Invasive Electrophysiological Study Research Articles

Prognostic value of electroanatomic-guided endomyocardial biopsy in patients with myocarditis, arrhythmogenic cardiomyopathy and non dilated left ventricular cardiomyopathy

A wide variety of non-invasive and invasive techniques for SCD risk stratification in non ischemic cardiomyopathy (NICM) have been proposed, including left ventricular (LV) ejection fraction, QRS duration, late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) and invasive electrophysiologic study with or without three-dimensional electroanatomic mapping (3D-EAM), to identify and characterize the arrhythmogenic substrate. There is still no clear consensus on the risk stratification in this clinical setting.The aim of our study is to characterize the 3D-EAM substrate in patients with the same clinical presentation of unexplained complex VAs and NICM using CMR, three-dimensional electranatomic mapping (3D-EAM) in association with endomyocardial biopsy (EMB) and genetic screening, as a more precise and early diagnostic assessment may provide important subsequent prognostic impact. The study was designed as a prospective multi-center observational evaluation and the patient follow-up was scheduled at 6 months interval. We enrolled 125 patients distinct into four different group by complete diagnostic work-up: myocarditis, non-dilated left ventricular cardiomyopathy, arrhythmogenic cardiomyopathy and control group. The four groups were compared in terms of clinical, imaging and 3D-EAM data. At multivariate analysis sustained VT/VF on admission [HR: 3.64 (1.79–7.4), p < 0.001], total bipolar scar area of left and right ventricle detected by 3D-EAM [HR: 2.24 (1.13–4.49), p = 0.02], histological diagnosis of myocarditis by 3D-EAM guided endomyocardial biopsy (EBM) [HR: 2.79 (1.04–7.44), p = 0.01] were independent predictors of complex VAs or death at follow-up. 3D-EAM guided EMB represent not only a valid diagnostic tool to identify the arrhythmogenic substrate in patients with NICM and ventricular arrhythmic phenotype but also an important predictor of complex Vas at long term follow-up.

Frequency of Atypical AVNRT in Patients Presenting with Narrow Complex Tachycardia

ABSTRACT Objective: To determine the frequency of atypical AVNRT in patients presenting with Narrow Complex Tachycardia. Study Design: Descriptive Cross Sectional Place and Duration of Study: Department of Cardiology, MTI-Hayatabad Medical Complex, Peshawar, from March, 2021 to March, 2022. Methodology: Ninety-three patients of either aged 30 to 80 years diagnosed with narrow complex tachycardia by consultant cardiac electrophysiologist on ECG showing QRS duration of less than 120 milliseconds were included in this study. Patients were managed as per standard protocol which included comprehensive clinical evaluation such as patient history, physical examination and invasive electrophysiological study for the diagnosis and characterization of atypical Atrioventricular Nodal Reentrant Tachycardia (AVNRT). Results: A total of ninety-three patients were studied with mean age of 43.08 years (SD = 9.07). Among the participants, 58.1% were male, while 41.9% were female. Majority of patients had Slow-Fast AVNRT (7.5%) followed by Fast-Slow AVNRT (3.2%), and Slow-Slow AVNRT in 2.2% patients. Conclusion: This study underscored the importance of gender-specific variations in the prevalence of different AVNRT types and highlighted the impact of gender as a potential influencing factor in the manifestation of specific types of AVNRT within the study population.

Accuracy of Different Surface Electrocardiogram Algorithms for Localization of Accessory Pathway in Comparison to Invasive Electrophysiological Localization: An Observational Study

