Nonspecific Intraventricular Conduction Delay Research Articles

P3856Timing and associated predictors of onset of new conduction disturbances requiring permanent pacemaker implantation after transcatheter aortic valve implantation

Abstract Objectives This study aimed to investigate the onset and the associated predictors of new conduction disturbances (CDs) requiring permanent pacemaker implantation (PPI) after transcatheter aortic valve implantation (TAVI). Background The onset and associated predictors of onset of new CDs leading to PPI are still unknown. However, these are essential for safe and early discharge. Currently, these CDs lead to prolonged post-procedural monitoring after TAVI, limiting early discharge possibilities. Methods We retrospectively analyzed data from five centers in Europe. Post-TAVI electrocardiograms and telemetry data were evaluated to identify the onset of new CD in all patients who required a PPI within 30 days after TAVI. Early onset CDs were defined as within 48 hours after procedure, and late onset CDs as after 48 hours. Results A total of 2,804 patients were included for analysis. The PPI rate was 11%, of which 18% was due to late onset (>48h) CDs. Independent predictors for late onset CDs requiring PPI were pre-existing non-specific intraventricular conduction delay (IVCD), pre-existing right bundle branch block (RBBB), self-expandable valves, and predilation (Figure). Patients with a balloon-expandable valve without predilation did not develop CDs requiring PPI after 48 hours. Figure 1 Conclusions Associated predictors of late onset conduction disturbances leading to PPI after TAVI were pre-existing IVCD, pre-existing RBBB, the use of self-expandable valves, and predilation. Patients without CDs in the first 48 hours after TAVI and without risk factors for late onset CDs requiring PPI are possible candidates for early discharge after 48 hours.

Effect of Left Ventricular Conduction Delay on All-Cause and Cardiovascular Mortality (from the PRECISION Trial)

The prognosis associated with prolonged intraventricular conduction on electrocardiogram (ECG) remains uncertain. We aimed to compare clinical outcomes of narrow versus prolonged intraventricular conduction on ECG stratified by QRS morphology and cardiovascular disease (CVD) status. A post-hoc analysis was performed of the randomized-control PRECISION trial. Patients with centrally adjudicated, nonpaced baseline ECGs were included. QRS duration was classified narrow (≤100 ms) versus prolonged (>100 ms) with additional categorization into left (LBBB) or right (RBBB) bundle branch block or nonspecific intraventricular conduction delay (IVCD). IVCD was subclassified if left ventricular conduction delay (LVCD) was present (L-IVCD) or absent (O-IVCD). The primary outcome was adjudicated all-cause and cardiovascular (CV) mortality. Of 24,081 patients randomized, 22,067 (92%) were included with follow-up 34 ± 13 months. Study patients were 63 ± 9 years, 64% female, 75% Caucasian, 23% with established CVD. The prevalence of QRS prolongation was 5.6% (1,240): 760 right bundle branch block (3.4%), 313 LBBB (1.4%), and 161 IVCD (0.7%), 95 subclassified L-IVCD (0.4%). After adjustment, LBBB and L-IVCD were similarly associated with increased all-cause (LBBB: 2.3 [1.4 to 3.8], p = 0.001; L-IVCD: 4.0 [2.1 to 7.9], p <0.001) and CV (LBBB: 3.6 [2.0 to 6.5], p <0.001; L-IVCD 3.6 [1.3 to 9.7], p = 0.001) mortality. The presence of LVCD (LBBB or L-IVCD) was associated with all-cause (2.8 [1.8 to 4.2], p <0.001) and CV (3.6 [2.2 to 6.1], p <0.001) mortality exceeding the observed risks of coronary artery disease, left ventricular hypertrophy, or diabetes. The LVCD hazard persisted across QRS durations (100 to 120 vs >120 ms) and CVD status. In conclusion, LVCD, whether LBBB or L-IVCD, was strongly associated with increased mortality in patients with and at-risk for CVD.

