Showing papers on "QRS complex published in 2010"

Cardiac-Resynchronization Therapy for Mild-to-Moderate Heart Failure

Abstract: Background Cardiac-resynchronization therapy (CRT) benefits patients with left ventricular systolic dysfunction and a wide QRS complex. Most of these patients are candidates for an implantable cardioverter–defibrillator (ICD). We evaluated whether adding CRT to an ICD and optimal medical therapy might reduce mortality and morbidity among such patients. Methods We randomly assigned patients with New York Heart Association (NYHA) class II or III heart failure, a left ventricular ejection fraction of 30% or less, and an intrinsic QRS duration of 120 msec or more or a paced QRS duration of 200 msec or more to receive either an ICD alone or an ICD plus CRT. The primary outcome was death from any cause or hospitalization for heart failure. Results We followed 1798 patients for a mean of 40 months. The primary outcome occurred in 297 of 894 patients (33.2%) in the ICD–CRT group and 364 of 904 patients (40.3%) in the ICD group (hazard ratio in the ICD–CRT group, 0.75; 95% confi dence interval [CI], 0.64 to 0.87; P<0.001). In the ICD–CRT group, 186 patients died, as compared with 236 in the ICD group (hazard ratio, 0.75; 95% CI, 0.62 to 0.91; P = 0.003), and 174 patients were hospitalized for heart failure, as compared with 236 in the ICD group (hazard ratio, 0.68; 95% CI, 0.56 to 0.83; P<0.001). However, at 30 days after device implantation, adverse events had occurred in 124 patients in the ICD-CRT group, as compared with 58 in the ICD group (P<0.001). Conclusions Among patients with NYHA class II or III heart failure, a wide QRS complex, and left ventricular systolic dysfunction, the addition of CRT to an ICD reduced rates of death and hospitalization for heart failure. This improvement was accompanied by more adverse events. (Funded by the Canadian Institutes of Health Research and Medtronic of Canada; ClinicalTrials.gov number, NCT00251251.)

Several common variants modulate heart rate, PR interval and QRS duration

Abstract: Electrocardiographic measures are indicative of the function of the cardiac conduction system. To search for sequence variants that modulate heart rate, PR interval and QRS duration in individuals of European descent, we performed a genome-wide association study in approximately 10,000 individuals and followed up the top signals in an additional approximately 10,000 individuals. We identified several genome-wide significant associations (with P < 1.6 x 10(-7)). We identified one locus for heart rate (MYH6), four for PR interval (TBX5, SCN10A, CAV1 and ARHGAP24) and four for QRS duration (TBX5, SCN10A, 6p21 and 10q21). We tested for association between these loci and subjects with selected arrhythmias in Icelandic and Norwegian case-control sample sets. We observed correlations between TBX5 and CAV1 and atrial fibrillation (P = 4.0 x 10(-5) and P = 0.00032, respectively), between TBX5 and advanced atrioventricular block (P = 0.0067), and between SCN10A and pacemaker implantation (P = 0.0029). We also replicated previously described associations with the QT interval.

Common variants in 22 loci are associated with QRS duration and cardiac ventricular conduction.

Abstract: The QRS interval, from the beginning of the Q wave to the end of the S wave on an electrocardiogram, reflects ventricular depolarization and conduction time and is a risk factor for mortality, sudden death and heart failure. We performed a genome-wide association meta-analysis in 40,407 individuals of European descent from 14 studies, with further genotyping in 7,170 additional Europeans, and we identified 22 loci associated with QRS duration (P < 5 × 10(-8)). These loci map in or near genes in pathways with established roles in ventricular conduction such as sodium channels, transcription factors and calcium-handling proteins, but also point to previously unidentified biologic processes, such as kinase inhibitors and genes related to tumorigenesis. We demonstrate that SCN10A, a candidate gene at the most significantly associated locus in this study, is expressed in the mouse ventricular conduction system, and treatment with a selective SCN10A blocker prolongs QRS duration. These findings extend our current knowledge of ventricular depolarization and conduction.

