Use of electroanatomic mapping to delineate transseptal atrial conduction in humans.

BACKGROUND: Interaction between wave fronts in the right and left atrium may be important for maintenance of atrial fibrillation, but little is known about electrophysiological properties and preferential routes of transseptal conduction. METHODS AND RESULTS: Eighteen patients (age 44+/-12 years) without structural heart disease underwent right atrial electroanatomic mapping during pacing from the distal coronary sinus (CS) or the posterior left atrium. During distal CS pacing, 9 patients demonstrated a single transseptal breakthrough near the CS os, 1 patient in the high right atrium near the presumed insertion of Bachmann's bundle and 1 patient near the fossa ovalis. The mean activation time from stimulus to CS os was 48+/-15 ms compared with 86+/-15 ms to Bachmann's bundle insertion (P<0.01) and 59+/-23 ms to the fossa ovalis (P=NS and P<0.01, respectively). During left atrial pacing, the earliest right atrial activation was near Bachmann's bundle in 5 and near the fossa ovalis in 4 patients. The activation time from stimulus to CS os was 70+/-15 ms compared with 47+/-16 ms to Bachmann's bundle (P<0.01) and 59+/-25 ms to the fossa ovalis (P=NS). Whereas the total septal activation time was not significantly different during CS pacing compared with left atrial pacing (41+/-16 versus 33+/-17 ms), the total right atrial activation time was longer during CS pacing (117+/-49 versus 79+/-15 ms; P<0.05). CONCLUSIONS: Three distinct sites of early right atrial activation may be demonstrated during left atrial pacing. These sites are in accord with anatomic muscle bundles and may have relevance for maintenance of atrial flutter or fibrillation.

Electrocardiographic identification of abnormal ventricular depolarization and repolarization in patients with idiopathic ventricular fibrillation.

OBJECTIVES: We sought to gain more insight into the arrhythmogenic etiology of idiopathic ventricular fibrillation (VF) by assessing ventricular depolarization and repolarization properties by means of various electrocardiographic (ECG) techniques. BACKGROUND: Idiopathic VF occurs in the absence of demonstrable structural heart disease. Abnormalities in ventricular depolarization or repolarization have been related to increased vulnerability to VF in various cardiac disorders and are possibly also present in patients with idiopathic VF. METHODS: In 17 patients with a first episode of idiopathic VF, 62-lead body surface QRST integral maps, QT dispersion on the 12-lead ECG and XYZ-lead signal-averaged ECGs were computed. RESULTS: All subjects of a healthy control group had a normal dipolar QRST integral map. In patients with idiopathic VF, either a normal dipolar map (29%,), a dipolar map with an abnormally large negative area on the right side of the thorax (24%) or a nondipolar map (47%) were recorded. Only four patients (24%) had increased QT dispersion on the 12-lead ECG and late potentials could be recorded in 6 (38%) of 16 patients. During a median follow-up duration of 56 months (range 9 to 136), a recurrent arrhythmic event occurred in 7 patients (41%), all of whom had an abnormal QRST integral map. Five of these patients had late potentials, and three showed increased QT dispersion on the 12-lead ECG. CONCLUSIONS: In patients with idiopathic VF, ventricular areas of slow conduction, regionally delayed repolarization or dispersion in repolarization can be identified. Therefore, various electrophysiologic conditions, alone or in combination, may be responsible for the occurrence of idiopathic VF. Body surface QRST integral mapping may be a promising method to identify those patients who do not show a recurrent episode of VF.

Body surface mapping of counterclockwise and clockwise typical atrial flutter: a comparative analysis with endocardial activation sequence mapping.

