Color Doppler tissue velocity imaging can disclose systolic left ventricular asynchrony independent of the QRS morphology in patients with severe heart failure

A QRS width greater than 120 ms is assumed to be a marker of inter- and intraventricular asynchrony in severe heart failure (HF) patients. Color Doppler tissue velocity imaging (c-TVI) with a time resolution of 10 ms was used to study regional left ventricular (LV) longitudinal systolic contraction pattern in HF patients with left and right bundle branch block (LBBB and RBBB) and in patients with normal QRS width. We studied 12 women and 23 men with severe HF, with a mean age of 66 +/- 11 years in New York Heart Association functional Class 2.9 +/- 0.6. Twenty patients had LBBB and 10 of those were accepted for cardiac resynchronization therapy by biventricular pacing (CRT). Ten patients had normal QRS width, and five had RBBB. In the echocardiographic apical four chamber view, regional peak LV tissue velocities and regional LV time differences of peak tissue velocities were compared at basal and mid-LV segments. There were no significant differences in regional mean peak tissue velocities among the patient groups. In patients with LBBB accepted for CRT, the LV lateral free-wall movement at basal LV was 29 ms delayed during main systole, almost significantly different from LBBB patients not accepted for CRT (P = 0.075). Even in HF patients with normal QRS width or RBBB, significant asynchronous longitudinal LV contraction was observed. Conclusions: For the detection of regional longitudinal LV contraction asynchrony in patients with severe HF, supplementary methods to the surface ECG, such as c-TVI, are strongly recommended.     

Ventricular Activation Onset-Triggered Left Ventricular Pacing:

Ventricular activation onset-triggered (VAOT) left ventricular pacing modalities synchronize left ventricular paced activation with existing intrinsic ventricular activation, in patients with complete LBBB and adequate rate. The purpose of this study was to evaluate the safety and feasibility of VAOT pacing with one left ventricular pacing lead, during temporary pacing in the postoperative period following open heart surgery. VAOT pacing was studied in five patients with LBBB and two patients with previously implanted right ventricular pacemakers. The VAOT pacing system used was assembled by modifying the function of existing equipment and its programming is described in detail. Comparative ECGs are reported, documenting the changes in ventricular activation produced by VAOT pacing. Stability of surface ECG acquisition was found to be essential to the success of temporary VAOT pacing and inappropriate pacing due to ECG instability is described. Patients were studied at rest and none experienced congestive heart failure. In the comparison of cardiac output, with and without VAOT pacing, no significant differences were found in LBBB patients or those with right ventricular pacemakers. In the comparison of arterial pressure, with and without VAOT pacing, no significant differences were found in six patients, however, in one LBBB patient with intrinsic predominant ventricular trigeminy, VAOT pacing was observed to have an antiarrhythmic effect resulting in suppression of ventricular ectopy and stabilization of arterial pressure. All patients survived VAOT pacing and the postoperative period without complications requiring additional intervention or treatment. (PACE 2004; 27[Pt. I]:730–739)     

The ECG Lead I Paradox in Cardiac Resynchronization Therapy

Background: In cardiac resynchronization therapy (CRT), the morphology of the QRS complex plays an important role in the determination of the pacing site and effectiveness of stimulation. Patients and Methods: Review of the electrocardiograms (ECGs) of 737 patients with a CRT device showed a negative QRS complex in lead I during right ventricular (RV) pacing and a positive QRS complex during left ventricular (LV) pacing in four patients. The RV lead was positioned in the high RV septum and the coronary sinus leads in a posterior or postero‐lateral basal level. Reversed ECG lead or pacemaker lead connection, anodal RV stimulation, and scar tissue‐related depolarization abnormalities were excluded as possible causes. Conclusion: Pacing from the high RV septum may rarely lead to a negative QRS complex and basal positions of the LV lead to a positive QRS complex in lead I during LV pacing. The lead I paradox becomes obvious when both phenomena, that are not interrelated, are present in the same patient.     