Introduction: Detection of accessory pathway (AP) on surface ECG in sinus rhythm helps in the diagnosis of Wolff-Parkinson-White Syndrome (WPW Syndrome), Catheter ablation of AP was indicated in symptomatic patients with preexcitation. Pre-ablation AP localization inferred from the 12-lead surface electrocardiogram (ECG) facilitates a tailored ablation strategy; there by specific risk can be properly assessed. As they are based on pre-excitation in the basal state, available algorithms can lead to complex and ambiguous analysis, mostly due to the variable influence of the AP over QRS morphology. Though various algorithms on surface ECG are available to predict the site of AP on surface ECG, but none of them are accurate. So, we have compared the accuracy of different algorithms in predicting the AP localization in comparison to electrophysiological study (EPS) diagnosis. Methodology: This retrospective observational study cohort consisted of 100 consecutive patients above 15 years of age presented to the tertiary care center with the history of palpitations or for assessment of a manifest AP. Accessory pathways were identified according to the site where successful radiofrequency energy was applied. Arruda algorithm, Milstein algorithm, Fitzpatrick algorithm and Pambrun algorithm were applied on a sinus rhythm manifest preexcited ECG to predict the AP localization by two independent investigators who are unaware of site of successful catheter ablation. Then those were compared with the EPS localization to test the accuracy of individual algorithm. Then Cohen’s Kappa was run to determine if there was agreement between any of the four different algorithms with EPS using SPSS version 20.0. Results: In the study population of 100 patients, male to female ratio of study population was 1.6:1, with a mean age of presentation 43.86 ± 11.4 years with the most common age group of 31 to 45 year. when the AP locations were categorized based on EP Study 56 percent of the AP were found on the left side while 43 percent of the AP were found on right side, 77 percent of the AP were septal pathways. Among the leftsided pathways, left anteroseptal constitutes majority followed by left posteroseptal pathway. On right side majority were in right posteroseptal location in our study. Based on 4 surface ECG algorithms AP was localized and each algorithm was compared with invasive EPS localization for accuracy using Cohen’s Kappa agreement analysis. As per agreement analysis the kappa value for Milstein, Pambrun algorithm, Fitzpatrik and Arruda were 0.188, 0.343, 0.441, and 0.645 respectively. It was found that Arruda algorithm had moderate strength of agreement with the findings of EPS (κ = 0.645). This is the proportion of agreement over and above chance agreement and which was statistically significant and the strongest among all the four algorithms. Conclusion: Our study has compared the accuracy of 4 surface ECG algorithms in predicting the accessory pathway localization with the EPS; it has demonstrated that the Arruda algorithm is more precise and accurate among the available algorithms followed by Fitzpatrik, Pambrun algorithm and Milstein algorithm, Knowing the pathway prior to ablation allows for optimal procedure preparation, mapping pathways that are difficult to find and finally may lessen the catheter-related injury and shortens the procedural time.

Aberrancy masquerading as ventricular tachycardia: Importance of invasive electrophysiology study for diagnosis of wide complex tachycardias

BackgroundDifferentiation between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy based on the 12‑lead ECG alone can be imprecise. Implantable cardiac defibrillators (ICD) may be inserted for presumed VT, particularly in patients with syncopal presentation or atypical aberrancy patterns. Accurate diagnosis of these patients facilitated by an electrophysiology study (EPS) may alter diagnosis and management. MethodsWe present a prospective collection of cases across 3 cardiac centers of consecutive patients with WCT presumed to be VT who were referred for consideration of an ICD, and in whom further evaluation including an EPS ultimately demonstrated SVT with aberrancy as the culprit arrhythmia. Results22 patients were identified (17 male, mean age 50±13 years. Available rhythm data at the time of referral was presumptively diagnosed as monomorphic VT in 16 patients and polymorphic VT in 6 patients. Underlying structural heart disease was present in 20 (91%). EPS resulted in a diagnosis of SVT with aberrancy in all cases: comprising AV nodal re-entry tachycardia (n=10), orthodromic reciprocating tachycardia (n=3), focal atrial tachycardia (n=3), AF/AFL (n=3) and 'double fire' tachycardia (n=2). 21 (95%) patients underwent successful ablation. All patients remained free of arrhythmia recurrence at a median of 3.4 years of follow-up. ICD insertion was obviated in 18 (82%) patients, with 1 patient proceeding to ICD extraction. ConclusionSVT with atypical aberrancy may mimic monomorphic or polymorphic VT. Careful examination of all available rhythm data and consideration of an EPS can confirm SVT and obviate the need for ICD therapy.

