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Background: Assessment of origin of ventricular tachycardias (VTs) arising from epicardial vs endocardial sites are largely challenged by the available criteria and etiology of cardiomyopathy. Current electrocardiographic (ECG) criteria based on 12-lead ECG have varying sensitivity and specificity based on site of origin and etiology of cardiomyopathy., Objectives: This study sought to test the hypothesis that epicardial VT has a slower initial rate of depolarization than endocardial VT., Methods: We developed a method that takes advantage of the fact that electrical conduction is faster through the cardiac conduction system than the myocardium, and that the conduction system is primarily an endocardial structure. The technique calculated the rate of change in the initial VT depolarization from a signal-averaged 12-lead ECG. We hypothesized that the rate of change of depolarization in endocardial VT would be faster than epicardial. We assessed by applying this technique among 26 patients with VT in nonischemic cardiomyopathy patients., Results: When comparing patients with VTs ablated using epicardial and endocardial approaches, the rate of change of depolarization was found to be significantly slower in epicardial (6.3 ± 3.1 mV/s vs 11.4 ± 3.7 mV/s; P < 0.05). Statistical significance was found when averaging all 12 ECG leads and the limb leads, but not the precordial leads. Follow up analysis by calculation of a receiver-operating characteristic curve demonstrated that this analysis provides a strong prediction if a VT is epicardial in origin (AUC range 0.72-0.88). Slower rate of change of depolarization had high sensitivity and specificity for prediction of epicardial VT., Conclusions: This study demonstrates that depolarization rate analysis is a potential technique to predict if a VT is epicardial in nature., Competing Interests: Funding Support and Author Disclosures This work was supported in part by the University of Minnesota’s Medical School Academic Investment Education Program grant and the Institute for Engineering in Medicine. Dr Prisco is funded by the National Institutes of Health T32 HL144472. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. All rights reserved.)

Background: Bilateral cardiac sympathetic denervation (BCSD) is an effective therapy for ventricular arrhythmias (VAs) in cardiomyopathies (CMPs). After BCSD, residual autonomic nervous system (ANS) function is unknown., Objective: The purpose of this study was to assess ANS responses in patients with CMP before and after BCSD as compared with demographically matched healthy controls., Methods: Patients with CMP undergoing BCSD and matched healthy controls were recruited. Noninvasive measures-finger cuff beat-to-beat blood pressure (BP), electrocardiography, palmar electrodermal activity (EDA), and finger pulse volume (FPV)-were obtained at rest and during autonomic stressors-posture change, handgrip, and mental stress. Maximal as well as specific responses to stressors were compared., Results: Eighteen patients with CMP (mean age 54 ± 14 years; 16 men, 89%; left ventricular ejection fraction 36% ± 14%) with refractory VAs and 8 matched healthy controls were studied; 9 patients with CMP underwent testing before and after (median 28 days) BCSD, with comparable ongoing medication. Before BCSD, patients with CMP (n = 13) had lower resting systolic BP and FPV than did healthy controls (P < .01). Maximal FPV and systolic BP reflex responses, expressed as percent change were similar, while diastolic BP, mean BP, and EDA responses were blunted. After BCSD, resting measurements were unchanged relative to presurgical baseline (n = 9). EDA responses to stressors were abolished, confirming BCSD, while maximal FPV and BP responses were preserved. Diastolic BP, mean BP, and FPV responses to orthostatic challenge pointed toward a better tolerance of active standing after BCSD as compared with before. Responses to other stressors remained unchanged., Conclusion: Patients with CMP and refractory VAs on optimal medical therapy have detectable but blunted adrenergic responses, which are not disrupted by BCSD., (Copyright © 2020 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Several distinct risk factors for arrhythmia recurrence and mortality following ventricular tachycardia (VT) ablation have been described. The effect of concurrent risk factors has not been assessed so far; thus, it is not yet possible to estimate these risks for a patient with several comorbidities. The aim of the study was to identify specific risk groups for mortality and VT recurrence using the Survival Tree (ST) analysis method., Methods: In 1251 patients 16 demographic, clinical and procedure-related variables were evaluated as potential prognostic factors using ST analysis using a recursive partitioning algorithm that searches for relationships among variables. Survival time and time to VT recurrence in groups derived from ST analysis were compared by a log-rank test. A random forest analysis was then run to extract a variable importance index and internally validate the ST models., Results: Left ventricular ejection fraction, implantable cardioverter defibrillator/cardiac resynchronization device, previous ablation were, in hierarchical order, identified by ST analysis as best predictors of VT recurrence, while left ventricular ejection fraction, previous ablation, Electrical storm were identified as best predictors of mortality. Three groups with significantly different survival rates were identified. Among the high-risk group, 65.0% patients were survived and 52.1% patients were free from VT recurrence; within the medium- and low-risk groups, 84.0% and 97.2% patients survived, 72.4% and 88.4% were free from VT recurrence, respectively., Conclusions: Our study is the first to derive and validate a decisional model that provides estimates of VT recurrence and mortality with an effective classification tree. Preprocedure risk stratification could help optimize periprocedural and postprocedural care.