OBJECTIVES: This study was directed at developing spatial 62-lead electrocardiogram (ECG) criteria for classification of counterclockwise (CCW) and clockwise (CW) typical atrial flutter (Fl) in patients with and without structural heart disease. BACKGROUND: Electrocardiographic classification of CCW and CW typical atrial Fl is frequently hampered by inaccurate and inconclusive scalar waveform analysis of the 12-lead ECG. METHODS: Electrocardiogram signals from 62 torso sites and multisite endocardial recordings were obtained during CCW typical atrial Fl (12 patients), CW typical Fl (3 patients), both forms of typical Fl (4 patients) and CCW typical and atypical atrial Fl (1 patient). All the Fl wave episodes were divided into two or three successive time periods showing stable potential distributions from which integral maps were computed. RESULTS: The initial, intermediate and terminal CCW Fl wave map patterns coincided with: 1) caudocranial activation of the right atrial septum and proximal-to-distal coronary sinus activation, 2) craniocaudal activation of the right atrial free wall, and 3) activation of the lateral part of the subeustachian isthmus, respectively. The initial, intermediate and terminal CW Fl wave map patterns corresponded with : 1) craniocaudal right atrial septal activation, 2) activation of the subeustachian isthmus and proximal-to-distal coronary sinus activation, and 3) caudocranial right atrial free wall activation, respectively. A reference set of typical CCW and CW mean integral maps of the three successive Fl wave periods was computed after establishing a high degree of quantitative interpatient integral map pattern correspondence irrespective of the presence or absence of organic heart disease. CONCLUSIONS: The 62-lead ECG of CCW and CW typical atrial Fl in man is characterized by a stereotypical spatial voltage distribution that can be directly related to the underlying activation sequence and is highly specific to the direction of Fl wave rotation. The mean CCW and CW Fl wave integral maps present a unique reference set for improved clinical detection and classification of typical atrial Fl.

Value of body surface mapping in localizing the site of origin of ventricular tachycardia in patients with previous myocardial infarction.

OBJECTIVES: This study examined the performance of the 62-lead body surface electrocardiogram (ECG) in identifying the site of origin of ventricular tachycardia in patients with a previous myocardial infarction. BACKGROUND: Because the accuracy of ECG localization of ventricular tachycardia using standard 12-lead recordings is restricted to the identification of rather large ventricular areas, application of multiple torso lead recordings may augment the resolving power of the surface ECG and result in more discrete localization of arrhythmogenic foci. METHODS: Thirty-two patients were selected for electrophysiologically guided ablative therapy for drug-resistant postinfarction ventricular tachycardia. In these patients, QRS integral maps of distinct monomorphic ventricular tachycardia configurations were correlated with a previously generated infarct-specific reference data base of paced QRS integral maps. Each paced pattern in the data base corresponded with ectopic endocardial impulse formation at 1 of 18 or 22 discrete segments of the left ventricle with a previous anterior or inferior myocardial infarction, respectively. Electrocardiographic localization was compared with the results obtained during intraoperative or catheter endocardial activation sequence mapping. RESULTS: Body surface mapping was performed during 101 distinct ventricular tachycardia configurations. Compared with the activation mapping data that were acquired in 64 of 101 ventricular tachycardias, body surface mapping identified the correct segment of origin in 40 (62%) of 64 tachycardias, a segment adjacent to the segment where the arrhythmia actually originated in 19 (30%) of 64 tachycardias and a segment disparate from the actual segment of origin in 5 (8%) of 64 tachycardias. With respect to infarct location, the segment of origin was correctly identified in 28 (60%) of 47 ventricular tachycardias in patients with anterior, 7 (70%) of 10 tachycardias in patients with inferior and 5 (71%) of 7 tachycardias in patients with combined anterior and inferior myocardial infarction. CONCLUSIONS: This study shows that body surface mapping enables precise localization of the origin of postinfarction ventricular tachycardia in 62% and regional approximation in 30% of tachycardias. The multiple-lead ECG may be used to guide and shorten catheter-based mapping procedures during ventricular tachycardia and to provide relevant information on the origin of tachycardias that cannot be mapped with conventional single-site mapping techniques because of unfavorable characteristics.

Continuous localization of cardiac activation sites using a database of multichannel ECG recordings.

