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Objectives This study investigated the prevalence and prognostic significance of concealed myocardial abnormalities identified by cardiac magnetic resonance (CMR) imaging in patients with apparently idiopathic premature ventricular contractions (PVCs). Background The role of CMR imaging in patients with frequent PVCs and otherwise negative diagnostic workup is uncertain. Methods This was a multicenter, international study that included 518 patients (44 ± 15 years; 57% men) with frequent (>1,000/24 h) PVCs and negative routine diagnostic workup. Patients underwent a comprehensive CMR protocol including late gadolinium enhancement imaging for detection of necrosis and/or fibrosis. The study endpoint was a composite of sudden cardiac death, resuscitated cardiac arrest, and nonfatal episodes of ventricular fibrillation or sustained ventricular tachycardia that required appropriate implantable cardioverter-defibrillator therapy. Results Myocardial abnormalities were found in 85 (16%) patients. Male gender (odds ratio [OR]: 4.28; 95% confidence interval [CI]: 2.06 to 8.93; p = 0.01), family history of sudden cardiac death and/or cardiomyopathy (OR: 3.61; 95% CI: 1.33 to 9.82; p = 0.01), multifocal PVCs (OR: 11.12; 95% CI: 4.35 to 28.46; p Conclusions CMR can identify concealed myocardial abnormalities in 16% of patients with apparently idiopathic frequent PVCs. Presence of myocardial abnormalities on CMR predict worse clinical outcomes.

Background The presence of left ventricular (LV) late gadolinium enhancement (LGE) at cardiac magnetic resonance (CMR) has been correlated to life-threatening arrhythmic events in patients with apparently idiopathic ventricular arrhythmias (VAs). Aim of the present study was to investigate the prognostic significance of a specific LV-LGE phenotype characterized by a subepicardial/midmyocardial “ring-like” pattern of fibrosis. Methods Out of a total of 518 consecutive patients with apparently idiopathic VAs who underwent CMR study, 79 (15%) had evidence of LV-LGE. Of these, 23 (4%) patients had LV LGE with ring-like pattern, defined as subepicardial or midmyocardial LGE involving at least 3 contiguous segments in the same slice (group A), while 56 (11%) patients had LV LGE with no ring-like pattern (group B). The remaining 439 patients had no LGE (group C). The end-point of the study was a composite SCD, resuscitated cardiac arrest and nonfatal episodes of ventricular fibrillation or documented sustained ventricular tachycardia. Results Group A patients were more frequently males compared to groups B and C (96% vs. 79% vs. 52%; p Conclusion In patients with apparently idiopathic VAs, a nonischemic LV-LGE with a ring-like pattern at CMR is associated with a high rate of malignant arrhythmic events during follow-up. Funding Acknowledgement Type of funding source: None

Key Clinical Message Idiopathic ventricular tachycardia arising from the LV summit epicardial area can be successfully mapped and possibly ablated from the left atrial appendage.

Major vessel injury during right ventricular outflow tract ablation is not something widely recognized, and routine evaluation of the left anterior descending (LAD) artery location in relation to the septal right ventricle is not routinely performed. In the present article, we report a case of acute LAD occlusion after right ventricular outflow tract ablation and then illustrate the intimately close relationship of the LAD artery to the anterior septal site of the RVOT (approximately 2-3 cm under the pulmonic valve), using a combination of intracardiac echocardiography and 3-dimensional electroanatomical mapping recorded during a second case, in order to specifically point to the area at risk.

Two brothers with congenitally-acquired Chagas’ disease (CD) diagnosed during adulthood are reported. The patients were born in the USA to a mother from Bolivia who on subsequent assessment was found to be serologically positive for Trypanosoma cruzi. Serologic screening of all pregnant women who migrated from countries with endemic CD is strongly recommended.