Electrocardiographic patterns during: pacing the great cardiac and middle cardiac veins

BACKGROUND: The electrocardiogram (ECG) patterns during pacing from the great cardiac vein (GCV) and the middle cardiac vein (MCV) are not well known. METHODS: We recorded 12-lead ECGs during GCV and MCV pacing in 26 patients undergoing implantation of a cardiac resynchronization device. The left ventricular (LV) lead was passed down the GCV (n = 19) or MCV (n = 7) prior to moving it to a lateral or posterolateral vein for permanent implantation. RESULTS AND CONCLUSIONS: Pacing within the GCV resulted in a left bundle branch block (LBBB) morphology with no or minimal R-wave in V(1) in 14 patients and a right bundle branch block (RBBB) pattern (R > S in lead V(1)) in four patients. In one patient, lead V1 during GCV pacing was isoelectric (R = S). A more distal pacing site in the GCV yielded a LBBB pattern in all the patients. All leads placed in the MCV resulted in a LBBB configuration. An ECG pattern with a RBBB pattern was invariably recorded during LV pacing in 125 consecutive outpatients with biventricular pacemakers and LV leads in the posterolatral and lateral coronary veins. Knowledge of the ECG patterns from various pacing sites in the coronary venous system may be helpful for troubleshooting all types of pacing systems, especially those where the coronary venous pacing site is unintentional.     

Electrocardiographic Patterns during Left Ventricular Epicardial Pacing

Background: There is a paucity of data concerning the use of QRS morphology patterns for identifying pacing sites during left ventricle (LV)‐only epicardial pacing in patients with a biventricular device. The objective of this study was to identify QRS patterns during LV‐only pacing, and to establish their relationship with LV lead position. In addition, to validate the diagnostic performance of such electrocardiogram (ECG) patterns for predicting posterolateral versus anterior and apical versus nonapical LV pacing site. Methods: The study retrospectively analyzed data from 376 cardiac resynchronization therapy device patients. Data analyzed included ECGs registered during LV‐only VVI pacing, fluoroscopic projections, and lateral chest roentgenograms that documented postimplantation LV lead position. Phase one of the study involved categorization of the ECG patterns of the first 66 study cases. Phase two of the study examined the association between ECG pattern and different LV lead positions. Results: As the LV epicardial pacing site became more anteroapical, the LV‐only paced QRS complexes in the precordial leads became more negative. Three ECG patterns were identified (posterolateral, intermediate, and anteroapical), and their distribution was found to be associated with LV lead position (P < 0.001). The posterolateral ECG pattern was mostly observed in cases where the LV lead was in the posterolateral area (diagnostic accuracy of 89.1% for predicting a nonapical LV lead position). The anteroapical ECG pattern was associated with LV leads in anteroapical segments (specificity of 98.5%, accuracy of 89.1% for predicting an anteroapical pacing site). Conclusions: Posterolateral and anteroapical ECG patterns are highly predictive of LV lead position. (PACE 2012; 35:1361–1368)     

Clinical Significance of QRS Duration During Ventricular Pacing

To clarify the clinical significance of an abnormally prolonged paced QRS duration, we studied 114 patients who had undergone pacing for atrioventricular block (AVB). Patients were divided into two groups: group I consisted of 29 patients with at least one paced QRS duration greater than or equal to 180 msec during the follow-up period; group II consisted of 85 patients with paced QRS durations less than 180 msec. The clinical background, QRS complexes before pacing, and the echocardiographic findings were assessed. Males (P less than 0.05), those with H-V block (P less than 0.05) and a wider QRS complex of conducted and escape beats (both P less than 0.01) were dominant in group I. The incidence of underlying heart disease was greater in group I than in group II (83% vs 32%, P less than 0.01). Reduced left ventricular ejection fraction (LVEF) and increased left ventricular end-diastolic dimension (LVDd) were more prominent in group I than in group II (LVEF 0.49 +/- 0.17 vs 0.68 +/- 0.10, P less than 0.01, LVDd 57.1 +/- 7.9 mm vs 48.5 +/- 5.6 mm, P less than 0.01). The paced QRS duration correlated with LVEF (r = -0.61) and LVDd (r = 0.81). A paced QRS duration greater than or equal to 180 msec was sensitive and specific for a LVEF less than 0.5 (83.3% and 85.2%) and LVDd greater than or equal to 60 mm (100% and 81.4%). We conclude that patients with a prolonged paced QRS duration have more serious heart disease, and the paced QRS duration can be a useful indicator of impaired LV function.     