Ventricular arrhythmias are responsible for hundreds of thousands of deaths every year. Catheter ablation of ventricular tachycardia (VT) is an essential component of the management of these life-threatening arrhythmias. However, in many patients, despite medical and interventional therapy, VT recurs. Furthermore, some VT substrates (mid-myocardial, left ventricular summit, and intraseptal) are not easily targeted because of limitations of currently available technology. In certain clinical settings, ventricular fibrillation (VF) episodes that have premature ventricular contraction triggers can also be targeted with catheter ablation. However, in most patients there is no clear VF trigger to target, and therefore polymorphic VT or VF cannot be adequately treated with catheter ablation. The autonomic nervous system plays a crucial role in all aspects of ventricular arrhythmias, yet interventions specific to the cardiac neuronal axis have been largely underutilized. This underutilization has been most pronounced in patients with structural heart disease. However, there is a growing body of literature on the physiology and pathophysiology of cardiac neural control and the benefits of neuromodulation to treat refractory ventricular arrhythmias in these patients. We present case-based examples of neuromodulatory interventions currently available and a review of the literature supporting their use., (Copyright © 2018 Heart Rhythm Society. All rights reserved.)

Objectives: This study sought to prospectively evaluate the value of a dedicated electrocardiographic posterior lead to create an anteroposterior ratio to localize premature ventricular complexes (PVCs) between the right ventricular outflow tract and left ventricular outflow tract for catheter ablation., Background: The anteroposterior relationship between the right and left outflow tract has not been explored for electrocardiographic localization of ventricular arrhythmia., Methods: Standard V 5 and V 6 leads were placed posteriorly and ablation was performed with activation mapping. The site of successful ablation was correlated with the ratio of the R-wave in V 4 to the R-wave in V 8 . Normalization of the V 4 /V 8 ratio to a V 4 /V 8 index was achieved by dividing the V 4 /V 8 ratio by sinus V 4 /V 8 . After determination of optimal cutoffs, comparison with V 2 transition ratio and V 2S /V 3R was subsequently performed using receiver operating characteristic curves in a prospective validation cohort., Results: A total of 134 patients underwent ablation of PVCs with 2 modified posterior leads. PVCs successfully ablated from the left side had a statistically significantly higher V 4 /V 8 ratio compared with right-sided PVCs (11.7 ± 10.6 vs. 2.3 ± 2.4, p < 0.001). At a cutoff of >3, the V 4 /V 8 ratio had a sensitivity of 88% with a specificity of 77% for left-sided locations. At a cutoff of >2.28, the V 4 /V 8 index had a sensitivity of 67% with a specificity of 98%. In the prospective validation cohort (n = 40), the V 4 /V 8 ratio exhibited the highest sensitivity of 75% with a negative predictive value of 89% compared with the V 4 /V 8 index, V 2 transition ratio, and V 2S /V 3R . The V 4 /V 8 index had the highest specificity of 96% with positive predictive value of 89% compared to the other predictive ratios. When analyzing cases with a V 3 transition, the V 4 /V 8 index demonstrated 100% specificity and positive predictive value., Conclusions: A simple modification of V 5 to V 8 posteriorly may provide incremental diagnostic value for localizing PVCs arising from the outflow tracts. Normalizing PVC localization criteria to the sinus rhythm results in the highest specificity when compared with other validated