Monomorphic ventricular tachycardia and ventricular extrasystoles have a specific exit site that can be localized using the multichannel surface electrocardiogram (ECG) and a database of paced ECG recordings. An algorithm is presented that improves on previous methods by providing a continuous estimate of the coordinates of the exit site instead of selecting one out of 25 predetermined segments. The accuracy improvement is greatest, and most useful, when adjacent pacing sites in individual patients are localized relative to each other. Important advantages of the new method are the objectivity and reproducibility of the localization results.

Automatic QRS onset and offset detection for body surface QRS integral mapping of ventricular tachycardia.

A QRS onset and offset detection algorithm has been developed for use in body surface QRS integral mapping of ventricular tachycardia. To determine QRS intervals, the algorithm uses two computed signals: the sum of the absolute values of the first derivatives of all leads and the sum of the absolute values of all leads. The second order derivative of the latter parameter is used to detect the time instants of QRS onset and offset. Using the algorithm, QRS integral maps are subsequently computed, which are correlated with a database of QRS integral maps in order to localize the site of origin of ventricular tachycardia. Comparison of the performance of the algorithm with visual evaluation by a human expert in this procedure revealed, in 95% of the cases, an identical or adjacent localization of the site of origin.

The spatial dispersion of atrial refractoriness and atrial fibrillation vulnerability.

The local dispersion of conduction and refractoriness has been considered essential for induction of atrial arrhythmias. This study sought to determine whether a difference of refractoriness and vulnerability for induction of atrial fibrillation between trabeculated and smooth as well as high and low right atrium may contribute to initiation of atrial fibrillation in dogs. In 14 healthy mongrel dogs weighing 22.4 +/- 1 kg, closed-chest endocardial programmed stimulation was performed from four distinct right atrial sites. Atrial refractory periods and vulnerability for induction of atrial fibrillation or premature atrial complexes were determined during a basic cycle length of 400 and 300 ms and an increasing pacing current strength. For a pacing cycle length of 300 ms, atrial refractory periods were longer on the smooth, as compared to the trabeculated right atrium (102 +/- 25 vs. 97 +/- 17 ms, p < 0.05), whereas for a pacing cycle length of 400 ms, there was no significant difference. The duration of the vulnerability zone for induction of atrial fibrillation was longer on the smooth right atrium, for a cycle length of both 400 ms (40 +/- 30 vs. 31 +/- 22 ms; p < 0.05) and 300 ms (33 +/- 25 vs. 23 +/- 21 ms; p < 0. 01). When comparing high and low right atrium, refractory periods were longer on the the low right atrium, for a cycle length of both 400 ms (111 +/- 23 vs. 94 +/- 24 ms; p < 0.01) and 300 ms (104 +/- 20 vs. 96 +/- 23 ms; p < 0.01). For a pacing cycle length of 300 ms, the duration of the atrial fibrillation vulnerability zone was longer for the high, as compared to the low right atrium (34 +/- 22 vs. 22 +/- 22, p < 0.01). Seven dogs with easily inducible episodes of atrial fibrillation demonstrated significantly shorter refractory periods as compared to 7 non-vulnerable dogs, regardless of pacing site and current strength. In conclusion, significant differences in refractoriness and vulnerability for induction of atrial fibrillation can be observed in the area of the crista terminalis in healthy dogs. Thus, local anatomic factors may play a role in the initiation of atrial fibrillation.

Conversion of left ventricular endocardial positions from patient-independent co-ordinates into biplane fluoroscopic projections.

Electrocardiographic body surface mapping is used clinically to guide catheter ablation of cardiac arrhythmias by providing an estimate of the site of origin of an arrhythmia. The localisation methods used in our group produce results in left-ventricular cylinder co-ordinates (LVCCs), which are patient-independent but hard to interpret during catheterisation in the electrophysiology laboratory. It is preferable to provide these results as three-dimensional (3D) co-ordinates which can be presented as projections in the biplane fluoroscopic views that are used routinely to monitor the catheter position. Investigations were carried out into how well LVCCs can be converted into fluoroscopic projections with the limited anatomical data available in contemporary clinical practice. Endocardial surfaces from magnetic resonance imaging (MRI) scans of 24 healthy volunteers were used to create an appropriate model of the left-ventricular endocardial wall. Methods for estimation of model parameters from biplane fluoroscopic images were evaluated using simulated biplane data created from these surfaces. In addition, the conversion method was evaluated, using 107 catheter positions obtained from eight patients, by computing LVCCs from biplane fluoroscopic images and reconstructing the 3D positions using the model. The median 3D distance between reconstructed positions and measured positions was 4.3mm.

