS duration. Left ventricular function was maintained at SR level during LV septal, LV apex, and multisite pacing, was moderately depressed during pacing at epicardial LV free wall sites, and was most severely depressed during RV apex pacing. On average, RV septal pacing did not improve LV function, compared with RV apex pacing, but in each experiment one (variable) RV pacing site was found, which only moderately reduced LV function. CONCLUSIONS: During ventricular pacing, LV pump function is maintained best (i.e., at SR level) when pacing at the LV septum or LV apex, potentially because pacing from these sites creates a physiological propagation of electrical conduction.     

Impact of different activation wavefronts on ischemic myocardial scar electrophysiological properties during high-density ventricular tachycardia mapping and ablation

Introduction

Scar-related ventricular tachycardia (VT) usually results from an underlying reentrant circuit facilitated by anatomical and functional barriers. The later are sensitive to the direction of ventricular activation wavefronts. We aim to evaluate the impact of different ventricular activation wavefronts on the functional electrophysiological properties of myocardial tissue.

Methods

Patients with ischemic heart disease referred for VT ablation underwent high-density mapping using Carto®3 (Biosense Webster). Maps were generated during sinus rhythm, right and left ventricular pacing, and analyzed using a new late potential map software, which allows to assess local conduction velocities and facilitates the delineation of intra-scar conduction corridors (ISCC); and for all stable VTs.

Results

In 16 patients, 31 high-resolution substrate maps from different ventricular activation wavefronts and 7 VT activation maps were obtained. Local abnormal ventricular activities (LAVAs) were found in VT isthmus, but also in noncritical areas. The VT isthmus was localized in areas of LAVAs overlapping surface between the different activation wavefronts. The deceleration zone location differed depending on activation wavefronts. Sixty-six percent of ISCCs were similarly identified in all activating wavefronts, but the one acting as VT isthmus was simultaneously identified in all activation wavefronts in all cases.

Conclusion

Functional based substrate mapping may improve the specificity to localize the most arrhythmogenic regions within the scar, making the use of different activation wavefronts unnecessary in most cases.     

Epicardial and endocardial mapping of ventricular tachycardia in patients with myocardial infarction. Is the origin of the tachycardia always subendocardially localized?

BACKGROUND. Left ventricular endocardial reentry is the conventional concept underlying surgery for ventricular tachycardia (VT). We assessed the incidences of patterns showing complete reentry circuits at either the subendocardial or subepicardial level and of patterns in which left ventricular endocardial mapping could only in part account for a reentrant mechanism. METHODS AND RESULTS. We retrospectively analyzed epicardial and left ventricular endocardial isochronal maps of 47 VTs induced in 28 patients with chronic myocardial infarction (inferior, 14 patients; anteroseptal, 14 patients). Electrograms were recorded intraoperatively from 128 sites with epicardial sock and transatrial left ventricular endocardial balloon electrode arrays. Given the methodology used in this study, the mapping characteristics of the tachycardias suggested five types of activation patterns: 1) complete (90% or more of VT cycle length) subendocardial reentry circuits in seven VTs (15%) and seven patients (25%), 2) complete subepicardial reentry circuits in four VTs (9%) and four patients (14%), 3) incompletely mapped circuits with a left ventricular endocardial breakthrough preceding the epicardial breakthrough in 25 VTs (53%) and 21 patients (75%), 4) incompletely mapped circuits with a left ventricular epicardial breakthrough preceding the endocardial breakthrough in three VTs (6%) and three patients (11%), and 5) a right ventricular epicardial breakthrough preceding the left ventricular endocardial breakthrough in eight VTs (17%) and seven patients (25%). After surgery, one type 3 VT and three type 5 VTs were reinducible. Thus, left ventricular endocardial reentry substrates (types 1 and 3) accounted for 68% of VTs, but substrates involving subepicardial (types 2 and 4) and deep septal layers (type 5) accounted for 32% of VTs. CONCLUSIONS: In a substantial number of VTs, a substrate localization that is at variance with the conventional concept can be detected by simultaneous epicardial and endocardial mapping and may require modification of the surgical approach conventionally aimed at endocardial layers.     