Cardiac Resynchronization Defibrillator Therapy for Nonspecific Intraventricular Conduction Delay Versus Right Bundle Branch Block

BackgroundThe benefits of cardiac resynchronization therapy (CRT) in patients with non-left bundle branch block (LBBB) conduction abnormality have not been fully explored. ObjectivesThis study sought to evaluate clinical outcomes among Medicare-aged patients with nonspecific intraventricular conduction delay (NICD) versus right bundle branch block (RBBB) in patients eligible for implantation with a CRT with defibrillator (CRT-D). MethodsUsing the National Cardiovascular Data Registry implantable cardioverter-defibrillator (ICD) registry data between 2010 and 2013, the authors compared outcomes in CRT-eligible patients implanted with CRT-D versus ICD-only therapy among patients with NICD and RBBB. Also, among all CRT-D–implanted patients, the authors compared outcomes in those with NICD versus RBBB. Survival curves and multivariable adjusted hazard ratios (HRs) were used to assess outcomes including hospitalization and death. ResultsIn 11,505 non-LBBB CRT-eligible patients, after multivariable adjustment, among patients with RBBB, CRT-D was not associated with better outcomes, compared with ICD alone, regardless of QRS duration. Among patients with NICD and a QRS ≥150 ms, CRT-D was associated with decreased mortality at 3 years compared with ICD alone (HR: 0.602; 95% confidence interval [CI]: 0.416 to 0.871; p = 0.0071). Among 5,954 CRT-D–implanted patients, after multivariable adjustment NICD compared with RBBB was associated with lower mortality at 3 years in those with a QRS duration of ≥150 ms (HR: 0.757; 95% CI: 0.625 to 0.917; p = 0.0044). ConclusionsAmong non-LBBB CRT-D–eligible patients, CRT-D implantation was associated with better outcomes compared with ICD alone specifically in NICD patients with a QRS duration of ≥150 ms. Careful patient selection should be considered for CRT-D implantation in patients with non-LBBB conduction.

On-treatment comparison between corrective His bundle pacing and biventricular pacing for cardiac resynchronization: A secondary analysis of the His-SYNC Pilot Trial

The His-SYNC pilot trial was the first randomized comparison between His bundle pacing in lieu of a left ventricular lead for cardiac resynchronization therapy (His-CRT) and biventricular pacing (BiV-CRT), but was limited by high rates of crossover. To evaluate the results of the His-SYNC pilot trial utilizing treatment-received (TR) and per-protocol (PP) analyses. The His-SYNC pilot was a multicenter, prospective, single-blinded, randomized, controlled trial comparing His-CRT vs BiV-CRT in patients meeting standard indications for CRT (eg, NYHA II-IV patients with QRS >120 ms). Crossovers were required based on prespecified criteria. The primary endpoints analyzed included improvement in QRS duration, left ventricular ejection fraction (LVEF), and freedom from cardiovascular (CV) hospitalization and mortality. Among 41 patients enrolled (aged 64 ± 13 years, 38% female, LVEF 28%, QRS 168 ± 18 ms), 21 were randomized to His-CRT and 20 to BiV-CRT. Crossover occurred in 48% of His-CRT and 26% of BiV-CRT. The most common reason for crossover from His-CRT was inability to correct QRS owing to nonspecific intraventricular conduction delay (n = 5). Patients treated with His-CRT demonstrated greater QRS narrowing compared to BiV (125 ± 22 ms vs 164 ± 25 ms [TR], P < .001;124 ± 19 ms vs 162 ± 24 ms [PP], P < .001). A trend toward higher echocardiographic response wasalso observed (80 vs 57% [TR], P = .14; 91% vs 54% [PP], P= .078). No significant differences in CV hospitalization or mortality were observed. Patients receiving His-CRT on-treatment demonstrated superior electrical resynchronization and a trend toward higher echocardiographic response than BiV-CRT. Larger prospective studies may be justifiable with refinements in patient selection and implantation techniques to minimize crossovers.

Prognostic Implication of Ventricular Conduction Disturbance Pattern in Hospitalized Patients with Acute Heart Failure Syndrome.

Background and ObjectivesConflicting data exist regarding the prognostic implication of ventricular conduction disturbance pattern in patients with heart failure (HF). This study investigated the prognostic impact of ventricular conduction pattern in hospitalized patients with acute HF.MethodsData from the Korean Acute Heart Failure registry were used. Patients were categorized into four groups: narrow QRS (<120 ms), right bundle branch block (RBBB), left bundle branch block (LBBB), and nonspecific intraventricular conduction delay (NICD). The NICD was defined as prolonged QRS (≥120 ms) without typical features of LBBB or RBBB. The primary endpoint was the composite of all-cause mortality or rehospitalization for HF aggravation within 1 year after discharge.ResultsThis study included 5,157 patients. The primary endpoint occurred in 39.7% of study population. The LBBB group showed the highest incidence of primary endpoint followed by NICD, RBBB, and narrow QRS groups (52.5% vs. 49.7% vs. 44.4% vs. 37.5%, p<0.001). In a multivariable Cox-proportional hazards regression analysis, LBBB and NICD were associated with 39% and 28% increased risk for primary endpoint (LBBB hazard ratio [HR], 1.392; 95% confidence interval [CI], 1.152–1.681; NICD HR, 1.278; 95% CI, 1.074–1.520) compared with narrow QRS group. The HR of RBBB for the primary endpoint was 1.103 (95% CI, 0.915–1.329).ConclusionsLBBB and NICD were independently associated with an increased risk of 1-year adverse event in hospitalized patients with HF, whereas the prognostic impacts of RBBB were limited.Trial RegistrationClinicalTrials.gov Identifier: NCT01389843