Genetic variation in SCN10A influences cardiac conduction

Abstract: To identify genetic factors influencing cardiac conduction, we carried out a genome-wide association study of electrocardiographic time intervals in 6,543 Indian Asians. We identified association of a nonsynonymous SNP, rs6795970, in SCN10A (P = 2.8 x 10(-15)) with PR interval, a marker of cardiac atrioventricular conduction. Replication testing among 6,243 Indian Asians and 5,370 Europeans confirmed that rs6795970 (G>A) is associated with prolonged cardiac conduction (longer P-wave duration, PR interval and QRS duration, P = 10(-5) to 10(-20)). SCN10A encodes Na(V)1.8, a sodium channel. We show that SCN10A is expressed in mouse and human heart tissue and that PR interval is shorter in Scn10a(-/-) mice than in wild-type mice. We also find that rs6795970 is associated with a higher risk of heart block (P < 0.05) and a lower risk of ventricular fibrillation (P = 0.01). Our findings provide new insight into the pathogenesis of cardiac conduction, heart block and ventricular fibrillation.

ECG criteria to identify epicardial ventricular tachycardia in nonischemic cardiomyopathy.

Abstract: Background— ECG criteria identifying epicardial (EPI) origin for ventricular tachycardia (VT) in nonischemic cardiomyopathy have not been determined Endocardial (ENDO) and EPI basal left ventricle fibrosis characterizes the VT substrate Methods and Results— We assessed the QRS from 102 basal-superior/lateral EPI and 67 comparable ENDO pace maps in 14 patients with nonischemic cardiomyopathy Pace mapping focused on low bipolar voltage areas Published morphology criteria: q wave in lead I (QWLI) and no q waves in inferior leads and interval criteria: pseudo-delta wave ≥34 ms, intrinsicoid deflection time ≥85 ms, shortest RS complex ≥121 ms, and maximum deflection index ≥055 were assessed for ability to identify EPI origin Sixteen EPI and 8 ENDO of the 34 mapped VTs (71%) in the study population and 14 EPI and 7 ENDO VTs from an 11-patient validation cohort were localized to basal-superior/lateral left ventricle and corroborated pacing data A QWL1 was seen in EPI but not ENDO pace maps (91% versus 4%; P <0001), identified 14 of 16 EPI VTs (sensitivity, 88%), and was seen in 1 of 8 ENDO VTs (specificity, 88%) None of the remaining criteria achieved similar sensitivity without specificity <50% We identified 4 criteria (q waves in inferior leads, pseudo-delta wave ≥75 ms, maximum deflection index ≥059, and QWL1) having ≥95% specificity and ≥20% sensitivity in identifying EPI/ENDO origin for pace maps This 4-step algorithm identified the origin in 109 of 115 pace maps (95%), 21 of 24 VTs (88%) in the study population, and 19 of 21 VTs (90%) in validation cohort Conclusions— Morphological ECG features that describe the initial QRS vector can help identify basal-superior/lateral EPI VTs in nonischemic cardiomyopathy Received February 22, 2009; accepted December 3, 2009

Early repolarization associated with ventricular arrhythmias in patients with chronic coronary artery disease.

Abstract: Background— Early repolarization, indicated on the standard 12-lead ECG, has recently been associated with idiopathic ventricular fibrillation in patients without structural heart disease. It is unknown whether there is an association between early repolarization and ventricular arrhythmias in the coronary artery disease (CAD) population. Methods and Results— Patients with CAD with implantable cardioverter-defibrillators in the healed phase of myocardial infarction were analyzed. In a case-control design, 60 patients who had ventricular arrhythmic events were matched for age and sex with 60 control subjects. ECGs were analyzed for early repolarization, defined as notching or slurring morphology of the terminal QRS complex or J-point elevation ≥0.1 mV above baseline in at least 2 lateral or inferior leads. Results were adjusted for left ventricular ejection fraction. Overall, early repolarization in 2 or more leads was more common in cases than control subjects (32% versus 8%, P =0.005). Early repolarization was noted more commonly in inferior leads (23% versus 8%, P =0.03), and a trend was noted in leads V4 through V6 (12% versus 3%, P =0.11). Early repolarization was uncommon in leads I and aVL in cases and control subjects (3% versus 0%). Notching was more common in cases than control subjects (28% versus 7%, P =0.008). Slurring and J-point elevation were not associated with ventricular arrhythmias. Conclusions— Early repolarization and, in particular, notching in the inferior leads is associated with increased risk of life-threatening ventricular arrhythmias in patients with CAD, even after adjustment for left ventricular ejection fraction. Our findings suggest early repolarization, and a notching morphology should be considered in a risk prediction model for arrhythmias in patients with CAD.