Evolution of paced QRS and QTc intervals in children with epicardial pacing leads

AIMS : Permanent ventricular pacing in children is associated with ventricular dysfunction due to asynchronous activation. It is unclear whether paced QRS intervals increase disproportionately over time, which could potentially cause ventricular dysfunction. METHODS : A total of 52 children, with bipolar steroideluting epicardial leads implanted at a median age of 5.6 years (0.0-17.4), was analyzed and followed up to 12.2 years (median 3.7). Patients were subdivided in two groups: right (RV, n = 21) and left (LV, n = 31) ventricular pacing. To correct for age, standard deviation scores (Z-scores) for paced QRS and QTc intervals were calculated from published standard-ECG norm-values. As a measure for individual paced QRS and QTc interval changes, a regression slope coefficient (incline(i)) was calculated for each patient's course. RESULTS : Mean Z-scores for paced QRS intervals at first and last follow-up were 4.7 +/- 1.2 and 4.9 +/- 0.9 for group RV, 4.4 +/- 1.1 and 4.8 +/- 1.1 for group LV. Incline(i) of paced QRS (group RV: 0.038 [-0.27-0.12], group LV: 0.147 [-0.05-0.30]; p = 0.07) and QTc intervals (group RV: 0.026 [-0.08-0.06], group LV: 0.023 [-0.04-0.09]; p = 0.63) did not differ between both groups and indicated limited interval changes over time. CONCLUSION : Neither epicardial pacing of the right nor left ventricle caused disproportionate paced QRS or QTc interval increases over time. An age-related prolongation of the electrical activation unlikely causes ventricular dysfunction.     

Changes in Morphology of the Paced QRS Complex Related to Atrial Contraction

A patient with 2:1 AV block underwent temporary ventricuJar pacing. AU the paced stimuli resuited in ventricular capture, but a marked variability in morphology of the paced QRS complexes occurred. Two different types of paced QRS complex (labeled A and B) were recognized. Type B complexes were manifest only when the pacing stimulus was preceded hy a sinus P wave within a time interval ranging from 0.15 to 0.52 sec. The P wave-induced changes in morphology of the paced QRS complexes were interpreted as due to displacement of the pacing ventricular lead caused by atrial systole.     

Fusion with the Prolonged First Postpacing Interval in Pacing of Ventricular Tachycardia

In cases of recurrent sustained ventricular tachycardia (VT), constant fusion and progressive fusion in fhe surface electrogram were observed during overdrive pacing of VT. However, following cessation of pacing, the return cycle of VT (stimulus to the first nonpaced QRS) was longer than the VT cycle length. This phenomenon can be explained by orthodromic capture of the exit site of the VT current with a conduction time (stimulus to QRS) exceeding the VT cyde length. This site can therefore be activated during entrainment of VT during the mid-to-terminal portion of the paced QRS complex, resulting in constant fusion.     

The effect of variation in the interval between right and left ventricular activation on paced QRS duration

Pacing of the RV and LV is a promising technique for treating patients with dilated cardiomyopathy and bundle branch block. The salutary effects of biventricular pacing may be due to resynchronization of LV activation. Currently, available biventricular pacemakers and implanted defibrillators produce simultaneous ventricular output pulses. The purpose of the current study was to assess the effects of variation in the timing of RV and LV activation, using the paced QRS duration as a marker of resynchronization. Twenty-six patients undergoing transvenous biventricular pacemaker implantation were studied. After stable lead positions were achieved, activation of the LV and RV was varied over a range of +/- 50 ms and the QRS duration measured on a 12-lead ECG. Only 6 (23%) of the 26 patients had maximal shortening of the paced QRS with simultaneous activation of the LV and RV. The shortest paced QRS duration was most often produced by an LV to RV interval of -30 ms (LV activation preceding RV activation). Optimization of LV to RV interval resulted in an additional 13% shortening of the paced QRS compared to simultaneous activation (P < 0.0001). Patients with leads located on the lateral or anterolateral walls of the LV were more likely to benefit from preexcitation of the LV than did patients with leads in the posterior position. Results of this study suggest that the ability to program the LV to RV interval may be useful to optimize the benefit of biventricular pacing.     

