Paced QRS Complex Research Articles

The paced electrocardiogram cannot be used to identify left and right ventricular pacing sites in cardiac resynchronization therapy: validation by cardiac computed tomography.

Paced electrocardiogram characteristics to confirm left ventricular (LV) and right ventricular (RV) pacing sites in cardiac resynchronization therapy (CRT) have not been validated with accurate knowledge of pacing lead positions. We aimed to evaluate the ability of the paced QRS morphology to differentiate between various LV and RV lead positions using cardiac computed tomography (CT) as the reference for LV and RV pacing site. Ninety-seven CRT patients were included. The QRS morphology was evaluated during forced LV-only and RV-only pacing. Pacing lead positions were assessed in a standard LV 16-segment model and a simplistic RV 6-segment model using cardiac CT. Ten patients with LV lead displacement or a LV pacing site outside the non-apical free wall were excluded from the analysis of the LV paced QRS complex. Pacing within the LV free wall was associated with a superior and a right-axis deviation (P = 0.02 and 0.04, respectively). Pacing from basal LV segments mainly produced a late (V5 or later) precordial QRS transition as compared with mid-LV pacing (P = 0.001). No significant associations were found between RV pacing site and QRS axis or precordial transition. Different QRS morphologies were observed during single-chamber pacing from identical LV or RV myocardial segments. Weak associations exist between LV and RV pacing sites and the paced QRS axis. None of the paced QRS characteristics can be used to reliably confirm specific LV and RV pacing sites in CRT patients.

Navigating the 7 cs of certified practice.

Navigating the 7 cs of certified practice.

A change in QRS morphology in right ventricular apical pacing: is it a red flag sign?

A 74-year-old man with symptomatic complete heart block underwent right ventricular apical permanent pacemaker implantation. The postoperative ECG showed, as expected, completely paced left bundle branch block QRS morphology. However,...

Universal Algorithm for Diagnosis of Biventricular Capture in Patients with Cardiac Resynchronization Therapy

An accurate and universal method for diagnosis of biventricular (BiV) capture using a standard 12-lead electrocardiogram (ECG) would be useful for assessment of cardiac resynchronization therapy (CRT) patients. Our objective was to develop and validate such an ECG method for BiV capture diagnosis that would be independent of pacing lead positions-a major confounder that significantly influences the morphologies of paced QRS complexes. On the basis of an evaluation of 789 ECGs of 443 patients with heart failure and various right ventricular (RV) and left ventricular (LV) lead positions, the following algorithm was constructed and validated. BiV capture was diagnosed if the QRS in lead I was predominantly negative and either V1 QRS was predominantly positive or V6 QRS was of negative onset and predominantly negative (step 1), or if QRS complex duration was <160 ms (step 2). All other ECGs were classified as loss of LV capture. The algorithm showed good accuracy (93%), sensitivity (97%), and specificity (90%) for detection of loss of LV capture. The performance of the algorithm did not differ among apical, midseptal, and outflow tract RV lead positions and various LV lead positions. LV capture leaves diagnostic hallmarks in the fused BiV QRS related to different vectors of depolarization and more rapid depolarization of the ventricles. An accurate two-step ECG algorithm for BiV capture diagnosis was developed and validated. This algorithm is universally applicable to all CRT patients, regardless of the positions of the pacing leads.

The effect of hyperkalaemia on cardiac rhythm devices

In patients with pacemakers, hyperkalaemia causes three important abnormalities that usually become manifest when the K level exceeds 7 mEq/L: (i) widening of the paced QRS complex from delayed intraventricular conduction velocity, (ii) Increased atrial and ventricular pacing thresholds that may cause failure to capture. In this respect, the atria are more susceptible to loss of capture than the ventricles, and (iii) Increased latency (usually with ventricular pacing) manifested by a greater delay of the interval from the pacemaker stimulus to the onset of depolarization. First-degree ventricular pacemaker exit block may progress to second-degree Wenckebach (type I) exit block characterized by gradual prolongation of the interval from the pacemaker stimulus to the onset of the paced QRS complex ultimately resulting in an ineffectual stimulus. The disturbance may then progress to 2 : 1, 3 : 1 pacemaker exit block, etc., and eventually to complete exit block with total lack of capture. Ventricular undersensing is uncommonly observed because of frequent antibradycardia pacing. During managed ventricular pacing, hyperkalaemia-induced marked first-degree atrioventricular block may induce a pacemaker syndrome. With implantable cardioverter-defibrillators (ICDs) oversensing of the paced or spontaneous T-wave may occur. The latter may cause inappropriate shocks. A raised impedance from the right ventricular coil to the superior vena cava coil may become an important sign of hyperkalaemia in the asymptomatic or the minimally symptomatic ICD patient.