Derivation of an optimal lead set for measuring ectopic atrial activation from the pulmonary veins by using body surface mapping.

Atrial fibrillation is often initiated by atrial premature beats originating in the pulmonary veins. Non-invasive localization of these ectopic beats would be of significant value in guiding therapy. Body surface potential mapping was performed in nine patients undergoing invasive electrophysiologic study. Signals were recorded from 62 electrodes during pace mapping from each of the pulmonary veins. Optimal electrodes for localizing pulmonary vein activation were sequentially chosen. Seven optimal electrodes (6 anterior, 1 posterior) for recording ectopic atrial activation originating in the pulmonary veins were selected. The seven optimal electrode set performed better than the standard 9 electrode ECG at estimating the full body surface map (correlation 97 vs. 95.7%; p < 0.05). Seven optimally selected electrodes can estimate the body surface potential distribution during ectopic atrial activation orignating from the pulmonary veins. The ability of this electrode configuration to discriminate the site of origin of ectopic atrial beats requires prospective evaluation.

Relationship between atrial fibrillation and typical atrial flutter in humans: activation sequence changes during spontaneous conversion.

BACKGROUND: A transitional rhythm precedes the spontaneous onset of atrial flutter in an animal model, but few data are available in man. METHODS AND RESULTS: In 10 patients, 16 episodes of atrial fibrillation (166+/-236 seconds) converting into atrial flutter during electrophysiological evaluation were analyzed. A 20-pole catheter was used for mapping the right atrial free wall. Preceding the conversion was a characteristic sequence of events: (1) a gradual increase in atrial fibrillation cycle length (150+/-25 ms after onset, 166+/-28 ms before conversion, P<.01); (2) an electrically silent period (267+/-45 ms); (3) "organized atrial fibrillation" (cycle length, 184+/-24 ms) with the same right atrial free wall activation direction as during atrial flutter; (4) another delay on the lateral right atrium (283+/-52 ms); and (5) typical atrial flutter (cycle length, 245+/-38 ms). The coronary sinus generally had a different rate than the right atrial free wall until the beat that initiated flutter, when right atrium and coronary sinus were activated in sequence. During 1313 seconds of fibrillation, there were 171 episodes of "organized atrial fibrillation." An additional activation delay at least 30 ms longer than the mean organized atrial fibrillation cycle length was sensitive (100%) and specific (99%) for impending organization into atrial flutter. During organized atrial fibrillation, right atrial free wall activation was craniocaudal in 70% and caudocranial in 30%, which may explain why counterclockwise flutter is a more common clinical rhythm than clockwise flutter. Atrial flutter never degenerated into fibrillation, even after adenosine infusion. CONCLUSIONS: Anatomic barriers, along with statistical properties of conduction and refractoriness during atrial fibrillation, may explain the remarkably stereotypical pattern of endocardial activation during the initiation of atrial flutter via fibrillation and the rarity of degeneration of flutter to fibrillation once it stabilizes.

Body surface mapping during percutaneous transluminal coronary angioplasty. QRS changes indicating regional myocardial conduction delay.