criteria., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: The occurrence of ventricular tachyarrhythmias seems to follow circadian, daily, and seasonal distributions. Our aim is to identify potential temporal patterns of electrical storm (ES), in which a cluster of ventricular tachycardias or ventricular fibrillation, negatively affects short- and long-term survival., Methods and Results: The TEMPEST study (Circannual Pattern and Temperature-Related Incidence of Electrical Storm) is a patient-level, pooled analysis of previously published data sets. Study selection criteria included diagnosis of ES, absence of acute coronary syndrome as the arrhythmic trigger, and ≥10 patients included. At the end of the selection and collection processes, 5 centers had the data set from their article pooled into the present registry. Temperature data and sunrise and sunset hours were retrieved from Weather Underground, the largest weather database available online. Total sample included 246 patients presenting with ES (221 men; age: 65±9 years). Each ES episode included a median of 7 ventricular tachycardia/ventricular fibrillation episodes. Fifty-nine percent of patients experienced ES during daytime hours ( P <0.001). The prevalence of ES was significantly higher during workdays, with Saturdays and Sundays registering the lowest rates of ES (10.4% and 7.2%, respectively, versus 16.5% daily mean from Monday to Friday; P <0.001). ES occurrence was significantly associated with increased monthly temperature range when compared with the month before ( P =0.003)., Conclusions: ES incidence is not homogenous over time but seems to have a clustered pattern, with a higher incidence during daytime hours and working days. ES is associated with an increase in monthly temperature variation., Clinical Trial Registration: https://www.crd.york.ac.uk. Unique identifier: CRD42013003744., (© 2017 American Heart Association, Inc.)

Introduction: Reversible premature ventricular complexes-induced cardiomyopathy (PVC-CMP) is a well-described, multi-factorial entity. Single predictors, such as PVC burden or QRS duration, may not apply equally to all patients in contemporary unselected populations including patients with structural heart disease (SHD) or with particular origin such as epicardial (EPI) PVC. We sought to evaluate clinical criteria associated with PVC-CMP notably focusing on the EPI origin impact and ECG recognition and the value of a new composite predictor of PVC-CMP, the PVC-CMP-Index., Methods and Results: We studied 107 consecutive patients (69 men; mean age = 56 ± 16 years) with frequent PVC (23.1 ± 11.5%) referred for PVC ablation. Thirty-six patients (33.6%) had an underlying SHD and 25 patients (23.4%) an EPI PVC origin. After a mean follow-up of 22.7 ± 15.3 months, 72.9% achieved a long-term successful ablation and 54.2% had PVC-CMP. PVC-CMP prevalence was significantly higher in patients with an EPI compared to endocardial PVC focus (84.0% vs. 45.1%, respectively, P < 0.001). EPI PVC origin (OR = 68.7 IC95% [3.5-1363], P = 0.005), as well as SHD (OR = 12.3 IC95% [1.6-92.6], P = 0.015), was independent predictor of PVC-CMP. While PVC burden (AUC = 0.78) or PVC-QRS width (AUC = 0.68) independently predicted PVC-CMP, the PVC-CMP-Index (values ≥39) defined as: PVC burden (0-1) × PVC-QRS width (milliseconds) × a constant C (1.28 for SHD or 2 for ECG suggesting EPI origin based on our ECG 3-step algorithm), highly correlated with PVC-CMP (AUC = 0.91, sensitivity = 93%, specificity = 80%)., Conclusion: We developed a new index, which incorporates PVC burden, QRS width, and presence of SHD or suspected EPI origin that best predicted PVC-CMP., (© 2016 Wiley Periodicals, Inc.)

