Changes In QRS Morphology Research Articles

From a wide to a narrow QRS tachycardia and back. What is the mechanism?

Summary A 40-year-old man developed a near syncope during exercise due to a wide complex tachycardia with periods of changing RR intervals accompanied by changes in QRS morphology. The diff erential diagnosis of this electrocardiographic pattern is discussed.

Effects of heart failure status on electrocardiogram precordial leads and their value for monitoring body fluid changes in heart failure patients

Changes in QRS morphology in ECG precordial leads and the value of these leads for identifying worsening heart failure (HF) have not been fully determined, though the effects of HF status on changes in QRS amplitude [1,2] and transitional zone [3,4] in these leads have been briefly described. When considering the right ventricle being more compliant than the left, it would be expected that expansion of the right ventricle is more than the left under the volume overload in worsening HF, and vice versa at its recovery [5], causing changes in QRS morphology in precordial leads.

New Endpoint for Ablation of Ventricular Tachycardia: Change in QRS Morphology with Pacing at Protected Isthmus as Index of Isthmus Block

Endpoints confirming block in the critical isthmus in sinus rhythm and with pace mapping have not been established. A 44-year-old man with a history of Tetralogy of Fallot presented with recurrent ventricular tachycardia (VT). Entrainment mapping was consistent with a macroreentrant circuit rotating in a clockwise fashion under the pulmonic valve. After termination of the VT in a critical isthmus located on the conal free wall, a pace map proximal to the site of successful ablation was consistent with a change in QRS morphology. This change in QRS morphology suggested critical isthmus block and successful ablation, which was confirmed by noninducibility with programmed stimulation. Evidence of conduction block can be used as an additional endpoint for successful ablation of VT.

Fragmented QRS Complex: A Novel Marker of Cardiovascular Disease

QRS complex fragmentation, defined as changes in QRS morphology with different RSR' patterns: additional R waves, notched S wave, or > 1R' wave, has recently been linked with various cardiac conditions and even been postulated to be predictive of outcomes in certain pathologies. The current article aims to consolidate the available information about this morphological ECG abnormality and its predictive value.

Rate-related changes in QRS morphology in patients with fixed bundle branch block: implications for differential diagnosis of wide QRS complex tachycardia

To analyse QRS morphology in response to rapid atrial pacing (RAP) and supraventricular tachycardia (SVT) in patients with pre-existing bundle branch block (BBB). We prospectively studied 59 patients in sinus rhythm (SR), with QRS > or = 120 ms, and no pre-excitation. Trains of RAP were introduced at increasing rates until atrioventricular block. QRS during SR and last QRS complex of each RAP train were compared on the 12-leads. Previously described criteria for minor and major configuration differences were used to identify QRS changes. During RAP minor QRS changes were seen in 22 (37%) and major changes in 23 (39%) subjects. One patient showed major axis shifts and no one showed a change to the contralateral BBB pattern. QRS changes were significantly and independently related to RAP rate and type of BBB (more frequent if right-BBB). Of 14 subjects (24%) with SVT, 13 displayed the same QRS changes during RAP. In patients with organic BBB, important changes in QRS morphology, except for a change in the contralateral BBB, can appear during RAP and SVT. Thus, in these patients, a change in QRS morphology during tachycardia does not necessarily imply that it is ventricular tachycardia.

Relationship between intensive diuresis and QRS morphology change

Relationship between intensive diuresis and QRS morphology change

Idiopathic ventricular arrhythmias arising from the pulmonary artery: Prevalence, characteristics, and topography of the arrhythmia origin

The characteristics of idiopathic ventricular tachycardias (VTs) or idiopathic premature ventricular contractions (PVCs) arising from the pulmonary artery (PA) have not been sufficiently clarified. The purpose of this study was to clarify the prevalence, characteristics, and preferential sites of idiopathic VT/PVCs arising from the PA (PA-VT/PVCs). Data obtained from 276 patients with idiopathic VT/PVCs who underwent radiofrequency (RF) catheter ablation were analyzed. Twelve VT/PVCs (4%) were PA-VT/PVCs, and their onset (34 +/- 14 years) was the youngest among all subgroups. Because those QRS morphologies were similar to VT/PVCs arising from the right ventricular outflow tract (RVOT-VT/PVC) and the earliest ventricular activation was from the RVOT, an initial ablation was performed in the RVOT in all patients. However, RF catheter ablation at the RVOT resulted in a QRS morphology change in all patients, so thereafter PA mapping and ablation was performed. A characteristic potential during sinus rhythm and/or the arrhythmia was recorded at the successful PA ablation site in all patients. A perfect or good pace map was obtained in 7 (70%) of 10 patients. The successful ablation site was the septal side of the PA close to the posterolateral attachment in 9 patients (75%) and the septal side close to the anterior attachment in the remaining 3 (25%). No PA-VT/PVCs recurred during follow-up of 27 +/- 13 months. PA-VT/PVCs should always be considered when the ECG suggests RVOT-VT/PVCs and RF catheter ablation in the RVOT results in both a failed ablation and a change in QRS morphology. PA-VT/PVCs often originate from the septal side of the PA.