Functional capacity of patients with pacemaker due to isolated congenital atrioventricular block.

BackgroundIsolated congenital atrioventricular block (CAVB) is a rare condition with multiple clinical outcomes. Ventricular remodeling can occur in approximately 10% of the patients after pacemaker (PM) implantation.ObjectivesTo assess the functional capacity of children and young adults with isolated CAVB and chronic pacing of the right ventricle (RV) and evaluate its correlation with predictors of ventricular remodeling.MethodsThis cross-sectional study used a cohort of patients with isolated CAVB and RV pacing for over a year. The subjects underwent clinical and echocardiographic evaluation. Functional capacity was assessed using the six-minute walk test. Chi-square test, Fisher's exact test, and Pearson correlation coefficient were used, considering a significance level of 5%.ResultsA total of 61 individuals were evaluated between March 2010 and December 2013, of which 67.2% were women, aged between 7 and 41 years, who were using PMs for 13.5 ± 6.3 years. The percentage of ventricular pacing was 97.9 ± 4.1%, and the duration of the paced QRS complex was 153.7 ± 19.1 ms. Majority of the subjects (95.1%) were asymptomatic and did not use any medication. The mean distance walked was 546.9 ± 76.2 meters and was strongly correlated with the predicted distance (r = 0.907, p = 0.001) but not with risk factors for ventricular remodeling.ConclusionsThe functional capacity of isolated CAVB patients with chronic RV pacing was satisfactory but did not correlate with risk factors for ventricular remodeling.

The Ventriculophasic Response: Relationship to Sinus Arrhythmia and the Duration of Interposed QRS Complexes

The ventriculophasic response (VR) refers to shortening of sinus cycle length during heart block when a QRS complex is interposed between 2 P waves. Our purpose was to analyze its relationship to respiratory sinus arrhythmia (SA) and to compare VR in relation to paced versus intrinsic QRS complexes. Patients with advanced heart block had their pacer devices temporarily programmed to ventricular inhibited mode at 30 ppm. In 35 subjects, we analyzed VR and SA before, during and after 3 cycles of deep breathing. In 16 other patients we compared VR in the presence of paced versus narrower intrinsic QRS complexes. The magnitude of P-P interval shortening surrounding QRS complexes during inspiration correlated with SA (r = 0.36, P = 0.03). The prevalence of VR increased from 37% at baseline to 77% of subjects during deep breathing (P = 0.02). The mean P-P interval shortening was greater surrounding intrinsic QRS complexes than paced QRS complexes (3.6 ± 3.6% vs. 1.4 ± 1.1%, P = 0.02). The prevalence of VR increased from 25% during paced rhythm to 56% when intrinsic complexes were present. VR, like SA, increases with deep breathing and likely reflects intact parasympathetic nervous system function. Its increase in the presence of narrower beats suggests it may reflect ventricular synchrony.

Electrocardiographic Patterns during Left Ventricular Epicardial Pacing

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. 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. 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). Posterolateral and anteroapical ECG patterns are highly predictive of LV lead position.

Optimizing the pacing site in the ventricular septum by fluoroscopy and morphology of the paced QRS complex

To analyze the paced QRS duration in various septal positions of the right ventricular leads and with different paced QRS vectors. To use the results to assess parameters suggesting the optimal site for right ventricular pacing. A total of 609 patients with leads implanted in the right ventricular septum were classified using fluoroscopy in the lateral view (the primary pacing site), and in the anteroposterior view (the secondary pacing site), according to the QRS vector in leads I and III. Significantly shortened paced QRS was found in the primary pacing site with the true septal compared with the anteroseptal site, with the vector being negative or isoelectric in lead I plus positive in lead III. In secondary pacing sites, no significant difference in pacing QRS duration was found between RVOT-HS, RVOT-LS, mid-septum and inferior-septum. For optimization of the pacing site in the ventricular septum, the following are significant: the primary site based on the lateral view, and the paced QRS vector in leads I and III.

Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part II

The interval from the pacemaker stimulus to the onset of the earliest paced QRS complex (latency) may be prolonged during left ventricular (LV) pacing. Marked latency is more common with LV than right ventricular (RV) pacing because of indirect stimulation through a coronary vein and higher incidence of LV pathology including scars. During simultaneous biventricular (BiV) pacing a prolonged latency interval may give rise to an ECG dominated by the pattern of RV pacing with a left bundle branch block configuration and commonly a QS complex in lead V1. With marked latency programming the V-V interval (LV before RV) often restore the dominant R wave in lead V1 representing the visible contribution of the LV to overall myocardial depolarization. When faced with a negative QRS complex in lead V1 during simultaneous BiV pacing especially in setting of a relatively short PR interval, the most likely diagnosis is ventricular fusion with the intrinsic rhythm. Fusion may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate BiV capture. The diagnosis of fusion depends on temporary reprogramming a very short atrio-ventricular delay or an asynchronous BiV pacing mode. Sequential programming of various interventricular (V-V) delays may bring out a diagnostic dominant QRS complex in lead V1 that was previously negative with simultaneous LV and RV apical pacing even in the absence of an obvious latency problem. The emergence of a dominant R wave by V-V programming strongly indicates that the LV lead captures the LV from the posterior or the posterolateral coronary vein and therefore rules out pacing from the middle or anterior coronary vein. In some cardiac resynchronization systems LV pacing is achieved with the tip electrode of the LV lead as the cathode and the proximal electrode of the bipolar RV as the anode. This arrangement creates a common anode for both RV and LV pacing. RV anodal capture can occur at a high LV output during BiV pacing when it may cause slight ECG changes. During LV only pacing (RV channel turned off) RV anodal pacing may also occur in a more obvious form so that the ECG looks precisely like that during BiV pacing. RV anodal stimulation may complicate threshold testing and ECG interpretation and should not be misinterpreted as pacemaker malfunction. Programming the V-V interval (LV before RV) in the setting of RV anodal stimulation cancels the V-V timing to zero.

Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part I

Cardiac resynchronization therapy (CRT) has added a new dimension to the electrocardiographic evaluation of pacemaker function. During left ventricular (LV) pacing from the posterior or posterolateral coronary vein, a correctly positioned lead V1 registers a tall R wave and there is right axis deviation in the frontal plane with few exceptions. During simultaneous biventricular stimulation from the right ventricular (RV) apex and LV site in the coronary venous system, the QRS complex is often positive (dominant) in lead V1 and the frontal plane QRS axis usually points to the right superior quadrant and occasionally the left superior quadrant. The reported incidence of a dominant R wave in lead V1 during simultaneous biventricular pacing (RV apex) varies from 50% to almost 100% for reasons that are not clear. During simultaneous biventricular pacing from the posterior or posterolateral coronary vein with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). A negative paced QRS complex in lead V1 during simultaneous biventricular pacing with the RV lead at the apex can be caused by incorrect placement of the lead V1 electrode (too high on the chest), lack of LV capture, LV lead displacement, pronounced latency (true exit block), conduction delay around the LV stimulation site, ventricular fusion with the intrinsic QRS complex, coronary venous LV pacing via the middle or anterior cardiac vein, unintended placement of two leads in the RV and severe conduction abnormalities within the LV myocardium. Most of these situations can cause a QS complex in lead V1 which should be interpreted (excluding fusion) as reflecting RV preponderance in the depolarization process. Barring the above causes, a negative complex in lead V1 is unusual and it probably reflects a different activation of a heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation). The latter is basically a diagnosis of exclusion. With a non-dominant R wave in lead V1, programming the V-V interval with LV preceding RV may bring out a diagnostic dominant R wave in lead V1 representing the contribution of LV stimulation to the overall depolarization process. In this situation the emergence of a dominant R wave confirms the diagnosis of prolonged LV latency (exit delay) or an LV intramyocardial conduction abnormality near the LV pacing site but it rules out the various causes of LV lead malfunction or misplacement.

Cardiac resynchronisation improves survival in mild heart failure!

Cardiac resynchronisation improves survival in mild heart failure!

Characteristics of Surface Electrocardiogram during RV Mid Septal Pacing Compared with RV Outflow Pacing

Aims: To reduce a risk of perforation, the RV mid septum (RVMS) may be more appropriate pacing site compared with RV outflow tract (RVOT). Our aim was to investigate whether the paced QRS complex can be useful to confirm RVMS pacing. Methods: 20 patients (77±10 years) with an implanted a permanent pacemaker were classified into 3 groups, high RVOT (N=5), low RVOT (N=7) and RVMS (N=8), using by the computed tomography. The surface 12 leads electrocardiograms were analyzed and compared among 3 groups. Results: In RVMS pacing, the QRS duration (144±12 ms) and QRS transition (5.3±0.7) had no significant difference compared with those of high RVOT (154±14 ms, 5.4±0.5) and low RVOT (146±9 ms, 5.6±0.5). The voltage of lead of I in RVMS (0.61±0.2 mV), were significantly higher than that in high RVOT (−0.21±0.27 mV; P<0.001) and tended to be higher than that in low RVOT (0.23±0.19 mV). The presence of a q-wave in lead of I in RVMS (0/8) was infrequent compared with those in high RVOT (4/5) and low RVOT (2/5). A RS pattern/R pattern in lead II was infrequent in RVMS (6/2) than in high RVOT (0/5) and low RVOT (3/4). Conclusion: A QRS complex in lead I and/or II may be useful to confirm a RVMS pacing.