Objectives: The objective of this study was to determine whether premature ventricular contractions (PVCs) arising from the aortic sinuses of Valsalva (SOV) and great cardiac vein (GCV) have coupling interval (CI) characteristics that differentiate them from other ectopic foci., Background: PVCs occur at relatively fixed CI from the preceding normal QRS complex in most patients. However, we observed patients with PVCs originating in unusual areas (SOV and GCV) in whom the PVC CI was highly variable. We hypothesized that PVCs from these areas occur seemingly randomly because of the lack of electrotonic effects of the surrounding myocardium., Methods: Seventy-three consecutive patients referred for PVC ablation were assessed. Twelve consecutive PVC CIs were recorded. The ΔCI (maximum - minimum CI) was measured., Results: We studied 73 patients (age 50 ± 16 years, 47% male). The PVC origin was right ventricular (RV) in 29 (40%), left ventricular (LV) in 17 (23%), SOV in 21 (29%), and GCV in 6 (8%). There was a significant difference between the mean ΔCI of RV/LV PVCs compared with SOV/GCV PVCs (33 ± 15 ms vs. 116 ± 52 ms, p < 0.0001). A ΔCI of >60 ms demonstrated a sensitivity of 89%, specificity of 100%, positive predictive value of 100%, and negative predictive value of 94%. Cardiac events were more common in the SOV/GCV group versus the RV/LV group (7 of 27 [26%] vs. 2 of 46 [4%], p < 0.02)., Conclusions: ΔCI is more pronounced in PVCs originating from the SOV or GCV. A ΔCI of 60 ms helps discriminate the origin of PVCs before diagnostic electrophysiological study and may be associated with increased frequency of cardiac events., (Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: The sympathetic nervous system is thought to play a role in the genesis of ventricular tachyarrhythmias (VT). Left and added right cardiac sympathectomy have been shown to reduce the burden of arrhythmias in the setting of a VT storm. However, the contribution of the right stellate ganglion (RSG) and the left stellate ganglion (LSG) to the innervation of the anterior left ventricular (LV) wall is not well understood., Objective: To evaluate the innervation of the anterior LV wall by the LSG and the RSG., Methods: The heart and stellate ganglia were exposed via sternotomy in pigs with normal hearts (n = 8). A 20-electrode catheter was placed on the anterior LV wall to record activation recovery interval (ARI), a surrogate measure of action potential duration. A microdialysis catheter was inserted in a similar location to sample interstitial norepinephrine (NE) content. ARI and NE measurements were recorded at baseline and during LSG and RSG stimulation., Results: LSG stimulation shortened ARI by 17.1% ± 10.5% (mean ± standard error), while RSG stimulation shortened ARI by 42.1% ± 15.7%, P = .04 (LSG vs RSG). LSG stimulation increased interstitial NE levels by 200% ± 65%, while RSG stimulation increased the NE content by 260% ± 40% (P = .012). LSG stimulation increased dispersion in ARI from 376.0 ± 83.7 ms(2) to 1242.5 ± 566 ms(2) (P = .03) and caused ventricular fibrillation in 2 pigs. During RSG stimulation, dispersion increased from 419 ± 65.8 to 474.8 ± 81 ms(2) (P = .4)., Conclusions: Both the LSG and the RSG provide significant innervation to the anterior LV wall as demonstrated by both ARI shortening and NE concentrations. LSG stimulation significantly increases ARI dispersion. This study provides mechanistic insight into the beneficial effects of left sympathectomy and the additional role of right sympathectomy in reducing arrhythmias in patients with anterior myocardial scars and VT storm., (Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Activation of cardiac sympathetic nerves alters ventricular repolarization; however, these changes remain poorly characterized. The goal of this study was to examine effects of sympathetic stimulation on repolarization to identify electrocardiographic markers of sympathetic activation. Pigs underwent median sternotomy and bilateral thoracotomy to expose the stellate ganglia. Changes in T-wave duration, amplitude, repolarization vector, and time from peak to end (Tp-Te) were continuously monitored. Within 15 seconds of unilateral left or right stellate ganglion (LSG/RSG) stimulation, T-wave amplitude increased 6- and 4.5-fold, respectively, in lead aVF. T-wave duration and Tp-Te both increased 200% during LSG stimulation but only 50% and 30%, respectively, with RSG stimulation. During LSG stimulation, frontal and horizontal T-wave vectors, respectively, changed from 1.9° ± 22.8° and 333.8° ± 9.7° at