Mapping and Ablation of Epicardial Idiopathic Ventricular Arrhythmias From Within the Coronary Venous System

Abstract: Background— The prevalence of epicardial idiopathic ventricular arrhythmias that can be ablated from within the coronary venous system (CVS) has not been described. Methods and Results— In a consecutive group of 189 patients with idiopathic ventricular arrhythmias referred for ablation, the site of origin (SOO) of ventricular tachycardia and/or premature ventricular contractions was determined by activation mapping and pace mapping. Mapping was performed within the CVS if endocardial mapping did not reveal an SOO. Venography of the CVS and coronary angiography were performed before ablation in the CVS. In 27 of 189 patients (14%±5%; 95% confidence interval), the SOO of the ventricular arrhythmia was identified from within the coronary venous system, either in the great cardiac vein (n=26) or the middle cardiac vein (n=1). The mean activation time at the SOO was −29±8 ms. Twenty of 27 patients (74%) underwent successful ablation within the CVS. Epicardial ventricular arrhythmias displayed a broader R wave in V1 compared with arrhythmias in the control group (85 ms [interquartile range, 40] versus 65 ms [interquartile range, 95]; P <0.01). Two patients had recurrent premature ventricular contractions within 2 weeks after ablation, and no recurrences occurred in the remaining patients during a median follow-up of 13 months (range, 25). In the 7 patients with unsuccessful ablation, failure was because the ablation catheter could not be advanced to the SOO within the great cardiac vein (n=4), inadequate power delivery at the SOO (n=1), proximity to the phrenic nerve (n=1), or proximity of the SOO to a major coronary artery (n=1). Transcutaneous epicardial ablation was effective in 1 of 2 patients in whom it was attempted. Conclusions— Almost 15% of idiopathic ventricular arrhythmias have an epicardial origin. ECG characteristics help to differentiate epicardial arrhythmias from endocardial ventricular arrhythmias. The SOO of epicardial arrhythmias can be ablated from within the CVS in approximately 70% of patients.

Atrioventricular Nodal Reentrant Tachycardia

Abstract: Atrioventricular nodal reentrant tachycardia (AVNRT) represents the most common regular supraventricular arrhythmia in humans.1 The precise anatomic site and nature of the pathways involved have not yet been established, and several attempts to provide a reasonable hypothesis based on anatomic or anisotropic models have been made.2 There has been considerable evidence that the right and left inferior extensions of the human atrioventricular (AV) node and the atrionodal inputs they facilitate may provide the anatomic substrate of the slow pathway, and a comprehensive model of the tachycardia circuit for all forms of AVNRT based on the concept of atrionodal inputs has been proposed.2 Still, however, the circuit of AVNRT remains elusive. Recently, time-honored conventional schemes for the diagnosis and classification of the various forms of the arrhythmia have been refuted in part by evolving evidence. Recognition of the various types of AVNRT is important, however, to expedite diagnosis and allow implementation of appropriate ablation therapy without complications. We present an update on AVNRT with a particular emphasis on electrophysiological criteria used for the differential diagnosis of regular, supraventricular tachycardias. Typically, AVNRT is a narrow-complex tachycardia, ie, QRS duration <120 ms, unless aberrant conduction, which is usually of the right bundle-branch type, or a previous conduction defect exists. Tachycardia-related ST depression and RR-interval variation may be seen. RR alternans in AVNRT has been attributed to the proposed model of a figure of 8 reentry with continuous crossing over of antegrade activation through an inferior input to the contralateral superior input via the node.2 In the typical form of AVNRT (slow-fast), abnormal (retrograde) P′ waves are constantly related to the QRS and in the majority of cases are indiscernible or very close to the QRS complex (RP′/RR <0.5). Thus, P′ waves are either masked by the QRS complex or …

