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Aims: Leadless pacing has emerged as an alternative to conventional transvenous pacemakers to mitigate the risks of pocket‐ and lead‐related complications but its use remains controversial in young adults mostly because experience in this patient population is limited. We sought to examine the feasibility and safety of implanting leadless single chamber pacemakers in young adults. Methods: This multicenter, retrospective, observational study sought to evaluate the safety, efficacy, and electrical performance of the Micra VR Transcatheter Pacemaker System (Medtronic) in patients between 18 and 40 years who underwent implantation of a leadless pacemaker for any indication at the university medical centers of Bordeaux, Clermont‐Ferrand, Toulouse, and Tours (France), between 2015 and 2021. The primary safety endpoint was freedom from system‐related or procedure‐related major complications at 6 months. The primary efficacy endpoint was the combination of a low (≤2 V) and stable (increase within 1.5 V) pacing capture threshold at 6 months. Results: Leadless pacemaker implantation was successful in all 35 patients. At 6 months, safety endpoint was met for 35 (100%) and efficacy endpoint for 34 (97%) patients. During a follow‐up of 26 ± 15 months (range: 6–60 months), Safety endpoint remained 100% and efficacy endpoint was 94%. Leadless pacemaker retrieval was not required in any patient. Approximately one‐third of patients (n = 13, 37%) had >40% ventricular pacing burdens at 1 year, including all 10 patients with a complete AV block but also 3 patients with normal AV conduction during implantation. One patient reported symptoms of pacemaker syndrome which was confirmed using Holter recording and successfully treated using reprogramming. Conclusion: In this observational study, leadless pacemakers demonstrated favorable short‐ and intermediate‐term safety and effectiveness in young adults. [ABSTRACT FROM AUTHOR]

Background: Temporary transvenous pacing in critically ill patients requiring prolonged cardiac pacing is associated with a high risk of complications. We sought to evaluate the safety and efficacy of self‐contained intracardiac leadless pacemaker (LPM) implantation in this population. Methods and Results: Consecutive patients implanted with a Micra LPM during the hospitalization in an intensive care unit were retrospectively included. Inclusion criteria were: more than or equal to 1 supracaval central venous line, or a ventilation tube, or intravenous antibiotic therapy for ongoing sepsis or bacteremia. Patients with a history of the previous implantation of a pacemaker were excluded. Out of 1016 patients implanted with an LPM, 99 met the inclusion criteria. Mean age was 75 years and Charlson comorbidity index 7. LPM implantation was successfully performed in 98% of cases, with a perioperative complication rate of 5%, mainly cardiac injuries. In‐hospital mortality rate was 6%. No late (>30 days) device‐related complication occurred, especially no infection. Conclusions: LPM appears as an acceptable alternative to conventional temporary transvenous pacing in selected critically ill patients requiring prolonged cardiac pacing, especially regarding the risk of infection. [ABSTRACT FROM AUTHOR]

Background: Loss of biventricular stimulation can result in nonresponse to cardiac resynchronization therapy (CRT). Problems associated with the left ventricular (LV) lead and LV sensing can be challenging to detect and their incidence is unclear. The purpose of this study was to investigate mechanisms of loss of biventricular pacing due to LV lead‐ and LV sensing‐associated problems. Methods: In this bicentric study, CRT patients were surveilled using a novel remote monitoring algorithm from Biotronik (Germany) that registers LV electrograms (EGMs) during intermittent loss of resynchronization. The episodes were analyzed to assess the mechanisms of resynchronization interruptions. Results: We analyzed 582 EGMs from 61 patients. During a median follow‐up of 6 months, 59% of the patients had such episodes. The majority of the episodes (61%) were related to inappropriate inhibition of LV pacing, mostly due to upper rate lock‐in caused by LV sensing (58%). In contrast, 8% of episodes showed intermittent loss of LV capture, which was identified thanks to LV sensing. The remaining 31% of episodes were due to physiological reasons for resynchronization interruptions (eg, supraventricular tachycardia [18%], premature beats [8%], and others [5%]). Patients with CRT interruption episodes had lower resynchronization rates (median: 98.5% vs 100%, P =.044). Conclusions: Inadequate programming (active LV sensing with T‐wave protection) is the main cause of impaired resynchronization in devices with LV sensing. In general, we recommend the deactivation of the LV T‐wave protection function. [ABSTRACT FROM AUTHOR]