baseline to 83.4° ± 3.9° (inferiorly) and 306.7° ± 1.8° (posteriorly). During RSG stimulation, frontal and horizontal T-wave vectors changed from 348.2° ± 21.6° and 333.8° ± 10.3° before stimulation to 280.7° ± 4.6° (superiorly) and 118.1° ± 5.6° (anteriorly). During stellate stimulation, T-wave vectors are displaced to angles specific for LSG activation (posteroinferiorly) or RSG activation (anterosuperiorly); T-wave amplitude, duration, and Tp-Te increase; and ST-duration decreases. Displaced repolarization vector and changes in T-wave morphometrics provide a novel marker of unilateral sympathetic nerve stimulation., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Objectives: The purpose of this study was to compare the characteristics and prevalence of late potentials (LP) in patients with nonischemic cardiomyopathy (NICM) and ischemic cardiomyopathy (ICM) etiologies and evaluate their value as targets for catheter ablation., Background: LP are frequently found in post-myocardial infarction scars and are useful ablation targets. The relative prevalence and characteristics of LP in patients with NICM is not well understood., Methods: Thirty-three patients with structural heart disease (NICM, n = 16; ICM, n = 17) referred for catheter ablation of ventricular tachycardia were studied. Electroanatomic mapping was performed endocardially (n = 33) and epicardially (n = 19). The LP were defined as low voltage electrograms (<1.5 mV) with onset after the QRS interval. Very late potentials (vLP) were defined as electrograms with onset >100 ms after the QRS., Results: We sampled an average of 564 +/- 449 points and 726 +/- 483 points in the left ventricle endocardium and epicardium, respectively. Mean total low voltage area in patients with ICM was 101 +/- 55 cm(2) and 56 +/- 33 cm(2), endocardial and epicardial, respectively, compared with NICM of 55 +/- 41 cm(2) and 53 +/- 28 cm(2), respectively. Within the total low voltage area, vLP were observed more frequently in ICM than in NICM in endocardium (4.1% vs. 1.3%; p = 0.0003) and epicardium (4.3% vs. 2.1%, p = 0.035). An LP-targeted ablation strategy was effective in ICM patients (82% nonrecurrence at 12 +/- 10 months of follow-up), whereas NICM patients had less favorable outcomes (50% at 15 +/- 13 months of follow-up)., Conclusions: The contribution of scar to the electrophysiological abnormalities targeted for ablation of unstable ventricular tachycardia differs between ICM and NICM. An approach incorporating LP ablation and pace-mapping had limited success in patients with NICM compared with ICM, and alternative ablation strategies should be considered., (Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: The presence of epicardial fat can confound the quantification of scar during transpericardial electroanatomic mapping. The electrogram (EGM) characteristics of epicardial fat have not been systematically compared with infarct scar using gross and histopathological analysis as a gold standard., Objective: The purpose of this study was to compare the EGM characteristics of epicardial fat with infarct scar., Methods: A closed-chest infarction was created in 40-50 kg pigs by occlusion of the circumflex artery for 150 minutes using an angioplasty balloon. This artery was chosen to minimize any potential overlap of epicardial fat with infarct and to spare any septal involvement. After 4-12 weeks of infarct healing, epicardial mapping was performed. EGMs in low-voltage regions (<1.5 mV) were analyzed, and bipolar amplitude, duration, number of deflections, and the presence of late potentials were recorded. Statistical analysis was performed using unpaired t-test and chi(2) analysis. Gross and histopathological examination was used to confirm areas of fat and infarct scar., Results: Seven porcine hearts were analyzed after high-density epicardial mapping (364 +/- 92 points) was performed 48 +/- 19 days after infarction. The mean bipolar EGM amplitude was similar in fat and scar (0.77 +/- 0.34 vs. 0.75 +/- 0.38 mV; P = not significant). The mean EGM duration was longer in scar than in fat (68.8 +/- 18.9 vs. 50.1 +/- 11.6 ms; P <.0001) and exhibited more fractionation (8.5 +/- 3.1 vs. 4.7 +/- 1.8 deflections; P <.0001). The presence of late potentials was 99% specific for scar. Further, areas of fat >4 mm in thickness registered low-voltage bipolar EGMs., Conclusion: Scar from healed myocardial infarction exhibits more fractionation and longer EGM duration when compared with fat. Late potentials are highly specific for locating infarct scars., (Copyright 2010. Published by Elsevier Inc.)