Novel approach to discriminate left bundle branch block from nonspecific intraventricular conduction delay using pacing-induced functional left bundle branch block

Left bundle branch block (LBBB) has a predictive value for response to cardiac resynchronization therapy as reported by Zareba et al. (Circulation 123(10):1061-1072, 2011). However, based on ECG criteria, the discrimination between complete LBBB and nonspecific intraventricular conduction delay is challenging. We tested the hypothesis that discrimination can be performed using standard electrophysiological catheters and a simple stimulation protocol. Fifty-nine patients were analyzed retrospectively. Patients were divided into groups of narrow QRS (n = 20), wide QRS of right bundle branch block (RBBB) morphology (n = 14), and wide QRS of LBBB morphology (n = 25). Using a diagnostic catheter placed in the coronary sinus, left ventricular activation was assessed during intrinsic conduction as well as during right ventricular (RV) stimulation. In patients with narrow QRS and RBBB, the Q-LV/QRS ratio was 0.43 ± 0.013 (n = 20) and 0.41 ± 0.026 (n = 14), respectively. In patients with LBBB morphology, the Q-LV/QRS split up into a group of patients with normal (0.43 ± 0.022, n = 7) and a group with delayed left ventricular activation (0.75 ± 0.016, n = 18). By direct comparison of the Q-LV/QRS ratio during intrinsic conduction with the Q-LV/QRS ratio during RV pacing leading to a functional LBBB, a clear distinction between a group of "true LBBB" and another group of "apparent LBBB"/nonspecific intraventricular conduction delay (NICD) could be generated. We present a novel and practical method that might facilitate discrimination between patients with apparent LBBB and true LBBB by comparing Q-LV/QRS ratios during intrinsic activation and during RV stimulation. Although this method can already be directly applied, validation by 3D electrical mapping and prospective correlation to cardiac resynchronization therapy (CRT) response will be required for further translation into clinical practice.

Scar burden, not intraventricular conduction delay pattern, is associated with outcomes in ischemic cardiomyopathy patients receiving cardiac resynchronization therapy

Patients with nonspecific intraventricular conduction delay (IVCD) benefit less from cardiac resynchronization therapy (CRT) than patients with left bundle branch block (LBBB). The purpose of this study was to determine whether post-CRT outcome differences in patients with ischemic cardiomyopathy (ICM) relate to intrinsic QRS pattern and/or scar burden. We analyzed 393 consecutive ICM patients with left ventricular ejection fraction (LVEF) ≤35%, QRS duration >120 ms, and LBBB or nonspecific IVCD who underwent single-photon emission computed tomography myocardial perfusion imaging and CRT-defibrillator implant. We compared scar burden; QRS duration; LVEF change; risk of death, transplant, or ventricular assist device; and risk of appropriate device shocks between LBBB and IVCD patients, using multivariable analyses to determine relative associations between QRS pattern vs scar burden and outcomes. Nonspecific IVCD is associated with greater scar burden and narrower baseline QRS duration than LBBB. IVCD patients demonstrated less QRS narrowing with CRT than LBBB patients, even when excluding IVCD patients with QRS duration <150 ms. LVEF improved less in patients with IVCD vs LBBB, but only scar burden not QRS morphology or duration was associated with LVEF increase ≥5%. During 39-month follow-up, IVCD was associated with shorter survival free from transplant/ventricular assist device and shorter time to first appropriate device shock. Scar burden but not QRS morphology was independently associated with these outcomes on multivariate analysis. IVCD is associated with greater scar burden than LBBB in ICM CRT-defibrillator recipients. Scar burden, not QRS pattern, is independently associated with adverse clinical outcomes.

Electrocardiogram (ECG) patterns of left anterior fascicular block and conduction impairment in ventricular myocardium: a whole-heart model-based simulation study.