Spontaneous stellate ganglion nerve activity and ventricular arrhythmia in a canine model of sudden death

Little information is available on the temporal relationship between instantaneous sympathetic nerve activity and ventricular arrhythmia in ambulatory animals. The purpose of this study was to determine if increased sympathetic nerve activity precedes the onset of ventricular arrhythmia. Simultaneous continuous long-term recording of left stellate ganglion (LSG) nerve activity and electrocardiography was performed in eight dogs with nerve growth factor infusion to the LSG, atrioventricular block, and myocardial infarction (experimental group) and in six normal dogs (control group). LSG nerve activity included low-amplitude burst discharge activity (LABDA) and high-amplitude spike discharge activity (HASDA). Both LABDA and HASDA accelerated heart rate. In the experimental group, most ventricular tachycardia (86.3%) and sudden cardiac death were preceded within 15 seconds by either LABDA or HASDA. The closer to onset of ventricular tachycardia, the higher the nerve activity. The majority of HASDA was followed immediately by either ventricular arrhythmia (21%) or QRS morphology changes (65%). HASDA occurred in a circadian pattern. HASDA occurred twice as often in the experimental group than in the control group. Electrical stimulation of LSG increased transmural heterogeneity of repolarization (Tpeak-end intervals) and induced either ventricular tachycardia or fibrillation in the experimental group but not in the control group. Immunohistochemical studies revealed increased synaptogenesis and nerve sprouting in the LSG in the experimental group. Two distinct types of LSG nerve activity (HASDA and LABDA) are present in the LSG of ambulatory dogs. The majority of malignant ventricular arrhythmias are preceded by either HASDA or LABDA, with HASDA particularly arrhythmogenic.

Prognostic Significance of Fragmented QRS Complex for Predicting the Risk of Recurrent Cardiac Events in Patients With Q-Wave Myocardial Infarction

There are limited data regarding the prognostic value of QRS complex fragmentation, defined as changes in QRS morphology (<120 ms) with different RSR' patterns: additional R waves, notched S wave, or >1 R' wave. The purpose of our analysis was to assess the prognostic value of presence of Q waves and QRS fragmentation for predicting recurrent cardiac events, defined as cardiac death, nonfatal myocardial infarction (MI), or unstable angina, whichever occurs first, in 350 patients with first Q-wave MI. In follow-up (2 months on average) electrocardiograms (ECGs), 277 patients (79%) had persistent Q waves and 73 (21%) had resolution of Q waves. Independently of Q waves, presence of QRS complex fragmentation was found in 187 patients (53%). Resolved Q waves on 2-month ECGs was associated with worsened prognosis (adjusted hazard ratio [HR] 2.33, p = 0.007), whereas presence of any fragmented QRS did not increase risk of recurrent cardiac events (adjusted HR 0.93, p = 0.79). Among patients for whom Q waves disappeared on 2-month ECGs, patients with QRS fragmentation (n = 37) had over twofold higher risk of recurrent events (adjusted HR 2.68, p = 0.004) compared with those without fragmented QRS and persistent Q waves. In conclusion, presence of fragmented QRS independently of Q waves was not associated with increased risk of recurrent events in the general population of patients after MI. However, among patients with resolved Q waves, fragmented QRS was associated with increased risk of cardiac events. Fragmented QRS complex should not be neglected in patients with transient Q waves after myocardial infarction.

Activation Sequence Modification During Cardiac Resynchronization by Manipulation of Left Ventricular Epicardial Pacing Stimulus Strength

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. To determine whether increasing SS can alter VA during CRT. 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. 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. 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.