Body surface mapping of ectopic left and right ventricular activation. QRS spectrum in patients without structural heart disease

The value of simultaneous 62-lead electrocardiographic recordings in localizing the site of origin of ectopic ventricular activation in a structurally normal heart was assessed by examining body surface QRS integral maps in 12 patients during left and right ventricular (LV and RV) pacing at 182 distinct endocardial sites. A data base of 38 characteristic mean integral maps was composed after visually selecting subgroups with nearly identical total QRS integral morphology and numerically evaluating intrasubgroup pattern uniformity and intersubgroup pattern variability. Corresponding endocardial pacing site locations were computed by a biplane cineradiographic method and outlined as segments on a standardized LV and RV polar projection. LV pacing resulted in 25 markedly different mean total QRS integral patterns, showing higher electrocardiographic sensitivity for anteroseptal (18 patterns) compared with posterolateral regions (seven patterns). RV pacing demonstrated 13 mean total QRS integral patterns, exhibiting less intersubgroup variation and comparatively low electrocardiographic sensitivity for the basal anterior and outflow regions. Comparison of LV with RV pacing revealed that QRS configurations produced at LV apical and LV midseptal sites closely resembled QRS configurations generated at RV apical, RV septal, and RV anterior sites, respectively. Total QRS time integral amplitudes showed considerable intrasubgroup variation but permitted global differentiation of spatially similar QRS patterns obtained during pacing at LV and RV sites. This study demonstrates that the QRS pattern of the total body surface electrocardiogram allows discrimination among 38 different LV and RV segments of ectopic endocardial impulse formation in patients with normal cardiac anatomy.     

Mapping and ablation of ventricular tachycardia guided by virtual electrograms using a noncontact, computerized mapping system

OBJECTIVES: The purpose of this study was to describe a computerized mapping system that utilizes a noncontact, 64 electrode balloon catheter to compute virtual electrograms simultaneously at 3,360 left ventricular (LV) sites and to assess the clinical utility of this system for mapping and ablating ventricular tachycardia (VT). BACKGROUND: Mapping VT in the electrophysiology laboratory conventionally is achieved by sequentially positioning an electrode catheter at multiple endocardial sites. METHODS: Fifteen patients with VT underwent 18 electrophysiology procedures using the noncontact, computerized mapping system. A 9F 64 electrode balloon catheter and a conventional 7F electrode catheter for mapping and ablation were positioned in the LV using a retrograde aortic approach. Using a boundary element inverse solution, 3,360 virtual endocardial electrograms were computed and used to derive isopotential maps. An incorporated locator system was used in conjunction with or instead of fluoroscopy to position the conventional electrode catheter. RESULTS: A total of 21 VTs, 12 of which were hemodynamically-tolerated and 9 of which were not, were mapped. Isolated diastolic potentials, presystolic areas, zones of slow conduction and exit sites during VT were identified using virtual electrograms and isopotential maps. Among 19 targeted VTs, radiofrequency ablation guided by the computerized mapping system and the locator signal was successful in 15. CONCLUSIONS: The computerized mapping system described in this study computes accurate isopotential maps that are a useful guide for ablation of hemodynamically stable or unstable VT.     

Radiofrequency ablation of infarct scar-related ventricular tachycardia: correlation of electroanatomical data with post-mortem histology

Introduction: Histological data after VT ablation in humans is rare. We present a case of a patient who had ablation for VT storm and who died remotely from non-arrhythmic causes.
Methods and Results: A 69-year-old male with ischemic cardiomyopathy and a dual-chamber implantable cardioverter defibrillator (ICD) presented with VT storm and multiple ICD therapies. A voltage map of the left-ventricular (LV) scar was created using CARTO™. VT was induced. An isochronal map identified the VT exit site at the scar border. No diastolic potentials were seen in this territory, so VT exit site ablation was performed, as well as at a putative entry site. VT cycle length and morphology changed during ablation, but termination only occurred with burst pacing. Post-ablation, the patient had no further shocks. He died seven months later from acute pancreatitis. The two ablation sites were identified on the post-mortem heart and used to correlate with the electroanatomical map. Scar area correlated well, measuring approximately 58.4 cm² macroscopically and 63.3 cm² on the electroanatomical map. Histology at VT exit site demonstrated areas of viable epicardial myocardium, suggesting that the circuit was at the epicardial scar border, which would explain the lack of diastolic potentials. Ablation scar did not reach the epicardium and therefore, ablation may have modified the exit site without complete interruption of the VT circuit.
Conclusions: In this case, ablation was unable to terminate the VT due to failure to reach the epicardium, but was sufficient to modify the tachycardia, thereby reducing ICD therapy.     