Left anterior fascicular block (LAFB) is a heart disease identifiable from an abnormal electrocardiogram (ECG). It has been reported that LAFB is associated with an increased risk of heart failure. Non-specific intraventricular conduction delay due to the lesions of the conduction bundles and slow cell to cell conduction has also been considered as another cause of heart failure. Since the location and mechanism of conduction delay have notable variability between individual patients, we hypothesized that the impaired conduction in the ventricular myocardium may lead to abnormal ECGs similar to LAFB ECG patterns. To test this hypothesis, based on a computer model with a three dimensional whole-heart anatomical structure, we simulated the cardiac exciting sequence map and 12-lead ECG caused by the block in the left anterior fascicle and by the slowed conduction velocity in the ventricular myocardium. The simulation results showed that the typical LAFB ECG patterns can also be observed from cases with slowed conduction velocity in the ventricular myocardium. The main differences were the duration of QRS and wave amplitude. In conclusion, our simulations provide a promising starting point to further investigate the underlying mechanism of heart failure with LAFB, which would provide a potential reference for LAFB diagnosis.

NEW APPROACH TO OLD CONCEPTS: PROGNOSIS AND NATURAL HISTORY OF CONDUCTION SYSTEM DISEASE; PROGNOSTIC IMPLICATIONS OF CONDUCTION SYSTEM DISEASE

Conduction abnormalities are commonly identified in approximately 10% of patients on standard 12-lead electrocardiograms (ECGs). While there have been previous attempts at characterizing the prognostic implications of these findings, the association between intraventricular conduction delays (IVCD) and outcomes are still poorly understood. We performed a retrospective cohort study of patients enrolled in the APPROACH registry. We included patients who had an ECG recorded in the MUSE database in the 180 days before coronary angiography or within 3 subsequent days. We excluded patients with reduced left ventricular ejection fraction (LVEF), paced rhythms, and those who died the day of coronary angiography. We used multivariable Cox proportional hazards models to assess associations between IVCD and all-cause mortality after correcting for age, sex, medical co-morbidities, LVEF and extent of coronary artery disease. We modeled conduction system disease as a baseline and as a time-varying exposure. We identified 11,267 patients (mean age 62.3 +/- 12.4, 70.1% male) who underwent coronary angiography between May 2006 and March 2014, 10,227 (90.8%) of whom presented with ACS. Over a median follow-up of 3.6 years, 922 (8.2%) patients died. IVCD was identified in 2,738 (24.3%) patients at baseline. After adjusting for all baseline factors, right bundle branch block (adjusted HR 1.41, 95% CI 1.15-1.72, p < 0.01) and non-specific intraventricular conduction delay (adjusted HR 1.60, 95% CI 1.24-2.06, p < 0.01) were independently associated with increased all-cause mortality. However, after similar adjustments left bundle branch block (Adjusted HR 0.79, 95% CI 0.61-1.02, p=0.07) was not associated with all-cause mortality. Our results were similar when modeling conduction disease as a baseline feature and as a time-varying exposure. After correction for medical co-morbidities and extent of coronary artery disease, right bundle branch block and non-specific intraventricular conduction delay is associated with increased all-cause mortality. However, in contrast to earlier studies, we found no association with left bundle branch block.

Assessment of cardiac resynchronisation therapy in patients with wide QRS and non-specific intraventricular conduction delay: rationale and design of the multicentre randomised NICD-CRT study

IntroductionCardiac resynchronisation therapy (CRT) was initially developed to treat patients with left bundle branch block (LBBB). However, many patients with heart failure have a widened QRS but neither left-BBB nor...

ECG parameters predict left ventricular conduction delay in patients with left ventricular dysfunction

Estimating left ventricular electrical delay (Q-LV) from a 12-lead ECG may be important in evaluating cardiac resynchronization therapy (CRT). The purpose of this study was to assess the impact of Q-LV interval on ECG configuration. One hundred ninety-two consecutive patients undergoing CRT implantation were divided electrocardiographically into 3 groups: left bundle branch block (LBBB), right bundle branch block (RBBB), and nonspecific intraventricular conduction delay (IVCD). The IVCD group was further subdivided into 81 patients with left (L)-IVCD and 15 patients with right (R)-IVCD (resembling RBBB, but without S wave in leads I and aVL). The Q-LV interval in the different groups and the relationship between ECG parameters and the maximum Q-LV interval were analyzed. Patients with LBBB presented a long Q-LV interval (147.7 ± 14.6 ms, all exceeding cutoff value of 110 ms), whereas RBBB patients presented a very short Q-LV interval (75.2 ± 16.3 ms, all <110 ms). Patients with an IVCD displayed a wide range of Q-LV intervals. In L-IVCD, mid-QRS notching/slurring showed the strongest correlation with a longer Q-LV interval, followed, in decreasing order, by QRS duration >150 ms and intrinsicoid deflection >60 ms. Isolated mid-QRS notching/slurring predicted Q-LV interval >110 ms in 68% of patients. The R-IVCD group presented an unexpectedly longer Q-LV interval (127.0 ± 12.5 ms; 13/15 patients had Q-LV >110 ms). Patients with LBBB have a very prolonged Q-LV interval. Mid-QRS notching in lateral leads strongly predicts a longer Q-LV interval in L-IVCD patients. Patients with R-IVCD constitute a subgroup of patients with a long Q-LV interval.