Introduction: We investigated whether pacing‐induced electrical dyssynchrony at the time of cardiac resynchronization therapy (CRT) device implantation was associated with chronic CRT response. Methods and Results: We included a total of 69 consecutive heart failure patients who received a CRT device. Left (LVp‐RVs) and right (RVp‐LVs) pacing‐induced interlead delays were measured intraoperatively and used to determine if there was paced left ventricular (LV) dyssynchrony, defined as present when LVp‐RVs is larger than RVp‐LVs. CRT response was defined as a reduction in LV end‐systolic volume ≥15%, 6 months after implantation. Paced left ventricular dyssynchrony (PLVD) was associated with ischemic cardiomyopathy (ICM) (χ2: 8; P =.005) but not with QRS morphology nor with pacing lead positions. In a univariate analysis, PLVD (odds ratio [OR], 6.53; 95% confidence interval [CI], 2.2‐18.9; P =.001), atypical left bundle branch block (LBBB) (OR, 3.3; 95% CI, 1.2‐9.4; P =.022), and ICM (OR, 5.2; 95% CI, 1.6‐17; P =.006) were associated with nonresponse. In a multivariate analysis, both PLVD (OR, 9.74; 95% CI, 2.8‐33.9; P <.0001) and atypical LBBB (OR, 5.6; 95% CI, 1.5‐20.3; P =.009) were independently associated with nonresponse. Adding PLVD to a model based on QRS morphology provided a significant and meaningful incremental value to predict LV reverse remodeling after CRT (χ2 to enter: 8; P <.005). Computer simulations corroborate these findings by showing that, while intrinsic electrical dyssynchrony is a prerequisite, the level of pacing‐induced dyssynchrony modulates acute CRT response. Conclusion: In addition to the intrinsic electrical substrate, PLVD is strongly associated with less LV reverse remodeling, demonstrating that measuring the electrical substrate during pacing has additional value for prediction of CRT response in an already well‐selected patient population. [ABSTRACT FROM AUTHOR]

Introduction: Some cardiac resynchronization therapy (CRT) device manufacturers (Biotronik, Germany; Boston Scientific, United States) have implemented left ventricular (LV) sensing functionality to prevent pacing into the vulnerable phase. Physicians are only partially aware of programming pitfalls related to LV sensing and general programming advice is lacking. Methods and Results: We provide an illustrative case–series‐based review of the variety of potential problems with LV sensing. LV sensing may inappropriately impair CRT delivery due to LV‐sensing issues or improper device programming. This can cause beat‐wise loss of resynchronization but also ongoing desynchronization. On the other hand, LV sensing provides additional diagnostic information, which may reveal intermittent problems of the LV lead such as capture loss. We summarize the available evidence to provide manufacturer‐specific recommendations on device programming and troubleshooting for daily clinical practice. Conclusion: CRT devices with LV sensing may suffer from impaired resynchronization due to programming pitfalls. If LV sensing is active (nominal setting in Biotronik and Boston Scientific devices), careful lookout for related problems and resynchronization percentage is required. Optimization is mandatory and even deactivation of LV sensing may have to be considered. [ABSTRACT FROM AUTHOR]