Robust R Peak and QRS detection in Electrocardiogram using Wavelet Transform

Abstract: In this paper a robust R Peak and QRS detection using Wavelet Transform has been developed. Wavelet Transform provides efficient localization in both time and frequency. Discrete Wavelet Transform (DWT) has been used to extract relevant information from the ECG signal in order to perform classification. Electrocardiogram (ECG) signal feature parameters are the basis for signal Analysis, Diagnosis, Authentication and Identification performance. These parameters can be extracted from the intervals and amplitudes of the signal. The first step in extracting ECG features starts from the exact detection of R Peak in the QRS Complex. The accuracy of the determined temporal locations of R Peak and QRS complex is essential for the performance of other ECG processing stages. Individuals can be identified once ECG signature is formulated. This is an initial work towards establishing that the ECG signal is a signature like fingerprint, retinal signature for any individual Identification. Analysis is carried out using MATLAB Software. The correct detection rate of the Peaks is up to 99% based on MIT-BIH ECG database.

New criteria during right ventricular pacing to determine the mechanism of supraventricular tachycardia.

Abstract: Background— Right ventricular pacing (RVP) during supraventricular tachycardia produces progressive QRS fusion before the QRS morphology becomes stable. This transition zone (TZ) may provide useful information for differentiating orthodromic reciprocating tachycardia (ORT) from atrioventricular nodal reentrant tachycardia and atrial tachycardia independent of entrainment success. Methods and Results— We studied the effect of properly timed RVP on atrial timing during the TZ in 92 patients with supraventricular tachycardia who had RVP within 40 ms of the tachycardia cycle length. The TZ during RVP includes progressively fused QRS complexes and the first paced complex with a stable QRS morphology based on analysis of the 12-lead ECG. We also measured the stimulus-atrial interval from the end of the TZ and with each QRS complex thereafter until pacing was terminated or ventriculo-atrial block occurred. A fixed stimulus-atrial interval was defined as variation <10 ms during RVP. Atrial preexcitation, postexcitation, or supraventricular tachycardia termination with abrupt ventriculo-atrial block was observed within the TZ in 32 of 34 patients with ORT. A fixed stimulus-atrial interval was established within the TZ in 33 of 34 patients with ORT. At least 1 of these 2 responses was observed in all patients with ORT. None of the patients with atrioventricular nodal reentrant tachycardia or atrial tachycardia had atrial timing perturbed or a fixed stimulus-atrial interval established within the TZ. Conclusions— During RVP within 40 ms of the tachycardia cycle length, ORT is the likely mechanism when atrial timing is perturbed or a fixed stimulus-atrial interval is established within the TZ.

J Wave, QRS Slurring, and ST Elevation in Athletes With Cardiac Arrest in the Absence of Heart Disease Marker of Risk or Innocent Bystander?

Abstract: Background—QRS-ST changes in the inferior and lateral ECG leads are frequently observed in athletes. Recent studies have suggested a potential arrhythmogenic significance of these findings in the g...

Frequency bands effects on qrs detection

Abstract: In this paper, we investigate the QRS frequency bands in ECG signals. Any QRS detection algorithm accuracy depends on the frequency range of ECG being processed. The QRS complex has different morphology and frequency band for different arrhythmias and noises in ECG signals. A standard bandpass range that maximizes the signal (QRS complex)-to-noise (T-waves, 60 Hz, EMG, etc.) ratio will be useful in ECG monitoring and diagnostic tools. A sensitive QRS detection algorithm has been introduced to compare the performance of using different frequency bands. The results shows that the recommended bandpass frequency range for detecting QRS complexes is 8-20Hz which the best signal-to-noise ratio.

Fragmented QRS complex: a novel marker of cardiovascular disease.

Abstract: 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.