Ablation of Idiopathic Ventricular Tachycardia in Two Separate Regions of the Outflow Tract: Prevalence and Electrocardiographic Characteristics

Few studies have clarified the prevalence and characteristics of idiopathic outflow tachycardia (OT-VT) with an altered QRS morphology after radiofrequency catheter ablation (RFCA), requiring additional RFCA applications at a different portion of the outflow tract (OT) to abolish the OT-VT. Among 344 patients (97 VTs and 247 premature ventricular contractions), 12 (3.5%; VTs-7, PVCs-5; 6 women) had dynamic QRS morphology changes following the RFCA, requiring additional RFCA applications at a different portion to abolish the OT-VT. In 8 of 12 patients (67%), this phenomenon occurred following RFCA at right (RVOT; n = 7) or left ventricular (LVOT; n = 1) endocardial sites of the OT: The second OT-VT was consistently associated with an increase in the R-wave amplitude in the inferior leads, and in five it was finally abolished by RFCA at the left sinus of Valsalva (LSV). Conversely, in four patients (33%), the second OT-VT appeared after RFCA at the LSV: two required additional RFCA applications at the LVOT to abolish the second OT-VT, and one at the RVOT, and all were associated with a decrease in the R-wave amplitude in the inferior leads. This kind of dynamic QRS morphology change was often observed when RFCA was applied to either the first or second OT-VT at a right or left ventricular endocardial site, with the other site being the LSV. A detailed continuous observation of the QRS morphology, especially of the R-wave in the inferior leads, is important for identifying changes in the QRS morphology during RFCA.

A Robust Method for ECG-Based Estimation of the Respiratory Frequency During Stress Testing

A robust method is presented for electrocardiogram (ECG)-based estimation of the respiratory frequency during stress testing. Such ECGs contain highly nonstationary noise and exhibit changes in QRS morphology which, when combined with the dynamic nature of the respiratory frequency, make most existing methods break down. The present method exploits the oscillatory pattern of the rotation angles of the heart's electrical axis as induced by respiration. The series of rotation angles, obtained from least-squares loop alignment, is subject to power spectral analysis and estimation of the respiratory frequency. Robust techniques are introduced to handle the nonstationary properties of exercise ECGs. The method is evaluated by means of both simulated signals, and ECG/airflow signals recorded from 14 volunteers and 20 patients during stress testing. The resulting respiratory frequency estimation error is, for simulated signals, equal to 0.5% +/- 0.2%, mean +/- SD (0.002 +/- 0.001 Hz), whereas the error between respiratory frequencies of the ECG-derived method and the airflow signals is 5.9% +/- 4% (0.022 +/- 0.016Hz). The results suggest that the method is highly suitable for analysis of noisy ECG signals recorded during stress testing.

A puzzling telemetry tracing

A 69-year-old female was admitted with the diagnosis of a non-ST-segment elevation myocardial infarction and placed on cardiac telemetry. Her resting ECG showed sinus rhythm and voltage criteria for left ventricular hypertrophy. A tracing was recorded by the telemetry monitor (Philips Med Systems) ( Figure 1 ); the patient was asymptomatic. What is the mechanism for the sudden change in QRS morphology? Figure 1 Telemetry monitor tracing (25 mm/s) displaying lead II (top, channel 1) …

P1-48: Dynamic changes in QRS morphology following radiofrequency ablation may require additional ablation at a different portion of the outflow tract to cure idiopathic outflow tract tachycardia

P1-48: Dynamic changes in QRS morphology following radiofrequency ablation may require additional ablation at a different portion of the outflow tract to cure idiopathic outflow tract tachycardia

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.

Purkinje fiber trigger for ventricular tachycardia: Local exit block with ablation leading to change in QRS morphology and difficulty with mapping

Background: Ventricular tachycardias (VT) are frequently initiated by reproducible ventricular premature beats (VPB) that originate from the Purkinje network (PN). We present one such case with a unique observation related to catheter ablation that made activation and pace mapping a challenge.

Prevalence and characteristics of idiopathic outflow tract tachycardia with QRS alteration following catheter ablation requiring additional radiofrequency ablation at a different point in the outflow tract.

Subtle variations in QRS morphology occurs during idiopathic outflow tract ventricular tachycardia (OTVT), but no studies have clarified the prevalence and characteristics of the OTVT with altered QRS morphology following radiofrequency catheter ablation (RFA), which then require an additional RF application at a different portion of the outflow tract to abolish OTVT. Of 202 patients with a monomorphic VT or premature ventricular contraction (PVC) originating from the outflow tract, 6 (3%) showed changes in QRS morphology in the OTVT following RFA, requiring an additional RF application to the outflow tract at a different portion. In all six patients, RFA was applied for the first or second OTVT to a right or left ventricular endocardial site, with the other site being the left sinus of Valsalva. In each patient, OTVT before or after the changes in QRS morphology had characteristic ECG findings originating from a particular portion of the outflow tract. Changes in QRS morphology consistently included an increase or decrease in R wave amplitude in all inferior leads. Detailed continuous observation of QRS morphology in OTVT, especially R wave amplitude in inferior leads, is important for identifying changes of QRS morphology during catheter ablation. Mapping and ablation at a different portion of the outflow tract is then needed for cure.