Cardiac resynchronization therapy (CRT) is an effective intervention in selected patients with moderate-to-severe heart failure with reduced ejection fraction and abnormal left ventricular activation time. The non-response rate of approximately 30% has remained nearly unchanged since this therapy was introduced 25 years ago. While intracardiac mapping is widely used for diagnosis and guidance of therapy in patients with tachyarrhythmia, its application in characterization of the electrical substrate to elucidate the mechanisms involved in CRT response remain anecdotal. In the present review, we describe the traditional determinants of CRT response before presenting novel non-invasive techniques used for CRT optimization. We discuss efforts to identify the target electrical substrate to guide the deployment of pacing electrodes during the operative procedure. Non-invasive body surface mapping technologies such as ECG imaging or ECG belt enables prediction of acute and chronic CRT response. While electrical dyssynchrony parameters provide high predictive accuracy for CRT response when obtained during intrinsic conduction, their predictive value is less when acquired during CRT or LV-pacing. Classic predictors of CRT response are female gender, NYHA class ≤ III, left ventricular ejection fraction ≥25%, QRS duration ≥150 ms and estimated glomerular filtration rate ≥60 mL/min. ECG-imaging is a comprehensive non-invasive mapping system which allows to express the amount of electrical asynchrony of a CRT candidate. Non-invasive body surface mapping technologies enables excellent prediction of acute and chronic CRT response before implantation. When performed during CRT or LV-pacing, the added value of these mapping systems remains unclear. [ABSTRACT FROM AUTHOR]

Abstract Background Electrocardiographic mapping (ECM) expresses electrical substrate through magnitude and direction of the activation delay vector (ADV). We investigated to what extent the response to cardiac resynchronization therapy (CRT) is determined by baseline ADV and by ADV modification through CRT and optimization of left ventricular (LV) pacing site. Methods ECM was performed in 79 heart failure patients (4 RBBB, 12 QRS < 120 ms, 23 non-specific conduction delay [NICD] and 40 left bundle branch block [LBBB]). 67 patients (QRS ≥ 120 ms) underwent CRT implantation and in 26 patients multiple LV pacing site optimization was performed. ADV was calculated from locations/depolarization times of 2000 virtual epicardial electrodes derived from ECM. Acute response was defined as ≥10% LVdP/d t max increase, chronic response by composite clinical score at 6 months. Results During intrinsic conduction, ADV direction was similar in patients with QRS < 120 ms, NICD and LBBB, pointing towards the LV free wall, while ADV magnitude was larger in LBBB (117 ± 25 ms) than in NICD (70 ± 29 ms, P < 0.05) and QRS < 120 ms (52 ± 14 ms, P < 0.05). Intrinsic ADV accurately predicted the acute (AUC = 0.93) and chronic (AUC = 0.90) response to CRT. ADV change by CRT only moderately predicted response (highest AUC = 0.76). LV pacing site optimization had limited effects: +3 ± 4% LVdP/d t max when compared to conventional basolateral LV pacing. Conclusion The baseline electrical substrate, adequately measured by ADV amplitude, strongly determines acute and chronic CRT response, while the extent of its modification by conventional CRT or by varying LV pacing sites has limited effects. Highlights • Activation delay vector expresses electrical substrate by its magnitude & direction. • Activation delay vector amplitude determines acute and chronic CRT response. • Varying left ventricular pacing sites has limited effects on CRT response. [ABSTRACT FROM AUTHOR]

Pacemaker-mediated tachycardia (PMT) is the term used to describe a repetitive sequence of sensed retrograde P waves followed by ventricular pacing at or below the maximum tracking rate. The following events can promote atrioventricular (AV) dissociation, retrograde conduction, and the onset of PMT: ventricular or atrial extrasystole, an excessively long programmed AV delay, external interference or myopotentials sensed by the atrial channel, atrial sensing or pacing failure, the absence of postventricular atrial refractory period extension after removal of a magnet, and VDD pacing at a higher rate than sinus rate. In contemporary devices, each manufacturer has a proprietary algorithm to detect and terminate PMT. Because of the increase in the number and complexity of the pacing algorithms and because of manufacturer-driven differences, a basic understanding of these new algorithms is important for patient care. We review here the main elements of the physiopathology of this type of tachycardia, describe the specific characteristics of the different manufacturers, and present representative clinical cases. [ABSTRACT FROM AUTHOR]