Acute Hemodynamic Effects of Alternate and Combined Site Pacing in Patients after Cardiac Surgery

We hypothesized that pacing at sites other them the right ventricular (RV) apex or at two or more ventricular sites would activate the myocardium more rapidly and improve cardiac function in patients undergoing coronary revascularization or aortic valve replacement. Epicardial electrodes were placed on the right atrium (A), RV paraseptal area close to the RV apex (B), RV outflow tract (C), LV apex (D), in patients undergoing bypass surgery. At constant rate and AV delay, we measured CO during A pacing, DV1 pacing at B, C, D, and various combinations of sites in random order in ten patients with EF > 50% and 27patients with EF ≤ 50%. When pacing at two sites, we made one electrode a cathode and one an anode and noted two distinct thresholds by careful observation of the 12-lead ECG. There were no significant differences in CO, systemic vascular resistance, systolic, or mean arterial pressure. Significant differences were noted in QRS duration, which increased progressively going from AAI to 3-site, 2-site, and single site pacing (P < 0.05 each comparison). Thus: (1) QRS duration correlated inversely with the number of ventricular sites paced; (2) despite this, CO did not improve irrespective of baseline EF; (3) multisite pacing produced multiple distinct thresholds which appeared to be related to the number of sites paced, and (4) unique ECG patterns confirmed multisite pacing.     

Importance of using standard rather than torso surface electrocardiographic leads for pacemapping at the right ventricular outflow tract

Although pacemapping has been used to localize the origin of ventricular tachycardia, the effect of changes in the position of ECG electrodes during ventricular pacing remains unknown. To clarify the relationship between the position of ECG limb electrodes and QRS configuration during pacemapping at the right ventricular outflow tract (RVOT), RVOT pacing was performed on 12 patients at eight pacing sites located in the anterior, septal, lateral, and posterior portions each in the high and low RVOT. Standard and torso ECGs were recorded simultaneously during each pacing protocol, and the QRS axis and amplitude were compared between the two ECGs. Differences between sites in the horizontal plane and in the longitudinal direction were also compared. The QRS axis on the torso ECG was significantly more rightward than that on the standard ECG at all eight pacing sites (72.1+/-17.4 vs 64.0+/-21.9 degrees). The magnitude of differences in the QRS axis and amplitude between the anterior and other sites at the same height was significantly greater in the standard ECG in all locations and in 7 of 18 comparable leads, respectively. The magnitude of differences between high and low sites was significantly greater in the standard ECG in three of four locations and in 5 of 12 comparable leads, respectively. In conclusion, the torso ECG is less sensitive to changes in pacing site at the RVOT than the standard ECG. The torso ECG is, therefore, not proper for pacemapping in attempts to ablate ventricular tachycardia arising from the RVOT.     

Reinitiation of ventricular macroreentry within the His-Purkinje system by back-up ventricular pacing - a mechanism of ventricular tachycardia storm

BACKGROUND: We describe immediate reinitiation of macroreentry ventricular tachycardia (VT) involving the His-Purkinje system by ventricular pacing from the electrode of an implantable cardioverter defibrillator (ICD) as a mechanism of VT storm refractory to ICD therapy. METHODS AND RESULTS: Repetitive reinitiation of bundle branch reentry tachycardia (BBRT), interfascicular tachycardia, or both VTs by ventricular pacing was identified in four ICD patients presenting with VT storm or incessant VT. All patients had a pre-existing prolonged HV interval (75 +/- 9 ms) and left bundle branch block (LBBB) or bifascicular block during sinus rhythm. The VTs included BBRT with LBBB in three patients and interfascicular tachycardia with right bundle branch block (RBBB) and left anterior or left posterior fascicular block in two patients. The paced beats from the ICD electrode exhibited a LBBB pattern of depolarization in two patients and a RBBB contour in V1 and V2 with left axis deviation in two patients. The QRS complex during pacing from the ICD electrode closely resembled that of the recurrent VT in all four patients suggesting that the pacing site of the ICD electrode was in proximity to the myocardial exit site of the bundle fascicle used for antegrade conduction during the reinitiated VT. Ventricular pacing from the ICD electrode after termination of the VT apparently encountered the retrograde refractoriness of this bundle fascicle and allowed immediate re-propagation of the wavefront orthodromically along the VT circuit. BBRT was eliminated by ablation of the right bundle branch. Successful ablation of the interfascicular tachycardias was achieved by targeting (1) an abnormal potential of the distal left posterior Purkinje network or (2) a diastolic potential during VT in the midinferior left ventricular (LV) septum. CONCLUSIONS: Repetitive reinitiation of BBRT and interfascicular tachycardia by ventricular pacing from the ICD electrode should be considered as a mechanism of VT storm refractory to ICD therapy in patients with a pre-existing conduction delay within the His-Purkinje system.     