Arrhythmias in Myotonic Dystrophy Patients Background Myotonic dystrophy (MD) is the most common muscular dystrophy in adults and is associated with sudden death. Reported predictors of sudden death in this population include atrial tachyarrhythmias, a PR interval greater than 240 milliseconds, aberrant QRS conduction, and any degree of AV block. Objective We sought to report on the arrhythmic outcome of a cohort of patients with a new diagnosis of genetically proven MD. Methods We performed a retrospective review of 37 patients with genetically confirmed MD referred to our electrophysiology clinic for primary cardiac screening. Results There were 25 patients with MD type 1 (MD1) and 12 patients with MD type 2 (MD2). Eight patients with MD1 (32%) had atrial fibrillation, compared to only one patient with MD2 (8.3%). Patients with MD1 were more likely to have evidence of conduction disease abnormalities (40% vs. 8.3%, P = ns) and had a higher all-cause mortality (16% vs. 0%) than those with MD2. Criteria for recommending ICD implantation were based on sudden death risk factors suggested by published literature. Eleven patients were offered an ICD, 2 refused and died within the next year. Of the 9 patients who received an ICD, 8 had MD1. Three patients received appropriate shocks, 2 for monomorphic VT, and one for polymorphic VT. Conclusion The presence of AV conduction disturbance in MD patients is associated with a greater risk for ventricular arrhythmias. MD1 was more likely to be associated with cardiac arrhythmias than MD2. The incidence of ventricular arrhythmias among those who received a primary prevention ICD was 33% over 22 months, with 2 patients experiencing monomorphic VT and one experiencing polymorphic VT.

Background The moderator band (MB) can be a source of premature ventricular contractions (PVCs), monomorphic ventricular tachycardia (VT), and idiopathic ventricular fibrillation (IVF). Objective The purpose of this study was to define the electrocardiographic (ECG) characteristics and procedural techniques to successfully identify and ablate MB PVCs/VT. Methods In 10 patients with left bundle branch block morphology PVCs/VT, electroanatomic mapping in conjunction with intracardiac echocardiography (ICE) localized the site of origin of the PVCs to the MB. Clinical characteristics of the patients, ECG features, and procedural data were collected and analyzed. Results Seven patients presented with IVF and 3 presented with monomorphic VT. In all patients, the ventricular arrhythmias (VAs) had a left bundle branch block QRS with a late precordial transition (>V4), a rapid downstroke of the QRS in the precordial leads, and a left superior frontal plane axis. Mean QRS duration was 152.7 ± 15.2 ms. Six patients required a repeat procedure. After mean follow-up of 21.5 ± 11.6 months, all patients were free of sustained VAs, with only 1 patient requiring antiarrhythmic drug therapy and 1 patient having isolated PVCs no longer inducing VF. There were no procedural complications. Conclusion VAs originating from the MB have a distinctive morphology and often are associated with PVC-induced ventricular fibrillation. Catheter ablation can be safely performed and is facilitated by ICE imaging.

Background Pacemaker (PM) interrogation requires correct manufacturer identification. However, an unidentified PM is a frequent occurrence, requiring time-consuming steps to identify the device. Objective The purpose of this study was to develop and validate a novel algorithm for PM manufacturer identification, using the ECG response to magnet application. Methods Data on the magnet responses of all recent PM models (≤15 years) from the 5 major manufacturers were collected. An algorithm based on the ECG response to magnet application to identify the PM manufacturer was subsequently developed. Patients undergoing ECG during magnet application in various clinical situations were prospectively recruited in 7 centers. The algorithm was applied in the analysis of every ECG by a cardiologist blinded to PM information. A second blinded cardiologist analyzed a sample of randomly selected ECGs in order to assess the reproducibility of the results. Results A total of 250 ECGs were analyzed during magnet application. The algorithm led to the correct single manufacturer choice in 242 ECGs (96.8%), whereas 7 (2.8%) could only be narrowed to either 1 of 2 manufacturer possibilities. Only 2 (0.4%) incorrect manufacturer identifications occurred. The algorithm identified Medtronic and Sorin Group PMs with 100% sensitivity and specificity, Biotronik PMs with 100% sensitivity and 99.5% specificity, and St. Jude and Boston Scientific PMs with 92% sensitivity and 100% specificity. The results were reproducible between the 2 blinded cardiologists with 92% concordant findings. Conclusion Unknown PM manufacturers can be accurately identified by analyzing the ECG magnet response using this newly developed algorithm.