Cardiac electrical asynchrony occurs as a result of cardiac pacing or conduction disorders such as left bundle-branch block (LBBB). Electrically asynchronous activation causes myocardial contraction heterogeneity that can be detrimental for cardiac function. Computational models provide a tool for understanding pathological consequences of dyssynchronous contraction. Simulations of mechanical dyssynchrony within the heart are typically performed using the finite element method, whose computational intensity may present an obstacle to clinical deployment of patient-specific models. We present an alternative based on the CircAdapt lumped-parameter model of the heart and circulatory system, called the MultiPatch module. Cardiac walls are subdivided into an arbitrary number of patches of homogeneous tissue. Tissue properties and activation time can differ between patches. All patches within a wall share a common wall tension and curvature. Consequently, spatial location within the wall is not required to calculate deformation in a patch. We test the hypothesis that activation time is more important than tissue location for determining mechanical deformation in asynchronous hearts. We perform simulations representing an experimental study of myocardial deformation induced by ventricular pacing, and a patient with LBBB and heart failure using endocardial recordings of electrical activation, wall volumes, and end-diastolic volumes. Direct comparison between simulated and experimental strain patterns shows both qualitative and quantitative agreement between model fibre strain and experimental circumferential strain in terms of shortening and rebound stretch during ejection. Local myofibre strain in the patient simulation shows qualitative agreement with circumferential strain patterns observed in the patient using tagged MRI. We conclude that the MultiPatch module produces realistic regional deformation patterns in the asynchronous heart and that activation time is more important than tissue location within a wall for determining myocardial deformation. The CircAdapt model is therefore capable of fast and realistic simulations of dyssynchronous myocardial deformation embedded within the closed-loop cardiovascular system. [ABSTRACT FROM AUTHOR]

Electrical Impact of the Left Ventricular Pacing Site in CRT Introduction Recent studies have demonstrated that left ventricular (LV) pacing site is a critical parameter in optimizing cardiac resynchronization therapy (CRT). The present study evaluates the effect of pacing from different LV locations on QRS duration (QRSd) and their relationship to acute hemodynamic response in congestive heart failure patients. Methods and Results Thirty-five patients with nonischemic dilated cardiomyopathy and left bundle branch block referred for CRT device implantation were studied. Eleven predetermined LV pacing sites were systematically assessed in random order: epicardial: coronary sinus (CS); endocardial: basal and mid-cavity (septal, anterior, lateral, and inferior), apex, and the endocardial site facing the CS pacing site. For each patient QRSd and +dP/dtmax during baseline (AAI) and DDD LV pacing at 2 atrioventricular delays were compared. Response to CRT was significantly better in patients with wider baseline QRSd (≥150 milliseconds). Hemodynamic response was inversely correlated to increase of QRSd during LV pacing (short atrioventricular [AV] delay: r = 0.44, P < 0.001; long AV delay: r = 0.59, P < 0.001). Compared to baseline, LV pacing at the site of shortest QRSd significantly improved +dP/dtmax (+18 ± 25%, P < 0.001) but was not superior to other conventional strategy (lateral wall, CS pacing, and echo-guided) and was inferior to a hemodynamically guided strategy. Conclusions In our study, we have demonstrated that changes of QRSd during LV pacing correlated with acute hemodynamic response and that LV pacing location was a primary determinant of paced QRSd. Although QRSd did not predict the maximum hemodynamic response, our results confirm the link between electrical activation and hemodynamic response of the LV during CRT. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to enhance understanding of the working mechanism of cardiac resynchronization therapy by comparing animal experimental, clinical, and computational data on the hemodynamic and electromechanical consequences of left ventricular pacing (LVP) and biventricular pacing (BiVP). Background: It is unclear why LVP and BiVP have comparative positive effects on hemodynamic function of patients with dyssynchronous heart failure. Methods: Hemodynamic response to LVP and BiVP (% change in maximal rate of left ventricular pressure rise [LVdP/dtmax]) was measured in 6 dogs and 24 patients with heart failure and left bundle branch block followed by computer simulations of local myofiber mechanics during LVP and BiVP in the failing heart with left bundle branch block. Pacing-induced changes of electrical activation were measured in dogs using contact mapping and in patients using a noninvasive multielectrode electrocardiographic mapping technique. Results: LVP and BiVP similarly increased LVdP/dtmax in dogs and in patients, but only BiVP significantly decreased electrical dyssynchrony. In the simulations, LVP and BiVP increased total ventricular myofiber work to the same extent. While the LVP-induced increase was entirely due to enhanced right ventricular (RV) myofiber work, the BiVP-induced increase was due to enhanced myofiber work of both the left ventricle (LV) and RV. Overall, LVdP/dtmax correlated better with total ventricular myofiber work than with LV or RV myofiber work alone. Conclusions: Animal experimental, clinical, and computational data support the similarity of hemodynamic response to LVP and BiVP, despite differences in electrical dyssynchrony. The simulations provide the novel insight that, through ventricular interaction, the RV myocardium importantly contributes to the improvement in LV pump function induced by cardiac resynchronization therapy. [ABSTRACT FROM AUTHOR]