A Three-Decade Survival Analysis of Intraventricular Conduction Delay in Adults Without Ischemic Heart Disease

BackgroundThe prognosis of an incidental finding of intraventricular conduction delay in individuals without ischemic heart disease is debatable. Intraventricular conduction delay presents electrocardiographically as bundle branch block or nonspecific intraventricular conduction delay. We aimed to assess the long-term survival of an incidental intraventricular conduction delay finding in a cohort of individuals without ischemic heart disease, followed up for 3 decades. MethodsA randomized stratified cohort of the adult Israeli population underwent medical examinations and electrocardiography between 1976 and 1982. Patients with ischemic heart disease were excluded, and the cohort was followed for all-cause mortality for a median of 30.4 years. Major intraventricular conduction delay was defined as having complete bundle branch block or nonspecific intraventricular conduction delay, and minor intraventricular conduction delay was defined as having incomplete bundle branch block. Cox proportional hazard model was performed, comparing individuals by electrocardiogram finding, adjusting for demographic, clinical, and electrocardiographic variables. ResultsOf 2465 subjects, 2385 (96.8%) were without intraventricular conduction delay, 38 (1.5%) had minor intraventricular conduction delay, and 42 (1.7%) had major intraventricular conduction delay. All-cause mortality rates were higher among minor and major intraventricular conduction delay groups (57.9% and 66.7%, P = .43 and P = .04, respectively) compared with no intraventricular conduction delay (52.1%). By controlling for sex, age, and body mass index, intraventricular conduction delay was not associated with all-cause mortality: hazard ratios, 0.82 (95% confidence interval, 0.52-1.25) and 1.06 (95% confidence interval, 0.72-1.54) for minor and major intraventricular conduction delay, respectively. ConclusionsIntraventricular conduction delay was not found to be an independent risk factor for all-cause mortality in individuals without ischemic heart disease.

Prevalence and prognosis of ECG abnormalities in normotensive and hypertensive individuals.

To define the prevalence and prognosis of ECG abnormalities in hypertensive individuals. ECG, blood pressure and other cardiovascular risk factors were recorded in a nationwide population sample of 5800 Finns. The presence of 15 ECG abnormalities was evaluated. Participants were divided into categories by blood pressure and followed for coronary heart (CHD) and cardiovascular disease (CVD) events. Mean follow-up was 10.4 ± 2.2 years. The age- and sex-adjusted prevalence rates of ECG abnormalities were generally higher in the hypertensive participants than in normotensive individuals. In multivariable-adjusted Cox models, the following ECG abnormalities predicted CHD in hypertensive participants: left ventricular hypertrophy (LVH) by Sokolow-Lyon criteria [hazard ratio, 1.47; 95% confidence interval (CI), 1.07-2.01; P = 0.02], LVH with ST-depression and negative T wave (ST/T changes) (hazard ratio, 2.31; 95% CI, 1.20-4.43, P = 0.01), ST/T changes (hazard ratio, 2.12; 95% CI, 1.34-3.36; P = 0.001), positive T wave in lead aVR (AVRT+) (hazard ratio, 1.74; 95% CI, 1.15-2.64; P = 0.009) and poor R-wave progression (hazard ratio, 2.02; 95% CI, 1.27-3.22; P = 0.003). These ECG abnormalities were also significant predictors of CVD in hypertensive participants (P ≤ 0.03 for all). Nonspecific intraventricular conduction delay predicted CVD in the whole population (hazard ratio, 1.50; 95% CI, 1.06-2.13; P = 0.02). Prolonged QT interval, abnormal P-wave indices, left axis deviation and early repolarization pattern were not associated with CHD or CVD. ECG abnormalities are highly prevalent in hypertensive individuals. LVH is still the cornerstone of cardiovascular risk assessment in hypertensive patients. The additional assessment of ST/T changes, AVRT+ and poor R-wave progression in ECGs could improve risk prediction in hypertensive patients.