Frequent ventricular premature depolarizations (VPDs) can cause cardiomyopathy (CMP). The mechanisms underlying its development remain unclear, with VPD burden being only a weak predictor of risk.To determine whether VPD QRS duration at the time of initial presentation could predict risk for the subsequent development of CMP in patients with normal left ventricular ejection fraction (LVEF).From consecutive patients referred for ablation between January 1, 2006, and April 2, 2013, with ≥10% VPDs on 24-hour Holter monitoring, we identified 45 patients with normal LVEF and an electrocardiogram of the targeted VPD, who were then followed for at least 6 months (median 14 months; interquartile range [IQR] 8-32 months) before intervention. We excluded patients with structural or genetic heart disease.Of the 45 patients, 28 (62%) maintained normal LVEF and 17(38%) developed VPD-induced CMP. VPD burden was similar (26.5% [IQR 19.3%-39.5%] vs 26.0% [IQR 16.4%-41.0%]; P = 0.4) between the 2 groups. Patients who developed VPD-induced CMP had significantly longer VPD QRS duration (159 ms vs 142 ms; P.001) and a longer sinus QRS duration (97 ms vs 89 ms; P = .04). A VPD QRS duration of ≥153 ms best predicted development of VPD CMP (82% sensitivity and 75% specificity). Longer VPD QRS duration and a non-outflow tract site of VPD origin were independent risk factors for left ventricular dysfunction after multivariate analysis.VPD QRS duration longer than 153 ms and a non-outflow tract site of origin might be useful predictors of the subsequent development of VPD-induced CMP.

Introduction: Thromboembolic (TE) and bleeding complications represent the most common adverse events during atrial fibrillation (AF) ablation. In order to prevent TE, unfractionated heparin (UFH) is recommended throughout the procedure, with a target ACT of 350-400 sec. In this study we compared periprocedural heparin requirements during different pre-procedure anticoagulation regimens and the potential clinical implications. Methods: We retrospectively analyzed every case of AF ablation performed at our institution over the last 2 years, including only first time ablations, and collected the amount of UFH per kilogram needed to achieve the target ACT. The groups were compared based on the periprocedural anticoagulation strategy (warfarin vs. dabigatran vs. rivaroxaban), and the number of doses held before the procedure. Patients on warfarin were all on uninterrupted warfarin, but for comparison we further subdivided this group into INR tertiles, based on INR at time of procedure. Results: We included 584 patients. Of those 391 (67%) were on warfarin, 162 (28%) were receiving dabigatran and 31 (5%) rivaroxaban. Baseline characteristics were not significantly different between the groups, including procedural duration and baseline creatinine. 54.1% had paroxysmal AF and 5.3% had a prior TIA/stroke. Patients that held ≥2 doses of dabigatran needed significantly more UFH-per-kilogram-per-procedure, as compared to patients on warfarin with INR No differences were observed between those on warfarin with INR ≤1.5 and those holding ≥2 doses rivaroxaban (p=0.56). No significant differences were observed in the rate of bleeding or TE complications between groups (P=0.18). Conclusions: Interrupted dabigatran is associated with significantly increased need for UFH compared to those functionally off warfarin, which may suggest a slight rebound procoagulant effect due to dabigatran interruption.

Background— Percutaneous epicardial ablation of ventricular arrhythmias arising from the left ventricular summit is limited by the presence of major coronary vessels and epicardial fat. We report the outcomes of percutaneous epicardial mapping and ablation of ventricular arrhythmias arising from the left ventricular summit and the ECG features associated with successful ablation. Methods and Results— Between January 2003 and December 2012, a total of 23 consecutive patients (49±14 years; 39% men) with ventricular arrhythmias arising from the left ventricular summit underwent percutaneous epicardial instrumentation for mapping and ablation because of unsuccessful ablation from the coronary venous system and multiple endocardial LV/right ventricular sites. Successful epicardial ablation was achieved in 5 (22%) patients. In the remaining 18 (78%) cases, ablation was aborted for either close proximity to major coronary arteries or poor energy delivery over epicardial fat. The Q-wave amplitude ratio in aVL/aVR was higher in the successful group, with a ratio of >1.85 present in 4 (80%) patients in the successful group versus 2 (11%) in the unsuccessful group ( P =0.008). The ratio of R/S wave in V1 was greater in the successful group, with 4 (80%) patients in the successful group having a R/S ratio of >2 in V1 versus 5 (28%) in the unsuccessful group ( P =0.056). None of the patients in the successful group had an initial q wave in lead V1, as opposed to 6 (33%) in the unsuccessful group. The presence of at least 2 of the 3 ECG criteria above predicted successful ablation with 100% sensitivity and 72% specificity. Conclusions— Epicardial instrumentation for mapping and ablation of ventricular arrhythmias arising from the left ventricular summit is successful only in a minority of patients because of close proximity to major coronary arteries and epicardial fat. A Q-wave ratio of >1.85 in aVL/aVR, a R/S ratio of >2 in V1, and absence of q waves in lead V1 help identify appropriate candidates for epicardial ablation.