MRI Predictors of Reverse Remodeling After CRT Introduction Response rate after cardiac resynchronization therapy (CRT) remains suboptimal. We sought to identify pre- and intraprocedural predictors of response using MRI. Methods and Results Sixty patients underwent MRI before CRT. Left ventricular (LV) volumes and ejection fraction were assessed on cine images. Intra-LV dyssynchrony was defined as the maximal delay between first peaks of radial wall motion over 20 segments. Myocardial scar extent was quantified using delayed-enhanced MRI. After CRT, the paced LV segment was characterized on preprocedural MRI with respect to presence of scar and mechanical delay, the latter being quantified using time to first peak of wall motion, expressed in percentage of the total LV activation. Echocardiography was performed before and 6 months after CRT to quantify reverse remodeling (RR). Mean RR at 6 months was 30 ± 29% of baseline LV end-systolic volume. At univariate analysis, RR related to baseline LV end-diastolic and end-systolic volumes (R2 = 0.101, P = 0.01; R2 = 0.072, P = 0.04), intra-LV mechanical dyssynchrony (R2 = 0.351, P < 0.0001), scar extent (R2 = 0.273, P < 0.0001), and presence of scar at pacing site (R2 = 0.100, P = 0.01). QRS duration and mechanical delay at pacing site were not found related to RR (R2 = 0.041, P = 0.12 and R2 = 0.012, P = 0.4, respectively). At multivariate analysis intra-LV mechanical dyssynchrony, scar extent, and LV end-diastolic volume were independent predictors of RR (R2 = 0.307, P = 0.001; R2 = 0.096, P = 0.002, R2 = 0.078, P = 0.005, respectively). Conclusion Intra-LV dyssynchrony and scar extent are independent predictors of RR after CRT. Scar at pacing site is associated to a lesser response to CRT. Mechanical delay at this site has no impact on the response. [ABSTRACT FROM AUTHOR]

Depression and Cardiac Resynchronization Therapy. Background: The relationship between depression and heart failure is neither coincidental nor trivial, since depression is a powerful predictor of re-hospitalization and mortality. We prospectively studied the prevalence and impact of depression on the clinical outcomes of patients attending for cardiac resynchronization therapy (CRT). We specifically examined whether patients with depression have a different rate of response to CRT and whether CRT has an effect on depressive symptoms. Methods: Sixty-eight recipients of CRT systems were included. The depressive status was evaluated before implant and after 6 months by a structured diagnostic interview measuring Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria of major depression and by a self-report questionnaire (Center for Epidemiological Studies Depression Scale, CES-D). The CRT response was assessed at 6 months by a clinical composite score. Results: At inclusion, DSM-IV criteria of major depression were identified in 41% of the population, while using the self-report questionnaire 65% were observed to have mild to major depressive symptoms (CES-D ≥ 16). Only 4 patients were taking antidepressants. At 6 months, 75% were considered responders to CRT. Response to CRT did not differ between those with and without depression at baseline. The rate of patients with depression at 6 months was significantly lower in responders to CRT compared with nonresponders. Conclusions: We found a high prevalence of depressive symptoms in patients receiving CRT systems. Patients with depression should not be excluded from CRT, because they demonstrate a similar rate of response than the persons without depression and the responders are less likely to be depressed at 6 months. (J Cardiovasc Electrophysiol, Vol. 23, pp. 631-636, June 2012) [ABSTRACT FROM AUTHOR]