Using a radiotransparent electrode array, body surface maps (BSMs) were constructed based on simultaneous recordings from 62 leads on the entire thorax before, during, and after balloon inflation during percutaneous transluminal coronary angioplasty (PTCA). Twenty-five patients were studied, and 30 angioplasties were performed; 20 patients had one-vessel disease, and five patients had two-vessel disease. In total, 15 dilations in the left anterior descending artery (LAD), seven in the right coronary artery (RCA), and eight in the left circumflex artery (LCx) were studied. For each patient, the BSM and the QRS integral map before, during, and after the inflation was compared by subtraction of recordings "during-minus-before" inflation and "before-minus-after" inflation. The subtraction was performed on the results of the QRS integral maps. The conclusions derived from the inspection of the BSMs and the difference maps show specific changes in the QRS complex during ischemia related to the corresponding ischemic segment in 21 of 25 patients in the three groups. An area of positive potentials remained present on the BSM during dilation, indicating a depolarization wave front. For the LAD group, positive potentials were seen on the anterior thorax and, for the RCA group, on the lower part of the thorax. By subtraction analysis, these changes were extracted and presented as difference maps. For the LCx group, the BSM revealed no changes in pattern but the difference map showed a difference vector pointing in a anteroposterior direction. A regional myocardial conduction delay was hypothesized as the most likely cause for the results.

The role of the crista terminalis in atrial flutter and fibrillation: a computer modeling study.

Although atrial fibrillation is a common arrhythmia, the underlying mechanisms are incompletely understood. Recent studies have determined the role of the crista terminalis in the mechanisms of a simpler arrhythmia, atrial flutter. We hypothesize that as transverse coupling across the crista terminalis increases, the activation pattern that results is less like typical atrial flutter and more like atrial fibrillation. 6480 Van Capelle elements were coupled in an icosahedron, simulating the right atrium. Atrial simulations were created which incorporated no heterogeneity, heterogeneous coupling, heterogeneous effective refractory periods, and both heterogeneous coupling and effective refractory periods. When the entire crista terminalis was uncoupled, typical atrial flutter occurred. When transverse coupling allowed activation to propagate across the crista terminalis, the flutter cycle length decreased (p<0.0001). In addition, when heterogeneity was present, both the coefficient of variation of cycle length and the number of activation wavelets increased (p<0.0001). Thus, a more rapid reentrant circuit in the superior right atrium drove fibrillatory activity in the remainder of the atrium, as predicted by the "mother wavelet hypothesis." While awaiting in vivo validation, our study indicates that transverse coupling along the crista terminalis may play an important role in the development of atrial fibrillation from atrial flutter.

Electrocardiographic analysis of ectopic atrial activity obscured by ventricular repolarization: P wave isolation using an automatic 62-lead QRST subtraction algorithm.

INTRODUCTION: Atrial activity on the surface ECG during premature beats and supraventricular arrhythmias frequently is obscured by the superimposed QRST complex of the previous cardiac cycle. This study examines the performance of a newly developed automatic QRST subtraction algorithm to isolate ectopic P waves from the preceding T-U wave. METHODS AND RESULTS: The 62-lead ECG recordings were obtained during (1) sinus rhythm and programmed right atrial stimulation in 12 patients (group A); and (2) sinus rhythm and atrial premature beats, atrial tachycardia, or paroxysmal atrial fibrillation in 5 patients (group B). Pacing in group A patients was conducted at a slow drive cycle length to generate an ectopic P wave not obscured by the previous QRST complex and by delivering single premature extrastimuli at progressively shorter coupling intervals to produce an ectopic P wave obscured by the upsloping (early T-U wave), peak (middle T-U wave), and downsloping component of the T-U wave (late T-U wave). All ectopic P waves in group B patients were concealed by the preceding T-U wave. Automatic QRST subtraction was attained using an adaptive template constructed from averaged QRST complexes (mean 83 +/- 25 complexes) obtained during sinus rhythm (groups A and B) or atrial overdrive pacing (group A). P wave integral maps subsequently were computed, visually compared, and mathematically correlated. A high correspondence in spatial map pattern was observed between integral maps of "nonobscured" and previously "obscured" paced P waves obtained in group A patients (mean r = 0.88 +/- 0.07) as well as between integral maps of two to three previously obscured P waves with the same atrial arrhythmia morphology obtained in group B patients (mean r = 0.94 +/- 0.05). Improved morphologic P wave replication in group A patients was acquired when concealment occurred in the early (mean r = 0.90 +/- 0.08) or late part of the T-U wave (mean r = 0.90 +/- 0.06) as opposed to the middle T-U wave (mean r = 0.85 +/- 0.07) (P = NS and P < 0.05 for early vs middle and late vs middle T-U wave, respectively). CONCLUSION: This novel automatic 62-lead QRST subtraction algorithm enables discrete isolation of T-U wave obscured ectopic atrial activity on the surface ECG while retaining the intricate spatial detail in P wave morphology. Future clinical application of the algorithm may enable improved ECG localization of focal triggers of paroxysmal atrial fibrillation, atrial tachycardia, and the atrial insertion of accessory pathways.