Myotonic dystrophy (MD) is the most common muscular dystrophy in adults and is associated with sudden death. Reported predictors of sudden death in this population include atrial tachyarrhythmias, a PR interval greater than 240 milliseconds, aberrant QRS conduction, and any degree of AV block.We sought to report on the arrhythmic outcome of a cohort of patients with a new diagnosis of genetically proven MD.We performed a retrospective review of 37 patients with genetically confirmed MD referred to our electrophysiology clinic for primary cardiac screening.There were 25 patients with MD type 1 (MD1) and 12 patients with MD type 2 (MD2). Eight patients with MD1 (32%) had atrial fibrillation, compared to only one patient with MD2 (8.3%). Patients with MD1 were more likely to have evidence of conduction disease abnormalities (40% vs. 8.3%, P = ns) and had a higher all-cause mortality (16% vs. 0%) than those with MD2. Criteria for recommending ICD implantation were based on sudden death risk factors suggested by published literature. Eleven patients were offered an ICD, 2 refused and died within the next year. Of the 9 patients who received an ICD, 8 had MD1. Three patients received appropriate shocks, 2 for monomorphic VT, and one for polymorphic VT.The presence of AV conduction disturbance in MD patients is associated with a greater risk for ventricular arrhythmias. MD1 was more likely to be associated with cardiac arrhythmias than MD2. The incidence of ventricular arrhythmias among those who received a primary prevention ICD was 33% over 22 months, with 2 patients experiencing monomorphic VT and one experiencing polymorphic VT.

Diabetic cardiomyopathy is characterized, in part, by calcium handling imbalances associated with ventricular dysfunction. The cardiac Na+/Ca2+ exchanger 1 (NCX1) has been implicated as a compensatory mechanism in response to reduced contractility in the heart; however, its role in diabetic cardiomyopathy remains unknown. We aimed to fully characterize the Akitains2 murine model of type 1 diabetes through assessing cardiac function and NCX1 regulation. The CXCL12/CXCR4 chemokine axis is well described in its cardioprotective effects via progenitor cell recruitment postacute myocardial infarction; however, it also functions in regulating calcium dependent processes in the cardiac myocyte. We therefore investigated the potential impact of CXCR4 in diabetic cardiomyopathy. Cardiac performance in the Akitains2 mouse was monitored using echocardiography and in vivo pressure-volume analysis. The Akitains2 mouse is protected against ventricular systolic failure evident at both 5 and 12 mo of age. However, the preserved contractility was associated with a decreased sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a)/phospholamban ratio and increased NCX1 content. Direct myocardial injection of adenovirus encoding anti-sense NCX1 significantly decreased NCX1 expression and induced systolic failure in the Akitains2 mouse. CXCL12 and CXCR4 were both upregulated in the Akitains2 heart, along with an increase in IκB-α and NF-κB p65 phosphorylation. We demonstrated that CXCR4 activation upregulates NCX1 expression through a NF-κB-dependent signaling pathway in the cardiac myocyte. In conclusion, the Akitains2 type 1 diabetic model is protected against systolic failure due to increased NCX1 expression. In addition, our studies reveal a novel role of CXCR4 in the diabetic heart by regulating NCX1 expression via a NF-κB-dependent mechanism.

In individuals with diabetes mellitus (DM), the haptoglobin (Hp) genotype is a major determinant of susceptibility to myocardial infarction. We have proposed that this is because of DM and Hp genotype–dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavenging receptor CD163 plays an essential role in the clearance of hemoglobin released from lysed red blood cells after intraplaque hemorrhage. We sought to test the hypothesis that expression of CD163 is DM and Hp genotype–dependent. CD163 was quantified in plaques by immunohistochemistry, on peripheral blood monocytes (PBMs) by FACS, and as soluble CD163 (sCD163) in plasma by ELISA. In DM plaques, despite an increase in macrophage infiltration, CD163 immunoreactivity was lower, resulting in a dramatic reduction in the percentage of macrophages expressing CD163 (27±2% versus 70±2%,P=0.0001). In individuals with DM as compared with individuals without DM, the percentage of PBMs expressing CD163 was reduced (3.7±0.6% versus 7.1±0.9%,PPP=0.01) and an increase in plasma soluble CD163 (3.0±0.2 μg/mL versus 2.3±0.2 μg/mL,P=0.04). Taken together, these results demonstrate an impaired hemoglobin clearance capacity in Hp 2-2 DM individuals and may provide the key insight explaining the increased incidence of myocardial infarction in this population.