Utility of the surface electrocardiogram for confirming right ventricular septal pacing: validation using electroanatomical mapping

When targeting the interventricular septum during pacemaker implantation, the lead may inadvertently be positioned on the anterior wall due to imprecise fluoroscopic landmarks. Surface electrocardiogram (ECG) criteria of the paced QRS complex (e.g. negativity in lead I) have been proposed to confirm a septal position, but these criteria have not been properly validated. Our aim was to investigate whether the paced QRS complex may be used to confirm septal lead position. Anatomical reconstruction of the right ventricle was performed using a NavX® system in 31 patients (70 ± 11 years, 26 males) to validate pacing sites. Surface 12-lead ECGs were analysed by digital callipers and compared while pacing from a para-Hissian position, from the mid-septum, and from the anterior free wall. Duration of the QRS complex was not significantly shorter when pacing from the mid-septum compared with the other sites. QRS axis was significantly less vertical during mid-septal pacing (18 ± 51°) compared with para-Hissian (38 ± 37°, P = 0.028) and anterior (53 ± 55°, P = 0.003) pacing, and QRS transition was intermediate (4.8 ± 1.3 vs. 3.8 ± 1.3, P < 0.001, and vs. 5.4 ± 0.9, P = 0.045, respectively), although no cut-offs could reliably distinguish sites. A negative QRS or the presence of a q-wave in lead I tended to be more frequent with anterior than with mid-septal pacing (9/31 vs. 3/31, P = 0.2 and 8/31 vs. 1/31, P = 1.0, respectively). No single ECG criterion could reliably distinguish pacing the mid-septum from the anterior wall. In particular, a negative QRS complex in lead I is an inaccurate criterion for validating septal pacing.

Reversal of primary and pseudo-primary T wave abnormalities by ventricular pacing. A novel manifestation of cardiac memory

"Cardiac memory" refers to abnormal T waves (TW) appearing after transient periods of altered ventricular depolarization. The aim of the study was to test the hypothesis that in the presence of abnormal TW, short periods of tailored ventricular pacing (VP) can be followed by normalization of ventricular repolarization. Ten patients with normal TW (control group) and 18 patients with abnormal TW (study group) underwent 15 min of VP at a cycle length of 500 ms. In the control group, VP was performed from the right ventricular apex, and in the study group from right or left ventricular sites that resulted in paced QRS complexes of opposite polarity to that of the abnormal TW. Before and after VP, atrial pacing was maintained at a stable cycle length. Simultaneous 12-lead electrocardiography (ECG) was recorded before, during, and following VP to assess changes in TW polarity, amplitude, electrical axis, QTc interval, and QTc interval dispersion. As expected, VP was followed by memory-induced changes in TW in eight of ten patients in the control group. Mean T wave axis shifted from +60 degrees + or - 21.2 degrees to +23.5 degrees + or - 50.7 degrees (p = 0.01) in the frontal plane. In the study group, complete or partial normalization of TW occurred in 17 of 18 patients. Mean T wave axis shifted from -23.7 degrees + or - 22.9 degrees to +19.7 degrees + or - 34.7 degrees (p < 0.0002) in the frontal plane when paced from right ventricular outflow tract. The QTc interval shortened after VP both in the control group (424 + or - 25 vs. 399 + or - 27 ms; p = 0.007) and in the study group (446 + or - 26 vs. 421 + or - 22 ms; p < 0.0002). No significant changes were found in QTc interval dispersion. Transient changes in the sequence of ventricular activation may either induce or normalize abnormal TW. The background of preceding ventricular depolarization needs to be taken into account before determining the clinical significance of a given pattern of ventricular repolarization.