Identifying delayed left ventricular lateral wall activation in patients with non-specific intraventricular conduction delay using coronary venous electroanatomical mapping.

BackgroundDelayed left ventricular (LV) lateral wall activation is considered the electrical substrate that characterises patients suitable for cardiac resynchronisation therapy (CRT). Although typically associated with left bundle branch block, delayed LV lateral wall activation may also be present in patients with non-specific intraventricular conduction delay (IVCD). We assessed LV lateral wall activation in a cohort of CRT candidates with IVCD using coronary venous electroanatomical mapping, and investigated whether baseline QRS characteristics on the ECG can identify delayed LV lateral wall activation in this group of patients.MethodsTwenty-three consecutive CRT candidates with IVCD underwent intra-procedural coronary venous electroanatomical mapping using EnSite NavX. Electrical activation time was measured in milliseconds from QRS onset and expressed as percentage of QRS duration. LV lateral wall activation was considered delayed if maximal activation time measured at the LV lateral wall (LVLW-AT) exceeded 75 % of the QRS duration. QRS morphology, duration, fragmentation, axis deviation, and left anterior/posterior fascicular block were assessed on baseline ECGs.ResultsDelayed LV lateral wall activation occurred in 12/23 patients (maximal LVLW-AT = 133 ± 20 ms [83 ± 5 % of QRS duration]). In these patients, the latest activated region was consistently located on the basal lateral wall. QRS duration, and prevalence of QRS fragmentation and left/right axis deviation, and left anterior/posterior fascicular block did not differ between patients with and without delayed LV lateral wall activation.ConclusionCoronary venous electroanatomical mapping can be used at the time of CRT implantation to determine the presence of delayed LV lateral wall activation in patients with IVCD. QRS characteristics on the ECG seem unable to identify delayed LV lateral wall activation in this subgroup of patients.

Ventricular conduction abnormalities as predictors of long‐term survival in acute de novo and decompensated chronic heart failure

AimsData on the prognostic role of left and right bundle branch blocks (LBBB and RBBB), and nonspecific intraventricular conduction delay (IVCD; QRS ≥ 110 ms, no BBB) in acute heart failure (AHF) are controversial. Our aim was to investigate electrocardiographic predictors of long‐term survival in patients with de novo AHF and acutely decompensated chronic heart failure (ADCHF).Methods and ResultsWe analysed the admission electrocardiogram of 982 patients from a multicenter European cohort of AHF with 3.9 years' mean follow‐up. Half (51.5%, n = 506) of the patients had de novo AHF. LBBB, and IVCD were more common in ADCHF than in de novo AHF: 17.2% vs. 8.7% (P < 0.001) and 20.6% vs. 13.2% (P = 0.001), respectively, and RBBB was almost equally common (6.9% and 8.1%; P = 0.5), respectively. Mortality during the follow‐up was higher in patients with RBBB (85.4%) and IVCD (73.7%) compared with patients with normal ventricular conduction (57.0%); P < 0.001 for both. The impact of RBBB on prognosis was prominent in de novo AHF (adjusted HR 1.93, 1.03–3.60; P = 0.04), and IVCD independently predicted death in ADCHF (adjusted HR 1.79, 1.28–2.52; P = 0.001). Both findings were pronounced in patients with reduced ejection fraction. LBBB showed no association with increased mortality in either of the subgroups. The main results were confirmed in a validation cohort of 1511 AHF patients with 5.9 years' mean follow‐up.ConclusionsConduction abnormalities predict long‐term survival differently in de novo AHF and ADCHF. RBBB predicts mortality in de novo AHF, and IVCD in ADCHF. LBBB has no additive predictive value in AHF requiring hospitalization.

Whole exome sequencing identifies the TNNI3K gene as a cause of familial conduction system disease and congenital junctional ectopic tachycardia