Triple-site pacing in patients with biventricular device-incidence of the phenomenon and cardiac resynchronization benefit.

In patients with biventricular pacing (BIV), triple-site pacing (TSP), i.e. standard biventricular cathodal pacing of the right and the left ventricle plus additional anodal capture of the right ventricle, is sometimes present. To evaluate the incidence of TSP phenomenon, to examine TSP-related QRS changes, and to assess the effect of TSP on intraventricular resynchronization by means of tissue Doppler imaging (TDI). 23 patients with a first generation biventricular device (Medtronic 8040) and 16 patients with a new generation device (Medtronic 8042) were evaluated to look for the presence of TSP. TSP was found in 6 patients (26%) with the Medtronic 8040 (group I) and in 13 patients (81%) with the Medtronic 8042 device (group II). QRS duration decreased by 10 to 20 ms and QRS amplitude of leads I and aVL increased in almost all patients in group I during TSP modality. In group II, QRS morphology, duration and amplitude did not change as obviously. TDI analysis of the left ventricular (LV) basal segments showed significant shortening of the systole, together with a corresponding prolongation of the diastole, at the inferior wall of the LV, during TSP compared to standard BIV in all patients ( p < 0.01). Other LV segments did not show any change. Qualitative TDI electro-mechanical activation pattern of all LV segments improved in 22%, while it remained unchanged in 72%. TSP phenomenon can be identified in approximately a quarter of patients with the first-generation biventricular devices on the basis of the QRS morphology changes. In the second-generation biventricular pacemakers it can be demonstrated in the vast majority of patients. TSP may increase the effectiveness of cardiac resynchronization therapy by counteracting the regional activation delay located at the inferior wall of the LV.

Altered atrial, atrioventricular, and ventricular conduction in patients with the long QT syndrome caused by the ΔKPQ SCN5A sodium channel gene mutation

The ΔKPQ sodium channel gene mutation causes an LQT3 form of the long QT syndrome (LQTS), in which prolongation of repolarization is due to impaired inactivation of sodium current during the repolarization process.1–3 Studies of sodium current kinetics of channels encoded by the mutated SCN5A have also shown that depolarization is affected in LQT3 conditions, with sodium current having faster inactivation of depolarizing current than is observed in normally functioning channels.4–6 Recently, the SCN5A sodium channel gene mutations were found to cause progressive conduction disorder,7 the disorder characterized by progressive prolongation of QRS morphology, with subsequent development of bundle branch blocks and complete atrioventricular blocks. The Brugada syndrome, in which QRS morphology is affected simultaneously with ST-T-wave abnormalities, also is caused by mutations on the same SCN5A sodium channel gene.8 Sodium current also plays an important role in atrial depolarization,9 and in atrioventricular conduction.10 Pathologic changes in the atrioventricular conduction system were reported in patients with LQTS.11 These observations indicate that sodium channel gene mutations cause a spectrum of depolarization (or conduction) abnormalities. Therefore, in this study, we investigated whether LQTS patients with the ΔKPQ mutation of SCN5A sodium channel gene have clinically detectable changes in QRS morphology, P-wave morphology, and PR interval duration quantified in the signal-averaged electrocardiogram (SAECG).

Mechanisms for spontaneous changes in QRS morphology sometimes resembling torsades de pointes during reentrant ventricular tachycardia in a canine infarct model.

Spontaneous changes in QRS morphology during sustained reentrant ventricular tachycardia, occurring gradually or abruptly, causing the tachycardia to be polymorphic, have been described in clinical cases. The purpose of this study was to determine the mechanism for such changes in a canine infarct model. Reentrant circuits were mapped in the epicardial border zone during sustained ventricular tachycardia in the canine heart, 4 days after left anterior descending coronary occlusion. In 10 tachycardias, there was either an abrupt change in QRS morphology or a gradual change that took up to 25 cycles. When the latter occurred, the ECG resembled torsades de pointes. Maps showed that the predominant mechanism for the change in QRS was a shift in the exit route by which the impulse left the reentrant circuit to activate the ventricles (9/10 tachycardias). Such shifts resulted from small changes in conduction velocity in segments of the circuit, either speeding or slowing, which modified the length of the functional lines of block. Movement of the circuit to a different region was responsible for the change in QRS in only one of these experiments, in which the reentrant mechanism also changed from functional to anatomic. Subtle changes in conduction in reentrant circuits can alter QRS morphology. Changes in the exit route from a stable reentrant circuit can cause the ECG characteristics to resemble torsades de pointes.