Supraventricular Electrical Interaction in Conjoined Twins with Common Coronary Sinus

Conjoined twins with echocardiographic evidence of continuity of the coronary sinuses had identical heart rates on ECG. Both had broad, polyphasic QRS complexes, and various imaging modalities were unable to determine whether there was ventricular myocardial continuity. Administration of adenosine demonstrated that the broad polyphasic complexes were a "fusion" of the twins' individual QRS complexes, which could be clearly distinguished after administration of the drug. Ventricular pacing resulted in dissociation of the individual QRS complexes, thus demonstrating an absence of ventricular myocardial continuity. This was confirmed when the twins were successfully separated at the age of 10 months.     

Site‐Specific Differences in Latency Intervals during Biventricular Pacing: Impact on Paced QRS Morphology and Echo‐Optimized V‐V Interval

Objective: To investigate differences in latency intervals during right ventricular (RV) pacing and left ventricular (LV) pacing from the (postero‐)lateral cardiac vein in cardiac resynchronization therapy (CRT) patients and their relationship to echo‐optimized interventricular (V‐V) intervals and paced QRS morphology. Methods: We recorded digital 12‐lead electrocardiograms in 40 CRT patients during RV, LV, and biventricular pacing at three output settings. Stimulus‐to‐earliest QRS deflection (latency) intervals were measured in all leads. Echocardiographic atrioventricular (AV) and V‐V optimization was performed using aortic velocity time integrals. Results: Latency intervals were longer during LV (34 ± 17, 29 ± 15, 28 ± 15 ms) versus RV apical pacing (17 ± 8, 15 ± 8, 13 ± 7 ms) for threshold, threshold ×3, and maximal output, respectively (P < 0.001), and shortened with increased stimulus strength (P < 0.05). The echo‐optimized V‐V interval was 58 ± 31 ms in five of 40 (12%) patients with LV latency ≥ 40 ms compared to 29 ± 20 ms in 35 patients with LV latency < 40 ms (P < 0.01). During simultaneous biventricular pacing, four of five (80%) patients with LV latency ≥ 40 ms exhibited a left bundle branch block (LBBB) pattern in lead V₁ compared to three of 35 (9%) patients with LV latency < 40 ms (P < 0.01). After optimization, all five patients with LV latency ≥ 40 ms registered a dominant R wave in lead V₁. Conclusions: LV pacing from the lateral cardiac vein is associated with longer latency intervals than endocardial RV pacing. LV latency causes delayed LV activation and requires V‐V interval adjustment to improve hemodynamic response to CRT. Patients with LV latency ≥ 40 ms most often display an LBBB pattern in lead V₁ during simultaneous biventricular pacing, but a right bundle branch block after V‐V interval optimization. (PACE 2010; 1382–1391)     

Optimization of Ventricular Function by Improving the Activation Sequence During Ventricular Pacing

Abnormal electrical activation occurring during ventricular pacing reduces left ventricular (LV) pump function. Two strategies were compared to optimize LV function using ventricular pacing, minimal asynchrony and optimal sequence of electrical activation. ECG and hemodynamics aortic flowpmbe, thermodilution cardiac output, LV pressure and its maximal rates of rise (LVdP/dtpos) and fall (LVdP/dtneg) were measured in anesthetized open-chest dogs (n = 7) with healthy hearts. The QRS duration (a measure of asynchrony of activation) was 47 ± 5 ms during sinus rhythm and increased to 110 ± 12 ms during DDD pacing at the right ventricular (RV) apex with a short AV interval. During pacing at the LV apex and LV base, the QRS duration was 8%± 7% and 15%± 7% (P < 0.05) longer than during RV apex pacing, respectively. Stroke volumes, LVdP/dtpos and LVdP/dtneg, however, were higher during LV apex(15%± 16%, 10%± 12% [P<0.05], and 15%± 10%, respectively) and LV base pacing (11%± 12% [P<0.05], 3%± 12%, and 3%± 11%, respectively) than during RV apex pacing. Systolic LV pressure was not influenced significantly by the site of pacing. Biventricular pacing (RV apex together with one or two LV sites) decreased the QRS duration by approximately 20% as compared with RV apex pacing, however, it did not improve stroke volumes, LVdP/dtpos and LVdP/dtneg beyond those during pacing at the LV apex alone. In conclusion, the sequence of electrical activation is a stronger determinant of ventricular function than the synchrony of activation. For optimal LV function the selection of an optimal single pacing site, like the LV apex, is more important than pacing from multiple sites.     