We report familial cardiac conduction disease (FCCD) in a 3-generation pedigree, including some family members with congenital junctional ectopic tachycardia (JET) (Fig. 1A). The proband presented during a febrile illness at 3.5-years of age with variable atrio-ventricular (AV) block (1st, 2nd, and 3rd degrees) together with left anterior fascicular block (LAFB) and right bundle branch block (RBBB) (Fig. 1B). Viral studies and echocardiogram were normal and he received a pacemaker; he subsequently developed clinical junctional tachycardia. Family history revealed a maternal grandmother with RBBB diagnosed at 5 years of age. The electrocardiogram (ECG) from the proband's mother revealed sinus rhythm (SR), 1st degree AV block and a nonspecific intraventricular conduction delay. Clinical genetic testing of SCN5A did not reveal any disease-associated mutations. Subsequently she gave birth to identical twin girls. Both girls had rapid JET in the immediate post-natal period that was initially difficult to control. There was rate dependent RBBB and LAFB in both children prior to use of antiarrhythmic drugs. The arrhythmia has resolved in one twin but persists in the other as a catecholamine dependent accelerated junctional rhythm/congenital JET that is modified by propranolol therapy (Fig. 1C). The resting ECGs now both show LAFB and intermittent incomplete RBBB. The mother has subsequently developed symptomatic palpitations and shows electrocardiographic features consistent with typical atrioventricular nodal re-entrant tachycardia (AVNRT) on symptom-rhythm correlation observed on loop recorder. Thus, the conduction defects in this family were of varying severity and the relationship to congenital JET in the three children is important as it is well recognized that congenital JET may progress to heart block [ 1 Henneveld H. Hutter P. Bink-Boelkens M. et al. Junctional ectopic tachycardia evolving into complete heart block. Heart. 1998; 80: 627-628 Crossref PubMed Scopus (23) Google Scholar , 2 Villain E. Vetter V.L. Garcia J.M. et al. Evolving concepts in the management of congenital junctional ectopic tachycardia. A multicenter study. Circulation. 1990; 81: 1544-1549 Crossref PubMed Scopus (211) Google Scholar ]. At this stage the conduction abnormalities are minor in the twins who presented with the JET and have not progressed.

Nonspecific intraventricular conduction delay: Definitions, prognosis, and implications for cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) is an electrical treatment of heart failure with reduced ejection fraction and wide QRS. It aims to correct the electrical dyssynchrony present in 30% to 50% of patients in this population. Dyssynchrony results in widening of the QRS complex on the electrocardiogram (ECG). CRT was initially developed to treat patients who had left bundle branch block (LBBB) and delayed activation of the lateral left ventricular wall. However, a large proportion of heart failure patients present with a widened QRS that is neither an LBBB nor a right bundle branch block (RBBB): nonspecific intraventricular conduction delay (NICD). Less studied than RBBB or LBBB, its pathophysiology is both complex and varied yet still reflects intramyocardial conduction delay. NICD is most often associated with cardiomyopathy (eg, ischemic or hypertensive). Conduction pathways can be either healthy or affected. Results from CRT are contradictory in this patient group, despite a seemingly neutral trend. Unfortunately, prospective studies are lacking. Guidelines recommending implantation of CRT devices in this group are based solely on analyses of subgroups with small sample sizes. A dedicated prospective study is therefore warranted for this question to be answered properly. A detailed study of the ECG and noninvasive study of ventricular electrical activation may enable clinicians to better identify patients with NICD who will respond to CRT.

Effects of Cardiac Resynchronization Therapy on Ventricular Electrical Remodeling in Patients With Heart Failure.

Cardiac resynchronization therapy (CRT) reverses structural remodeling of the left ventricle. We investigated whether CRT reverses left-ventricular electrical remodeling.Eighty patients were enrolled and implanted with CRT-devices. Echocardiography and electrocardiography data were obtained from each patient prior to implantation and two years after implantation. At two years after implantation, the patients were classified into a responder group and a non-responder group based on echocardiography.Over the next 2 years, 75 patients completed follow-up, and 5 patients had died. Echocardiography results showed that 23 patients could be classified as non-responders and 52 as responders. Larger numbers of non-responders were diagnosed with either ischemic cardiomyopathy (ICM) or nonspecific intraventricular conduction delay (NICD). The intrinsic QRS duration was not changed in responders, patients with dilated cardiomyopathy, or in the patient categories of male and female. However, the intrinsic QRS duration was significantly prolonged in non-responders and patients with ischemic cardiomyopathy (P = 0.041). The mean left ventricular end-diastolic diameter in the responder group was significantly decreased by CRT (P < 0.05), while there was no significant change in intrinsic QRS duration.While CRT does not reduce the intrinsic QRS duration, it can delay negative ventricular electrical remodeling. Continuous CRT is necessary.