Fragmented QRS and Mortality Risk in Patients With Left Ventricular Dysfunction

Abstract: Background— Fragmented QRS (fQRS) has been shown to predict cardiac events in select patient populations. Whether fQRS improves patient selection for primary prevention patients eligible for implantable cardioverter-defibrillator (ICD) therapy remains unknown. Methods and Results— In a prospective, multisite cohort of 842 patients with left ventricular dysfunction (ejection fraction ≤35%) representing both ischemic and nonischemic etiology, the presence of fQRS on ECG was assessed using standardized criteria. The association between fQRS and all-cause and arrhythmic mortality was evaluated overall and stratified by ICD status using multivariable Cox regression models, adjusted for demographic, clinical, and treatment variables. Fragmented QRS was present in 274 (32.5%) patients, and there were 191 (22.7%) deaths during a mean follow-up of 40±17 months. Rates of all-cause mortality did not differ between the fQRS+ (19.7%) and fQRS− (24.1%) groups; adjusted hazard ratio, 0.88; 95% confidence interval, 0.63–1.22; P =0.43. Additionally, rates of arrhythmic mortality were similar between the fQRS+ (9.9%) and fQRS− (12.7%) groups: adjusted hazard ratio, 0.77; 95% confidence interval, 0.49–1.31; P =0.38. Subgroup analyses found no association between fQRS and mortality when the cohort was further stratified by ICD status, etiology of left ventricular dysfunction, wide (≥120 ms) versus narrow (<120 ms) QRS duration, or fQRS myocardial territory. Conclusions— In this prospective, multisite cohort of primary prevention patients with left ventricular dysfunction, the presence of fQRS on ECG was not associated with a higher risk of either all-cause or arrhythmic mortality. These findings do not provide evidence that fQRS would be effective in risk stratifying primary prevention patients eligible for ICD therapy.

Myocardial Infarction Does Not Preclude Electrical and Hemodynamic Benefits of Cardiac Resynchronization Therapy in Dyssynchronous Canine Hearts

Abstract: Background— Several studies suggest that patients with ischemic cardiomyopathy benefit less from cardiac resynchronization therapy. In a novel animal model of dyssynchronous ischemic cardiomyopathy, we investigated the extent to which the presence of infarction influences the short-term efficacy of cardiac resynchronization therapy. Methods and Results— Experiments were performed in canine hearts with left bundle branch block (LBBB, n=19) and chronic myocardial infarction, created by embolization of the left anterior descending or left circumflex arteries followed by LBBB (LBBB+left anterior descending infarction [LADi; n=11] and LBBB+left circumflex infarction [LCXi; n=7], respectively). Pacing leads were positioned in the right atrium and right ventricle and at 8 sites on the left ventricular (LV) free wall. LV pump function was measured using the conductance catheter technique, and synchrony of electrical activation was measured using epicardial mapping and ECG. Average and maximal improvement in electric resynchronization and LV pump function by right ventricular+LV pacing was similar in the 3 groups; however, the site of optimal electrical and mechanical benefit was LV apical in LBBB hearts, LV midlateral in LBBB+LCXi hearts and LV basal-lateral in LBBB+LADi hearts. The best site of pacing was not the site of latest electrical activation but that providing the largest shortening of the QRS complex. During single-site LV pacing the range of atrioventricular delays yielding ≥70% of maximal hemodynamic effect was approximately 50% smaller in infarcted than noninfarcted LBBB hearts ( P <0.05). Conclusions— Cardiac resynchronization therapy can improve resynchronization and LV pump function to a similar degree in infarcted and noninfarcted hearts. Optimal lead positioning and timing of LV stimulation, however, require more attention in the infarcted hearts.

Segmentation of Holter ECG Waves Via Analysis of a Discrete Wavelet-Derived Multiple Skewness–Kurtosis Based Metric

Abstract: In this study, a simple mathematical-statistical based metric called Multiple Higher Order Moments (MHOM) is introduced enabling the electrocardiogram (ECG) detection–delineation algorithm to yield acceptable results in the cases of ambulatory holter ECG including strong noise, motion artifacts, and severe arrhythmia(s). In the MHOM measure, important geometric characteristics such as maximum value to minimum value ratio, area, extent of smoothness or being impulsive and distribution skewness degree (asymmetry), occult. In the proposed method, first three leads of high resolution 24-h holter data are extracted and preprocessed using Discrete Wavelet Transform (DWT). Next, a sample to sample sliding window is applied to preprocessed sequence and in each slid, mean value, variance, skewness, and kurtosis of the excerpted segment are superimposed called MHOM. The MHOM metric is then used as decision statistic to detect and delineate ECG events. To show advantages of the presented method, it is applied to MIT-BIH Arrhythmia Database, QT Database, and T-Wave Alternans Database and as a result, the average values of sensitivity and positive predictivity Se = 99.95% and P+ = 99.94% are obtained for the detection of QRS complexes, with the average maximum delineation error of 6.1, 4.1, and 6.5 ms for P-wave, QRS complex, and T-wave, respectively showing marginal improvement of detection–delineation performance. In the next step, the proposed method is applied to DAY hospital high resolution holter data (more than 1,500,000 beats including Bundle Branch Blocks—BBB, Premature Ventricular Complex—PVC, and Premature Atrial Complex—PAC) and average values of Se = 99.97% and P+ = 99.95% are obtained for QRS detection. In summary, marginal performance improvement of ECG events detection–delineation process, reliable robustness against strong noise, artifacts, and probable severe arrhythmia(s) of high resolution holter data can be mentioned as important merits and capabilities of the proposed algorithm.