Activation sequence modification during cardiac resynchronization by manipulation of left ventricular epicardial pacing stimulus strength

BACKGROUND: Success of cardiac resynchronization therapy (CRT) depends on altering electrical ventricular activation (VA) to achieve mechanical benefit. That increases in stimulus strength (SS) can affect VA has been demonstrated previously in cardiomyopathy patients undergoing ablation. OBJECTIVE: To determine whether increasing SS can alter VA during CRT. METHODS: In 71 patients with CRT devices, left ventricle (LV) pacing was performed at escalating SS. Timing from pacing stimulus to right ventricular (RV) electrogram, ECG morphology, and maximal QRS duration on 12 lead ECG were recorded. RESULTS: Demographics: Baseline QRS duration 153 +/- 25 ms, ischemic cardiomyopathy 48%, ejection fraction 24%+/- 7%. With increased SS, conduction time from LV to right ventricle (RV) decreased from 125 +/- 56 ms to 111 +/- 59 ms (P = 0.006). QRS duration decreased from 212 +/- 46 ms to 194 +/- 42 ms (P = 0.0002). A marked change in QRS morphology occurred in 11/71 patients (15%). The RV ring was the anode in 6, while the RV coil was the anode in 5. Sites with change in QRS morphology showed decrease in conduction time from LV to RV from 110 +/- 60 ms to 64 +/- 68 ms (P = 0.04). Twelve patients (16%) had diaphragmatic stimulation with increased SS. CONCLUSIONS: Increasing LV SS reduces QRS duration and conduction time from LV to RV. Recognition of significant QRS morphology change is likely clinically important during LV threshold programming to avoid unintended VA change.     

The effect of anodal stimulation on V-V timing at varying V-V intervals

We studied the effect of anodal capture at the ring electrode of the right ventricular (RV) lead on interventricular (V-V) timing during biventricular (BiV) pacing, in which left ventricular (LV) pacing was preceding RV pacing. The V-V interval was programmed from 80 to 4 ms (LV first) in the LV unipolar (LV tip--generator can) followed by the LV tip-RV ring pacing configuration. In the LV unipolar configuration, V-V programming leads to a continuous change in morphology of the QRS complex according to a change in collision of both activation fronts. When using the LV tip-RV ring configuration with anodal capture at the RV ring electrode no change in QRS morphology was recorded varying the V-V interval from 80 to 60 and 40 ms. However, at V-V intervals between 20 and 4 ms a change in morphology of the QRS complex was recorded, which was due to additional cathodal stimulation of the RV tip electrode during RV stimulation.     

Morphology of the RV electrogram during LV pacing is related to the hemodynamic effect in cardiac resynchronization therapy

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

Effects of Different Modes of Stimulation on the Morphology of the First QRS Complex Following Pacing During Digitalis-Induced Ventricular Tachycardia: Observations in the Conscious Dog With Chronic Complete Atrioventricular Block

During digitalis-induced, sustained, monomorphic ventricular tachycardia, programmed electrical stimulation was performed and the effect on the first post-pacing QRS morphology was determined. Ventricular tachycardia was induced in nine conscious dogs with chronic complete atrioventricular block by administering digoxin i.v. 0.1 mg/kg given in 1-½ hour. Spontaneous ventricular tachycardia most frequently had a right bundle branch block morphology and an extreme left axis suggesting an origin in the apex of the left ventricle. Less frequently, a left bundle branch block-like configuration with an intermediate axis was observed, compatible with an origin in the basal part of the right ventricle. Following pacing close to one of these predilection sites, the first post-pacing QRS morphology suggested an origin close to the site of stimulation. Pacing distant from these predilection sites resulted in fusion complexes between electrical activaion from these predilection sites and the stimulation site. The amount of fusion depended on interstimulus interval and the number of stimuli. Long interstimulus intervals and few stimuli induced a QRS complex similar to that of the spontaneous tachycardia. The faster and longer the stimulation train, the more the QRS complex became similar to the paced QRS complex. Similar findings were also observed on decreasing the last paced interval only. Our findings suggest that triggered activity is the underlying mechanism for the first post-pacing QRS complex. QRS configuration and the relation between the R-R interval and QRS configuration during tachycardia suggest that triggered activity is also the mechanism for the spontaneously occurring ventricular tachycardia during digitalis intoxication. These observations may have important clinical implications.