Objectives: This study sought to characterize left atrial (LA) sinus rhythm electrogram (EGM) patterns and their relationship to parasympathetic responses during atrial fibrillation (AF) ablation., Background: The mechanistic basis of fractionated LA EGMs in patients with paroxysmal AF is not well understood., Methods: We analyzed 1,662 LA ablation sites from 30 patients who underwent catheter ablation for paroxysmal AF. Pre-ablation EGM characteristics (number of deflections, amplitude, and duration) were measured in sinus rhythm. Parasympathetic responses during radiofrequency application (increase of atrial-His interval by > or =10 ms or decrease of sinus rate by > or =20%) were assessed at all sites. We also prospectively studied the effect of adenosine, a pharmacological agent mimicking acetylcholine signaling in myocytes, on LA EGMs. Finally, we performed mathematical simulations of atrial tissue to delineate possible mechanisms of fractionated EGMs in sinus rhythm., Results: A specific pattern of pre-ablation sinus rhythm EGM (deflections > or =4, amplitude > or =0.7 mV, and duration > or =40 ms) was strongly associated with parasympathetic responses (sensitivity 72%, specificity 91%). The sites associated with these responses were found to be located mainly in the posterior wall of the LA. Adenosine administration and mathematical simulation of the effect of acetylcholine were able to reproduce a similar EGM pattern., Conclusions: Parasympathetic activation during AF ablation is associated with the presence of pre-ablation high-amplitude fractionated EGMs in sinus rhythm. Local acetylcholine release could potentially explain this phenomenon.

Background: Many patients with appropriate indications fail to respond to cardiac resynchronization therapy (CRT)., Objective: The purpose of our study was to determine the relationship between CRT response and preimplantation apical wall motion abnormality., Methods: We analyzed data from 83 patients with ischemic cardiomyopathy who underwent CRT. All patients had New York Heart Association class III or IV symptoms despite maximal medical therapy, left ventricular ejection fraction (LVEF) < or =35%, and QRS duration > or =130 ms or <130 ms with left ventricular dyssynchrony. CRT responders at 6 months were defined as surviving patients with: (1) no hospitalization for heart failure, and (2) improvement of New York Heart Association classification. Patients underwent echocardiography before and 6 months after implantation to assess changes in regional wall motion and LVEF., Results: At baseline, CRT responders (n = 39) and nonresponders (n = 44) had similar LVEF (22.9% +/- 6.9% vs 23.1% +/- 8.3%), QRS duration (159 +/- 43 ms vs 159 +/- 36 ms), and medical treatment. CRT nonresponders had a higher prevalence of preimplantation apical wall motion abnormality (68% vs 33%, P = .003). Patients with baseline apical wall motion abnormalities (n = 43) were less likely than others (n = 40) to show improvement in wall motion at 6 months (30% vs 81%, P < .001) or clinical response to CRT (31% vs 64%, P = .003)., Conclusion: The presence of a preimplantation apical wall motion abnormality was associated with a lower rate of CRT response in patients with ischemic cardiomyopathy.