Organized activation during atrial fibrillation in man: endocardial and electrocardiographic manifestations.

INTRODUCTION: Atrial fibrillation is not entirely random, but little is known about the spatiotemporal endocardial organization and its surface ECG manifestations. METHODS AND RESULTS: In 16 patients with atrial fibrillation (chronic, n = 14), endocardial mapping of the trabeculated, the posteroseptal smooth right atrium, and the coronary sinus was performed using multipolar catheters. The surface ECG was analyzed by determining "fibrillation wave" (F wave) amplitude, rate, and polarity. During 50 minutes of atrial fibrillation, an organized activation was present 72% +/- 32% of the analyzed time on the trabeculated, 19% +/- 15% on the smooth right atrium (P < 0.01), and 51% +/- 33% along the coronary sinus (P < 0.05). The direction of organized activation was craniocaudal in 72% +/- 16%, caudocranial in 10% +/- 9% (P < 0.01), and indeterminable in 18% +/- 11%. The mean surface F wave amplitude in lead V1 was 0.128 +/- 0.06 mV during 28 seconds of atrial fibrillation with a craniocaudal direction of activation and 0.065 +/- 0.02 mV during a disorganized activation (P < 0.01). A stable relation between surface F waves and organized trabeculated right atrial activation was observed, and the mean F wave cycle length (190 +/- 27 msec) was highly comparable to the simultaneously measured endocardial cycle length (191 +/- 27 msec, correlation coefficient 0.97). F wave polarity in V1 was positive in 12 of 14 patients during craniocaudal and negative in 11 of 14 patients during caudocranial right atrial free-wall activation. CONCLUSION: An organized activation during atrial fibrillation with a predominant craniocaudal direction on the trabeculated right atrium is frequently present and influences the appearance of "coarse" or "fine" atrial fibrillation as well as F wave polarity on the surface ECG.

Association of left ventricular remodeling and nonuniform electrical recovery expressed by nondipolar QRST integral map patterns in survivors of a first anterior myocardial infarction. Captopril and Thrombolysis Study Investigators.

BACKGROUND: Progressive left ventricular dilatation after myocardial infarction is associated with a high mortality rate, the majority of which is arrhythmogenic in origin. The underlying mechanism of this relation remains unknown. It has been suggested, however, that left ventricular dilatation is accompanied by changes in repolarization characteristics that may facilitate the occurrence of life-threatening ventricular arrhythmias. METHODS AND RESULTS: We examined 62-lead body surface QRST integral maps during sinus rhythm in 78 patients at 349 +/- 141 days after thrombolysis for a first anterior myocardial infarction. Visual map analysis was directed at discriminating dipolar (uniform repolarization) from nondipolar (nonuniform repolarization) patterns. In addition, the nondipolar content of each map was assessed quantitatively with the use of eigenvector analysis. Nondipolar map patterns were present in almost one third of the patients (32%). Left ventricular end-systolic and end-diastolic volumes were assessed echocardiographically before discharge and after 3 and 12 months with the use of the modified biplane Simpson rule. The increase in left ventricular end-systolic volume 1 year after myocardial infarction was more pronounced in patients with nondipolar QRST integral map patterns (14.47 +/- 14.10 versus 4.22 +/- 8.44 mL/m2, P = .017). In patients with an increase in end-systolic volume of more than 16 mL/m2 (upper quartile), the prevalence of nondipolar maps was 89% compared with 29% in patients with dilatation of less than 16 mL/m2. In addition, the nondipolar content of maps in patients in the upper quartile was significantly increased compared with the lower quartiles (49 +/- 14% versus 37 +/- 12%, P = .013). Logistic regression analysis revealed that an end-systolic volume of more than 42 mL/m2 after 1 year contributed independently to the appearance of nondipolar maps. Patients with high-grade ventricular arrhythmias showed a higher nondipolar content (49 +/- 17% versus 39 +/- 10%, P = .013). QTc dispersion did not discriminate between patients with and those without high-grade ventricular arrhythmias. Also, the association between left ventricular remodeling and nondipolar map patterns was confirmed prospectively in an additional group of 15 patients. CONCLUSIONS: Nondipolar map patterns are present in 32% of patients after thrombolysis for a first anterior myocardial infarction and are associated with increased left ventricular dilatation. These data support the hypothesis that left ventricular dilatation after myocardial infarction leads to changes in repolarization characteristics that may facilitate the occurrence of life-threatening ventricular arrhythmias.