The relationship between right ventricular pacing voltage and QRS complex duration

Compared to the natural electrical activation of the myocardium through the His-Purkinje system, right ventricular pacing is associated with prolonged QRS complex duration, thereby impeding the synchronicity of contractions. In left ventricular pacing, a higher pacing voltage decreases the QRS complex duration. The aim of our study was to describe the relation between the right ventricular pacing voltage and the QRS complex duration. Fourteen patients (73.6 ± 7.6 years) with AV block and implanted pacemakers were paced at a frequency of 100 bpm with various pacing voltages. A signal-averaged QRS vector length was calculated at each degree of pacing voltage. The changes in the QRS complex duration were measured as a relative shift of the terminal region of the vectorcardiographic QRS complex (end-shift) and its most prominent peak (peak-shift) using the cross-correlation method. The nonlinear relationship between stimulation voltage and QRS duration was observed with the highest impact of stimulation voltage changes near the threshold value. The fourfold increase in the stimulation voltage above the threshold caused QRS complex shortening by 3.7 ± 2.1 ms (range 0.19–7.76 ms). Similar peak- and end-shift responses to altered stimulation energy demonstrated that the acceleration of depolarization occurred in the initial portion of the QRS complex. Older electrodes exhibited smaller and more linear changes in the QRS complex duration.

QRS complex widening due to loss of left bundle branch capture: pitfall of para-Hisian pacing

During para-Hisian pacing, widening of the paced QRS complex usually indicates loss of His bundle capture. We describe a patient without any accessory pathways in whom widening of the paced QRS complex occurred due to loss of left bundle branch capture during para-Hisian pacing. After initial widening of the QRS complex, further widening was observed due to loss of His bundle capture. With the initial QRS widening, the stimulus-atrial interval and retrograde atrial activation sequence were almost unchanged, so the findings mimicked retrograde conduction over an accessory pathway. This may be a pitfall of the para-Hisian pacing technique.

Attenuation (Augmentation) of Intrinsic and Paced QRS Complexes before (after) Hemodialysis

A patient with complete atrioventricular block after hemodialysis (HD) for which he had a permanent pacemaker implanted showed attenuation of the amplitude of the intrinsic and paced QRS complexes while awaiting HD, and augmentation of paced QRS complexes after HD. These QRS perturbations correlated with the changes in his weight. The mechanism of these phenomena and their clinical implications are discussed.

Analysis of the Electrocardiographic Waveforms Produced by Right Ventricular Pacing: Relation to the Nonpaced Patterns

Ventricular aberrant conduction has a confounding effect on the known relationships between the electrocardiogram (ECG) and left ventricular (LV) mass. By relating the ECG of right ventricular pacing to LV mass and to nonpaced recordings, clarification of these effects might emerge. In 30 patients (age, 81 +/- 7 years; 13 women) who had right ventricular paced ECGs and echocardiograms, 24 of who also had nonpaced ECGs, comparative analyses were performed. Although the nonpaced ECGs had strong correlations with various echocardiographic measurements, for paced ECGs, only QRS complex voltage and interventricular septal thickness (IVS) were significantly related. However, paced QRS complex voltage relationships correlated with those of nonpaced QRS complexes, ranging from an r = 0.54, P < 0.006, for the sum of the R in aVL and the S in V-3 to r = 0.78, P < 0.001, for the sum of the R in I and the S in III. Paced ECGs had a QRS complex with a greater spatial amplitude, a longer duration, and a more superior position, and had more deeply inverted T waves than nonpaced ECGs. The differences between the voltages of paced and nonpaced QRS complexes, moreover, diminished as LV mass and/or IVS increased. When compared with nonpaced ECGs, paced ECGs showed the most similarity to nonpaced ECGs having a left bundle branch block (LBBB) pattern. Except for the presence of more superiorly directed QRS complexes, paced impulses were not significantly different (P < 0.008) from nonpaced impulses having a LBBB pattern. Also, the nonpaced ECG pattern had no discernable effect on ECG produced by right ventricular (RV) pacing. Despite having weak relations with echocardiographic measurements, the QRS complex voltage of the paced ECG correlated with those of nonpaced ECGs, and the voltage differences between them were smaller as LV mass increased.

A Case with no Hemodynamic Benefit from Right Ventricular Anodal Capture during Biventricular Pacing

This case report describes a patient with a biventricular pacing system in whom right ventricular anodal capture had no hemodynamic benefit. While controlling the ventricular output, three morphologies of the paced QRS complex were obtained: right ventricular stimulation, biventricular stimulation, and biventricular pacing with additional stimulation from the anodal electrode in the right ventricle. While the QRS duration was 5 ms longer, the left ventricular systolic pressure and dP/dtmax during biventricular pacing without anodal capture of the right ventricle were greater than that during biventricular pacing with anodal capture. To avoid useless high output settings, the hemodynamic and clinical data should be compared with and without right ventricular anodal capture in each individual patient.