. Introduction: Preliminary studies have revealed a high correlation between peak endocardial acceleration (PEA) measured with a sensor embedded in a ventricular lead and human cardiac contractility. In this study we assessed (1) the contributions made by measurements of PEA1, an index of ventricular systolic contraction, from the right atrium, and (2) the feasibility of recording a fourth component of PEA (PEA4), coincident with atrial contraction and corresponding to the phonocardiographic fourth heart sound. Methods: We placed a PEA sensor embedded at the tip of a right atrial lead in 9 pigs. A 7F Millar catheter tip micromanometer was introduced into the left ventricular (LV) cavity to measure dP/dt. Myocardial contractility was increased by infusion of dobutamine and depressed by the infusion of esmolol. We searched, during VDD pacing, for PEA4 following atrial systole, while gradually lengthening the atrioventricular delay. Ventricular fibrillation was then triggered by rapid stimulation. Results: The changes in PEA1 were correlated with the changes in LV dP/dt (r = 0.91; P < 0.001). A low-frequency component of the endocardial signal (PEA4) was visible approximately 50 milliseconds after the atrial electrogram in all experiments. Following the induction of ventricular fibrillation, PEA4 remained visible on the endocardial recording, simultaneous with the sensed atrial electrogram. Conclusions: This study confirms the merit of embedding a PEA sensor in an atrial lead. The exploitation of the information provided by the PEA1 signal remains pertinent and the possibility to record an additional PEA4 component offers the perspective of new clinical applications. (J Cardiovasc Electrophysiol, Vol. 22, pp. 579-583 May 2011) [ABSTRACT FROM AUTHOR]

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Introduction: Biventricular pacing is associated with various electrocardiographic patterns depending on the position of the left ventricular (LV) lead. We aimed to develop an electrocardiogram-based algorithm to predict the position of the LV lead. Methods: The algorithm was developed in 100 consecutive recipients of cardiac resynchronization therapy (CRT) systems. QRS axis, morphology, and polarity were analyzed with a view to define the specific electrocardiographic characteristics associated with the various LV lead positions . The algorithm was prospectively validated in 50 consecutive CRT device recipients. Results: The first analysis of the algorithm was the QRS morphology in V1. A positive R wave in V1 suggested LV lateral or posterior wall stimulation. A QS pattern was specific of anterior LV leads. In the presence of an R wave in V1, V6 was analyzed to distinguish between an inferior and anterior LV lead. Inferior leads were never associated with a positive V6. To differentiate between lateral and posterior positions, we analyzed the pattern in V2. Lateral leads were associated with an R morphology in V1 and a negative V2. Posterior leads were associated with an R morphology in V1 and V2. The algorithm allowed a reliable distinction between an inferior or anterior and a lateral or posterior lead position in 90% of patients. Inferior, anterior, lateral, and posterior positions were reliably distinguished in 80% of patients. Conclusion: This algorithm predicted the position of the LV lead with a high sensitivity and predictive value. [ABSTRACT FROM AUTHOR]