Atlas of paced body surface QRS integral maps for localization of the site of origin of postinfarction ventricular tachycardia.

Current mapping during radiofrequency (RF) catheter ablation of postinfarction ventricular tachycardia (VT) is based primarily on the use of single-site mapping techniques. Although such techniques are highly suitable for distinguishing the ultimate site where RF energy is delivered by enabling detailed localization of the exit site or critical component of the VT reentrant circuit, they are time-consuming and inefficient for initial rapid identification of the arrhythmogenic target area. This study features the design and preliminary clinical application of a new noninvasive method that is aimed at speeding up the initial phase of the VT mapping procedure. This method is based on the use of an atlas of 62-lead body surface QRS integral map patterns that was previously developed using left ventricular pace mapping in patients with remote anterior or inferior myocardial infarction. The atlas contains 18 and 22 different paced QRS integral map patterns obtained in patients with previous anterior or inferior myocardial infarction, respectively. Each specific QRS pattern in the atlas provides a unique infarct-specific spatial electrocardiographic representation of the onset of ectopic ventricular activation in a circumscribed endocardial segment of the left ventricle. Localization of the segment of VT origin is obtained by visually or mathematically comparing the QRS integral map recorded during VT with one of the two sets of paced QRS integral maps contained within the atlas with the purpose of selecting the best matching paced QRS integral map pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Body-surface QRST integral mapping. Arrhythmogenic righ ventricular dysplasia versus idiopathic right ventricular tachycardia.

BACKGROUND: Ventricular tachycardia originating in the right ventricle may arise in the presence or absence of structural heart disease. The two main causes of right ventricular tachycardia are arrhythmogenic right ventricular dysplasia (ARVD) and idiopathic right ventricular tachycardia (IRVT) originating from the outflow tract. This study was carried out to determine whether body-surface QRST integral mapping can differentiate patients with ARVD from patients with IRVT. METHODS AND RESULTS: Body-surface QRST integral maps were obtained during sinus rhythm in 8 patients with ARVD, 8 patients with IRVT, and 27 healthy control subjects. QRST integral maps were analyzed both visually and mathematically. All control subjects had a normal dipolar QRST integral map. In all patients with ARVD, a specific dipolar QRST integral map with an abnormally large negative area covering the entire inferior and right anterior thorax was recorded. In 6 of 8 patients with IRVT, a normal map pattern was found, whereas the remaining 2 patients showed an abnormally large negative area on the right anterior thorax. CONCLUSIONS: Patients with ARVD display a specific abnormal QRST integral map that may be related to delayed repolarization in the structurally abnormal right ventricle. The majority of patients with IRVT demonstrate a normal QRST integral map. A slightly abnormal QRST integral map was noted in 2 of 8 patients with IRVT, which may be related to minor structural abnormalities, undetectable by the present routine diagnostic techniques. These preliminary results indicate that body-surface QRST integral mapping may become an important diagnostic tool to differentiate patients with ARVD from those with IRVT.

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.