Early repolarization syndrome – a new electrical disorder associated with sudden cardiac death –.

Abstract: Early repolarization (ER), consisting of a J-point elevation, notching or slurring of the terminal portion of the R wave (J wave), and tall/symmetric T wave, is a common finding on the 12-lead electrocardiogram. For decades, it has been considered as benign, barring sporadic case reports and basic electrophysiology research that suggested a critical role of the J wave in the pathogenesis of idiopathic ventricular fibrillation (VF). In 2007-2008, a high prevalence of ER in patients with idiopathic VF was reported and subsequent studies reinforced the results. This review summarizes the current state of knowledge concerning ER syndrome associated with sudden cardiac death. (Circ J 2010; 74: 2039-2044)

Fragmented QRS in prediction of cardiac deaths and heart failure hospitalizations after myocardial infarction.

Abstract: Background: Increased QRS fragmentation in visual inspection of 12-lead ECG has shown association with cardiac events in postmyocardial infarction (MI) patients We investigated user-independent computerized intra-QRS fragmentation analysis in prediction of cardiac deaths and heart failure (HF) hospitalizations after MI Methods: Patients (n = 158) with recent MI and reduced left ventricular ejection fraction (LVEF) were studied A 120-lead body surface potential mapping was performed at hospital discharge Intra-QRS fragmentation was computed as the number of extrema (fragmentation index FI) in QRS QRS duration (QRSd) was computed for comparison Results: During a mean follow-up of 50 months 15 patients suffered cardiac death and 23 were hospitalized for HF Using the mean + 1 SD as cut-point both parameters were univariate predictors of both end-points In multivariate analysis including age, gender, LVEF, previous MI, bundle branch block, atrial fibrillation, and diabetes FI was an independent predictor for cardiac deaths (HR 87, CI 30–256) and HF hospitalizations (HR 38, CI 16–93) whereas QRSd only predicted HF hospitalizations (HR 46, CI 20–107) In comparison to QRSd, FI showed better positive (PPA) and equal negative (NPA) predictive accuracy for both end-points, and PPA was further improved when combined to LVEF < 40% Limiting fragmentation analysis to 12-lead ECG or a randomly selected 8-lead set instead of all 120 leads resulted in an almost similar prediction Conclusions: Increased QRS fragmentation in post-MI patients predicts cardiac deaths and HF progression A computer-based fragmentation analysis is a stronger predictor than QRSd Ann Noninvasive Electrocardiol 2010;15(2):130–137

Mechanisms of drug induced QT interval prolongation.

Abstract: The long QT syndrome (LQTS) is characterized by a prolonged QT interval, as well as a propensity to develop syncope and sudden cardiac death caused by the malignant polymorphic ventricular arrhythmia called torsades de pointes (TdP). The QT interval is measured from the onset of the QRS complex to the end of the T wave and can be affected by both ventricular conduction velocities as well as by the velocity of repolarization. In most cases, QT prolongation is caused by factors that prolong the duration of the action potential, mainly by delaying the repolarization phase 3. The molecular mechanism is partially known. There are two well described mechanisms: blocking of the ion channel cavity of HERG; or causing an abnormal protein trafficking required for the location of HERG subunits in cell membrane. Both of them impair the I(Kr) current. However the blockade of ion channels is not the only condition to generate TdP. Other factors may play an important role, e.g. myocardium heterogeneity, drug-drug interaction, genetic polymorphism, and Electrolyte disturbances. Several drugs had been subject of withdrawal because QT-prolongation and arrhythmia. Understanding of processes involved in drug-induced QT prolongation is needed for the study and prevention of life-threatening arrhythmias.