Preferential conduction across the ventricular outflow septum in ventricular arrhythmias originating from the aortic sinus cusp.

OBJECTIVES: The purpose of this study was to examine the relationship between the origin and breakout site of idiopathic ventricular tachycardia (VT) or premature ventricular contractions (PVCs) originating from the myocardium around the ventricular outflow tract. BACKGROUND: The myocardial network around the ventricular outflow tract is not well known. METHODS: We studied 70 patients with idiopathic VT (n = 23) or PVCs (n = 47) with a left bundle branch block and inferior QRS axis morphology. Electroanatomical mapping was performed in both the right ventricular outflow tract (RVOT) and aortic sinus cusp (ASC) during VT or PVCs. RESULTS: The earliest ventricular activation (EVA) was recorded in the RVOT in 55 patients (group R) and in the ASC in 15 (group A). In all group R patients, the closest pace map and successful ablation were achieved at the EVA site. Although a successful ablation was achieved at the EVA site in all group A patients, the closest pace map was obtained at the EVA site in 8 and RVOT in 7 (with an excellent pace map in 4). The stimulus to QRS interval was 0 ms during pacing from the RVOT and 36 +/- 8 ms from the ASC. The distance between the EVA and perfect pace map sites in those 4 patients was 11.9 +/- 3.0 mm. CONCLUSIONS: Ventricular arrhythmias originating from the ASC often show preferential conduction to the RVOT, which may render pace mapping or some algorithms using the electrocardiographic characteristics less reliable. In some of those cases, an insulated myocardial fiber across the ventricular outflow septum may exist.     

Effects of right ventricular pacing on intra-left ventricular electromechanical activation in patients with native narrow QRS

Some patients with right ventricular (RV) apical pacing show contractile asynchrony of the left ventricle. Whether the asynchrony is due to RV pacing or was a preexistimg condition remains unknown. The aim of this study was to evaluate how much pacing from the RV apex affects left ventricular (LV) electromechanical activation and to assess whether the extent of LV asynchrony during RV pacing can be predicted by clinical, electrocardiographic, or echocardiographic findings obtained during spontaneous rhythm. We evaluated 56 patients with narrow QRS and preserved atrioventricular conduction who received permanent backup RV pacing. Intra-LV electromechanical activation was assessed during spontaneous rhythm and during pacing using tissue Doppler echocardiography. An abnormal intra-LV electromechanical delay (EMD) (defined as a >41-ms difference between the faster and slower activated LV wall) was found in 15 patients (27%) during spontaneous rhythm and 28 patients (50%) during RV pacing (p<0.001). Of the 9 baseline variables (age, gender, history of heart failure, QRS duration in spontaneous rhythm and during pacing, LV end-diastolic and end-systolic diameters, LV ejection fraction, and intra-LV EMD in spontaneous rhythm), an abnormal baseline intra-LV EMD and QRS duration of >85 ms were independent predictors of an abnormal intra-LV delay during RV pacing. RV apical pacing induces asynchrony of LV contractions in a substantial percentage of patients but not in all. Although normal baseline intra-LV electromechanical activation cannot exclude the development of significant asynchrony during RV pacing, the presence of preimplant LV asynchrony predicts for a worsening of this detrimental effect.     

Functional role of the epicardium in postinfarction ventricular tachycardia. Observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation

BACKGROUND. Conventionally, monomorphic sustained ventricular tachycardia in patients with remote myocardial infarction is believed to originate from the subendocardium. In a previous study, we demonstrated that electrical activation patterns during ventricular tachycardia occasionally suggest a subepicardial rather than subendocardial reentry. METHODS AND RESULTS. This study prospectively evaluated the functional role of the epicardium in postinfarction ventricular tachycardia with complex intraoperative techniques including computerized electrical activation mapping, entrainment, observation of changes in activation pattern during successful epicardial laser photoblation, and histological study. Five of 10 consecutive patients undergoing intraoperative computerized activation mapping had 10 ventricular tachycardia morphologies displaying epicardial diastolic activation These 10 "epicardial" ventricular tachycardias revealed the following global activation patterns: monoregional spread (two), figure-eight activation (five), and circular macroreentry (three). Entrainment of ventricular tachycardia using epicardial stimulation was successfully performed from an area of slow diastolic conduction in four tachycardia morphologies. During entrainment, global activation remained undisturbed with recordings showing a long stimulus to QRS interval, unchanged QRS morphology, and pacing capture of all components of the reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation was delivered during ventricular tachycardia to epicardial sites of presumed reentry. Epicardial photoablation terminated five of five figure-eight tachycardias, two of three circular macroreentry tachycardias but not the monoregional tachycardias. Electrophysiological recordings during epicardial laser photocoagulation demonstrated progressive prolongation of ventricular tachycardia cycle length and apparent interruption of the presumed reentrant circuit. Histological evaluation of the reentrant region (three patients) showed a rim of surviving myocardium under the epicardial surface. CONCLUSIONS. This study suggests that 1) chronic postinfarction ventricular tachycardia may result from subepicardial macroreentry, 2) slow conduction within the reentry circuit can be localized by computerized mapping and epicardial entrainment, and 3) ventricular tachycardia interruption by laser photocoagulation results from conduction delay and block within critical elements of the reentrant pathway. Viable subepicardial muscle fibers may constitute the underlying pathology.     

Novel mechanism of postinfarction ventricular tachycardia originating in surviving left posterior Purkinje fibers

BACKGROUND: Other than bundle branch reentry and interfascicular reentry, monomorphic postmyocardial infarction (post-MI) reentrant ventricular tachycardia (VT) including the His-Purkinje system has not been reported. Verapamil-sensitive idiopathic left VT includes the left posterior Purkinje fibers but develops in patients without structural heart disease. OBJECTIVES: The purpose of this study was to describe a novel mechanism of reentrant VT arising from the left posterior Purkinje fibers in patients with a prior MI. METHODS: The study consisted of four patients with a prior MI and symptomatic heart failure who underwent electrophysiologic study and catheter ablation for VT showing right bundle branch block (n = 3) or atypical left bundle branch block (n = 1) morphology with superior axis. In two patients, the VT frequently emerged during the acute phase of MI and required emergency catheter ablation. RESULTS: Clinical VT was reproducibly induced by programmed stimulation. In three patients, both diastolic and presystolic Purkinje potentials were sequentially recorded along the left ventricular posterior septum during the VT, whereas in the fourth patient, only presystolic Purkinje potentials were observed. During entrainment pacing from the right atrium, diastolic Purkinje potentials were captured orthodromically and demonstrated decremental conduction properties, whereas presystolic Purkinje potentials were captured antidromically and appeared between the His and QRS complex. Radiofrequency energy delivered at the site exhibiting a Purkinje-QRS interval of 58 +/- 26 ms successfully eliminated the VTs without provoking any conduction disturbances. CONCLUSION: Reentrant monomorphic VT originating from the left posterior Purkinje fibers, which is analogous to idiopathic left VT, can develop in the acute or chronic phase of MI. Catheter ablation is highly effective in eliminating this VT without affecting left ventricular conduction.     

右室心尖部起搏对左室电机械活动的影响

目的运用超声心动图和组织多普勒检查,分析右室心尖部起搏对左室电机械活动的影响;探讨能够预测右室心尖部起搏后左室内机械活动不同步性的因素。方法选取因病窦综合征置入双腔永久起搏器的患者28例,术后7天分别测量患者在自身心律、VVI起搏两种状态下的超声心动图和组织多普勒心功能指数(Tei指数)、左室内不同步指数(Ts-SD)等参数并分析左室内机械活动不同步的影响因素。结果64.2%的患者在右室起搏期间,表现为左室机械活动的不同步;Ts-SD显著增加(40.10±18.50 ms vs 29.96±18.87 ms,P=0.034);右室起搏后Tei指数明显增加(0.49±0.23 vs 0.38±0.21,P(0.01);自身心律状态下的Ts-SD指数是右室起搏时出现左室收缩不同步现象的独立预测因素(OR=1.079,P=0.029)。结论右室心尖部起搏导致左右心室之间及左室内收缩不同步,对患者心脏整体功能带来不利的影响。