Abstract 13286: Non-Specific Intraventricular Conduction Delay and Risk of Sudden Death

Introduction: We and others have reported an independent association between prolonged QRS duration and risk of sudden cardiac death (SCD) in the general population. Left and right bundle branch block have been studied previously, but there is little information regarding non-specific intraventricular conduction delay and risk of SCD. Hypothesis: Completed conduction defects, including non-specific IVCD, are associated with increased SCD risk. Methods: Sudden cardiac death cases and controls from an ongoing large population based study in the Northwestern US (2002 to 2010) were included if age ≥ 35 years with a non-paced 12-lead ECG (recorded prior and unrelated to SCD in cases). QRS morphology was subcategorized as normal, intermediate [left anterior fascicular block (LAFB), left posterior fascicular block (LPFB), and incomplete right or left bundle branch block (IRBBB/ILBBB)] or completed conduction defects [left bundle branch block (LBBB), right bundle branch block (RBBB), or nonspecific intraventricular conduction delay (IVCD)]. Comparisons were conducted using chi-square tests for categorical variables and independent samples t-tests for continuous variables. Logistic regression was used to evaluate the association of QRS morphology with SCD. Results: We evaluated 761 SCD cases (64% male) and 539 controls (65% male). Cases were significantly older (69.7 vs 66.3 years, p&lt;0.0001) with greater QRS duration (102 vs. 98 ms, p=0.001). For conduction categories, intermediate or completed conduction defects were significantly more common in cases whereas normal QRS morphology was more common among controls (p=0.01). And for specific morphology overall, QRS morphology patterns differed between cases and controls (p=0.03); abnormal QRS morphologies were more frequent in cases than controls except for LAFB. After adjustment for age and gender, however, only a finding of LBBB or non-specific IVCD remained a significant predictor of SCD [OR 1.34 (95% CI 1.03-1.75)]. Conclusions: LBBB and non-specific IVCD, but not RBBB, are significant predictors of SCD in the general population. These findings contribute to the utility of the 12-lead EKG for SCD risk stratification.

IS ST-SEGMENT DEPRESSION EQUIVALENT TO ST-SEGMENT ELEVATION IN PATIENTS PRESENTING WITH OUT-OF-HOSPITAL CARDIAC ARREST?

Following an out-of-hospital cardiac arrest (OHCA), systematic post-arrest care improves the likelihood of survival and neurological recovery. The immediate post resuscitation 12-lead electrocardiogram (ECG) aids in the diagnosis of an acute coronary syndrome (ACS); this can occur in up to 50% of adults presenting with OHCA. We aimed to characterize the relationship between the post-resuscitation ECG and coronary angiography (CA) during the index admission. A retrospective chart review of consecutive adult patients admitted to St. Paul’s and Mt. St. Joseph’s Hospitals following an OHCA, between January 2010 and December 2011, was undertaken. Patients were identified using the Resuscitation Outcomes Consortium Cardiac Arrest Epistry databases and included if they were admitted to hospital and had interpretable post-resuscitation ECG. ST-segment changes of >0.1mV in two contiguous leads were considered significant. A stenosis of >70% was classified as obstructive coronary artery disease (CAD) and >50% for left main stenosis. Coronary occlusion was defined as >99% stenosis. Our cohort consisted of n=65 patients with a mean age of 62 ± 17 years and 69% were male. The initial rhythm on paramedic arrival was ventricular tachycardia/fibrillation (n=29; 45%), asystole (n=15; 23%), pulseless electrical activity (n=8; 12%), and unspecified (n=13; 20%). The post-resuscitation ECG demonstrated sinus rhythm (n=44; 68%), atrial tachycardia (n=13; 20%), and other (n=8; 12%). The median heart rate was 95bpm (IQR=72-114bpm), QRS duration 112ms (IQR=94-146ms), and corrected QT interval 456ms (IQR=415-494ms). The QRS morphology included narrow complex (n=35; 54%), non-specific intraventricular conduction delay (n=11; 17%), RBBB (n=14; 22%), and LBBB (n=5; 8%). The rate of CA was 42% (n=27). The table below shows CA findings stratified by ST segment change. At CA the mean LVEDP was 20mmHg and LVEF was 41%. The odds ratios (OR) of coronary occlusion for ST-elevation was 21.6 (95% CI=2.1-218.6; p=0.002) and for non ST segment change was 0.07 (95% CI=0.01 - 0.5; p=0.004). In patients with ST-depression there was a trend towards coronary occlusion (OR 4.5 95% CI=0.5-41.2; p=0.17). A significant proportion of patients presenting with OHCA demonstrated ST-segment changes on the post-resuscitation ECG. Rates of coronary angiography in OHCA patients were low. The findings of significant CAD were frequent, irrespective of ST-segment shift. The presence of ST- depression showed a trend towards coronary occlusion. Systematic evaluation of patients with ST depression is warranted to further improve survival and neurological recovery post OHCA.