Background: The impact of cardiac resynchronization therapy (CRT) on dispersion of repolarization is controversial. The benefit of CRT on sudden cardiac death has been demonstrated only after 3 years follow-up., Objective: The purpose of this study was to explore the immediate effect of CRT on dispersion of repolarization and to define the value of dispersion of repolarization parameters as predictors of appropriate implantable cardioverter-defibrillator (ICD) therapy., Methods: Data from 100 patients who underwent CRT-ICD placement were analyzed retrospectively. Patients had symptoms of New York Heart Association functional class III or IV heart failure, left ventricular ejection fraction < or =35%, and QRS duration >130 ms or QRS < or =130 ms with left intraventricular dyssynchrony. ECG indices of dispersion of repolarization before and immediately after CRT implantation (QT dispersion, Tpeak-Tend [Tp-e], and Tp-e dispersion) were measured., Results: In patients who were upgraded to a biventricular system, Tp-e did not increase significantly after CRT. However, Tp-e increased significantly after CRT in patients with left bundle branch block or narrow QRS at baseline. After 12-month follow-up, 22 patients had received appropriate ICD therapy. ICD therapy and no ICD therapy groups had similar baseline characteristics, such as secondary prevention and ischemic cardiomyopathy. Postimplantation Tp-e was the only independent predictor of future ICD therapy (P = .02)., Conclusion: Immediately after CRT, Tp-e did not increase in patients who received a biventricular upgrade; however, Tp-e did increase in patients with preimplantation left bundle branch block or narrow QRS. Postimplantation Tp-e was the only independent predictor of appropriate ICD therapy.

Cardiac arrhythmias are a leading cause of mortality and morbidity in Western society. In some specific instances, these arrhythmias are caused by abnormalities of cardiac ion channels, such as sodium, calcium, and potassium channels, which carry ionic currents and are fundamental determinants of cardiac excitability. Abnormalities of these ion channels are attributed to mutations in the genes encoding the channel protein and cause altered function of channels, which can predispose to arrhythmias. During heart failure, many channels also malfunction because of altered expression, resulting in lethal arrhythmias.

We sought to establish pathogenetic links between electrophysiology, histopathology, and ventricular tachyarrhythmias in patients with Ebstein's anomaly. The atrialized right ventricle (ARV) is the site of mechanically inducible ventricular tachyarrhythmias, but relations between the arrhythmogenic substrate, the type of tachyarrhythmias, and the trigger(s) have not been established. This study comprised 23 patients (10 men and 13 women; aged 18 to 58 years; mean 32 +/- 3) who did not undergo surgery and 6 pre- and postoperative patients with Ebstein's anomaly, diagnosed by transthoracic and transesophageal echocardiography. Twenty-one patients had classic Ebstein's anomaly and 2 had mild forms. Signal-averaged electrocardiograms (SAECGs) identified slow conduction by using 3 time-domain variables calculated by an automated algorithm and inspected visually. Two variables were required to establish the presence of late potentials. SAECGs were repeated in 6 patients after surgical exclusion of the ARV. Five surgical specimens of the ARV and the true right atrium were examined histologically. Mathematic simulations were used to illustrate anchored and unanchored spiral/scroll waves. SAECGs were positive in 21 patients with classic Ebstein's anomaly and were negative postoperatively in the 6 so studied. The ARV was characterized histologically by clusters of cardiomyocytes isolated within a fibrous matrix. We hypothesize that SAECGs identify slow conduction residing in the ARV, and that excitation of this arrhythmogenic substrate provokes spiral/scroll waves that cannot anchor because clusters of cardiomyocytes are isolated within a fibrous matrix. The waves meander erratically as polymorphic ventricular tachycardia or break up into ventricular fibrillation.

Background: The upper limit of vulnerability (ULV) correlates with the defibrillation threshold and can be determined with 1 episode of ventricular fibrillation (VF). To automate the ULV in an implantable cardioverter-defibrillator (ICD), the most vulnerable intervals must be identified from an ICD electrogram rather than the latest-peaking surface T wave (Tpeak). We hypothesized that the recovery time (TR), defined as the maximum derivative (dV/dt) of the T wave of the shock electrogram, correlates with the most vulnerable intervals., Methods and Results: We determined ULV, defibrillation threshold, and the most vulnerable intervals in 25 patients at ICD implantation. The ULV was the weakest T-wave shock that did not induce VF. The most vulnerable intervals were the ones associated with the strongest shocks that induced VF. Telemetered shock electrograms were stored on digital tape and differentiated offline to measure TR. Tpeak and TR were highly correlated (Tpeak-TR=-2+/-11 ms; rho=0.80, P<0.001). At least 1 most vulnerable interval timed between -20 ms and +20 ms relative to Tpeak in all patients and between -40 ms and +20 ms relative to TR in 96% of patients., Conclusions: The recovery time of shock electrograms provides accurate information about global repolarization. TR closely approximates Tpeak. The ULV method may be automated in an ICD by timing T-wave shocks relative to TR.