Introduction: The peak of endocardial acceleration (PEA) is an index of myocardial contractility. We aimed to (1) demonstrate that the PEA measured by the noninvasive cutaneous precordial application of an accelerometer sensor is related to left ventricular (LV) d P/d t max and (2) assess the usefulness of PEA monitoring during graded ischemia and during different configurations of sequential biventricular pacing. Methods and Results: Measurements of invasive LV d P/d t max were compared with measurements of transcutaneous PEA in seven pigs at baseline and during acute drug infusions; increased heart rate; right, left, biventricular and sequential biventricular pacing before and after graded ischemia induced by the constriction of the left anterior descending coronary artery. A consistent PEA signal was obtained in all animals. PEA changes were highly related to LV d P/d t max changes ( r= 0.93; P < 0.001). The changes of LV contractility induced by the different pacing configurations were detected by PEA analysis in the absence of ischemia ( r= 0.94; P < 0.001) and in the presence of ischemic LV dysfunction ( r= 0.91; P < 0.001). Conclusion: Noninvasive PEA measurement allows monitoring of left ventricular contractility and may be a useful tool to detect global effect of ventricular ischemia and to optimize the choice of both pacing site and pacing configuration. [ABSTRACT FROM AUTHOR]

Reliability and Reproducibility of QRS Duration. Background: A QRS >120 ms remains the recommended criterion for the selection of cardiac resynchronization therapy (CRT) candidates. However, the reproducibility of this measurement has not been studied thoroughly. Methods: QRS duration was measured by 3 experienced cardiologists and by automatic measurement on 228 electrocardiograms (ECGs) randomly collected from 188 subjects, including neonates, healthy adults, patients with complete and incomplete bundle branch block, and CRT candidates. All ECGs were recorded at a 25 mm/s sweep speed. Forty recordings were duplicated and 50 ECGs were recorded at both 25 and 50 mm/s. Results: Significant interobserver differences (P < 0.001) were found between each combination of paired observers, with an up to 50-ms absolute variability between cardiologists and low concordance with computerized measurements. Intraobserver absolute variability was also significant (P < 0.01) for the 3 observers. These significant differences persisted (P < 0.01) when focusing our interest on the ECGs in the 100–140 ms range (defined as at least one out of the 4 measures in this range). Considering the 120 ms limit, 22 (27.5%) ECGs were differently classified by at least one of the cardiologists. We observed similar interobserver differences between each combination of paired observers with a 50 mm/s sweep speed. Conclusion: Manual QRS duration measurements were associated with significant inter- and intraobserver variability and low concordance with computerized measurements. The measurement of QRS is, therefore, operator-dependent and a reevaluation of the measurement methods may be essential to develop clinical and investigative standards. (J Cardiovasc Electrophysiol, Vol. 21, pp. 890-892, August 2010) [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Patients who have undergone repair of Tetralogy of Fallot (TOF) often present with right bundle branch block. Cardiac resynchronization therapy (CRT) with right ventricular (RV) or biventricular (BiV) stimulation has been proposed as a modality to correct electrical abnormalities and improve cardiac contractility in patients with repaired TOF. We aimed to 1) compare ventricular electrical activation in adults with repaired TOF during RV versus BiV stimulation, using a non-invasive epicardial mapping system, and 2) examine the clinical mid-term effects of BiV resynchronization. Methods: 9 adults with repaired TOF were implanted with a CRT system and underwent 1) a non-invasive epicardial mapping (n=9) during sinus intrinsic rhythm, RV and BiV pacing 2) a clinical evaluation (n=7) before and after 6months CRT with assessment of NYHA class and exercise capacity. Results: During intrinsic rhythm, non-invasive mapping demonstrated delayed activation of the right compared with the left ventricle in all patients, with the greatest activation delay noted near the infundibulum. However, we observed important differences among patients, in the severity of activation delays. Global activation time and an index of dyssynchrony were improved (p<0.05) during BiV pacing compared with RV pacing and spontaneous rhythm. BiV pacing increased (p<0.05) exercise tolerance and lowered the mean NYHA functional class at 6months of follow up. Conclusion: Patients with corrected TOF present with different patterns of ventricular activation. RV stimulation modestly improved RV activation sequence and was associated with a delayed LV activation. Biventricular stimulation significantly decreased right and left ventricular dyssynchrony. [Copyright &y& Elsevier]