Objective/background: It has been shown that patients with an acute myocardial infarction and persistent electrocardiographic ST-segment depression are at high risk for subsequent cardiac events. The purpose of this retrospective analysis was to examine the long-term effects of propranolol therapy in patients with their first acute myocardial infarction and persistent electrocardiographic ST-segment depression., Methods: The outcomes of 2877 patients enrolled in the Beta-Blocker Heart Attack Trial (BHAT) with their first myocardial infarction (75% of patients in BHAT) were reviewed. Patients were divided into three groups on the basis of presence or absence of > or =1 mm ST-segment depression in two contiguous leads of the 12-lead electrocardiogram obtained soon after admission or at the time of randomization, which occurred 10.1+/-3.5 days after the index myocardial infarction. Group 1 included 774 patients (392 randomly assigned to placebo and 382 to propranolol) with no ST-segment depression; group 2 included 1447 patients (713 placebo, 734 propranolol) with ST-segment depression at admission or at the time of randomization (labeled as transient); and group 3 included 656 patients (339 placebo and 317 propranolol) who had electrocardiographic ST-segment depression from the time of admission to the time of randomization (labeled as persistent)., Results: In group 3, patients with persistent electrocardiographic ST depression, the mortality rate in patients randomly assigned to placebo was 13.6% compared with 7.6% in patients with propranolol (p = 0.012; log rank test). Sudden death in the placebo arm was 9.7% compared with 4.7% in the propranolol group (p = 0.012, log rank test). The results of the Cox regression analysis, adjusting for all baseline variables with p values <0.25, showed the relative risk of overall mortality rate and the relative risk of sudden death were 2.13 ( 1.22, 3.70) and 2.56 (1.27, 5.26), respectively, for the placebo group compared with the propranolol group. Patients with persistent ST-segment depression had the greatest benefit from propranolol (47.2 fewer events [deaths/reinfarctions] per 1000 person-years compared with 78 and 2.1 fewer events in patients with transient and no ST-segment depression, respectively)., Conclusions: It appears that the greatest benefit for beta-blocker therapy in patients after myocardial infarction is observed in patients with persistent ST-segment depression who are at greatest risk for death and reinfarction. Definitive conclusions regarding therapy with beta-adrenergic blocking agents in patients with persistent ST-segment depression cannot be made because our analysis, given its retrospective nature, is only hypothesis generating.

The prognostic significance of ST segment depression in patients with their first acute myocardial infarction was investigated in 1444 patients with an acute myocardial infarction, who were randomly assigned to the placebo arm of the Beta-Blocker Heart Attack Trial (BHAT). Patients were divided retrospectively into three groups based on the presence or absence of > or = 1 mm ST segment depression in two contiguous leads of a 12-lead electrocardiogram obtained during the first few days after admission and at the time of randomization, which occurred at 9.7 +/- 3.3 days after the index myocardial infarction. Group 1 included 392 patients with no ST segment depression, group 2 comprised 713 patients with transient ST segment depression in the first few days after admission or at the time of randomization, and group 3 included 339 patients with persistent ST segment depression in the first few days after admission and at the time of randomization. At a median follow-up of 26 months, the mortality rate was 4.9% in group 1, 7.6% in group 2, and 13.6% in group 3. When Cox regression was used to adjust for baseline differences in other variables, the differences between the three groups continued to be highly significant (p = 0.005; 95% confidence intervals [0.6 and 1.4]). We conclude that persistent and transient ST segment depression in patients with their first myocardial infarction are strong predictors of increased long-term mortality when compared to patients without ST segment depression. These findings should be taken into consideration when stratifying patients at risk in the post-myocardial infarction period.