Machine-learning guided differentiation between photoplethysmography waveforms of supraventricular and ventricular origin

Abstract Aims To test, whether a neural network-based classifier could aid in distinguishing photoplethysmographic (PPG) pulse waveforms of ventricular from those of supraventricular origin. Methods Thirty patients undergoing invasive electrophysiological studies for documented narrow complex tachycardias between May and December 2021 at a university medical centre were included in the trial. PPG waveforms were recorded using a PPG wristband (Empatica E4) in parallel to 12-lead surface electrograms (ECGs) and intracardiac electrograms from diagnostic catheters. Pulse waves were then annotated to either supraventricular (sinus rhythm, atrial pacing) or ventricular origin (ventricular pacing) based on invasive electrogram recordings, ECGs and stimulation protocols. 21147 data sets were split into test, training and validation data sets and used to develop, train and validate a convolutional neural network (CNN) for classifying PPG waveforms according to their origin into sinus rhythm, atrial or ventricular pacing. Results Datasets were complete for 27 patients. 74% were female and median age was 53 (range 18, 78) years, median BMI was 27±5, 19% had arterial hypertension, 11% had diabetes and 15% had coronary artery disease. During the electrophysiological study, typical AV-nodal re-entrant tachycardias could be induced in 63% of patients, 15% had inducible atrial tachycardias and the other patients had no inducible tachyarrhythmias. Our CNN-based classifier was able to correctly predict the origins of pulse waves in 95±1% for sinus rhythm, 96±1% for atrial paced rhythms and 95±1% for ventricular rhythms. Conclusion A neural network-based classifier trained on ground truth PPG data obtained by using invasive EP measurements for annotation could accurately predict atrial or ventricular origin from PPG waveforms alone.Graphical abstract

Arrhythmic Mitral Valve Prolapse and Sports Activity: Pathophysiology, Risk Stratification, and Sports Eligibility Assessment.

Although mitral valve prolapse (MVP) is the most prevalent valvular abnormality in Western countries and generally carries a good prognosis, a small subset of patients is exposed to a significant risk of malignant ventricular arrhythmias (VAs) and sudden cardiac death (SCD), the so-called arrhythmic MVP (AMVP) syndrome. Recent work has emphasized phenotypical risk features of severe AMVP and clarified its pathophysiology. However, the appropriate assessment and risk stratification of patients with suspected AMVP remains a clinical conundrum, with the possibility of both overestimating and underestimating the risk of malignant VAs, with the inappropriate use of advanced imaging and invasive electrophysiology study on one hand, and the catastrophic occurrence of SCD on the other. Furthermore, the sports eligibility assessment of athletes with AMVP remains ill defined, especially in the grey zone of intermediate arrhythmic risk. The definition, epidemiology, pathophysiology, risk stratification, and treatment of AMVP are covered in the present review. Considering recent guidelines and expert consensus statements, we propose a comprehensive pathway to facilitate appropriate counseling concerning the practice of competitive/leisure-time sports, envisioning shared decision making and the multidisciplinary "sports heart team" evaluation of borderline cases. Our final aim is to encourage an active lifestyle without compromising patients' safety.

Clonal Hematopoiesis of Indeterminate Potential With Loss of Tet2 Enhances Risk for Atrial Fibrillation Through Nlrp3 Inflammasome Activation.

Clonal hematopoiesis of indeterminate potential (CHIP), a common age-associated phenomenon, associates with increased risk of both hematological malignancy and cardiovascular disease. Although CHIP is known to increase the risk of myocardial infarction and heart failure, the influence of CHIP in cardiac arrhythmias, such as atrial fibrillation (AF), is less explored. CHIP prevalence was determined in the UK Biobank, and incident AF analysis was stratified by CHIP status and clone size using Cox proportional hazard models. Lethally irradiated mice were transplanted with hematopoietic-specific loss of Tet2, hematopoietic-specific loss of Tet2 and Nlrp3, or wild-type control and fed a Western diet, compounded with or without NLRP3 (NLR [NACHT, LRR {leucine rich repeat}] family pyrin domain containing protein 3) inhibitor, NP3-361, for 6 to 9 weeks. Mice underwent in vivo invasive electrophysiology studies and ex vivo optical mapping. Cardiomyocytes from Ldlr-/- mice with hematopoietic-specific loss of Tet2 or wild-type control and fed a Western diet were isolated to evaluate calcium signaling dynamics and analysis. Cocultures of pluripotent stem cell-derived atrial cardiomyocytes were incubated with Tet2-deficient bone marrow-derived macrophages, wild-type control, or cytokines IL-1β (interleukin 1β) or IL-6 (interleukin 6). Analysis of the UK Biobank showed individuals with CHIP, in particular TET2 CHIP, have increased incident AF. Hematopoietic-specific inactivation of Tet2 increases AF propensity in atherogenic and nonatherogenic mouse models and is associated with increased Nlrp3 expression and CaMKII (Ca2+/calmodulin-dependent protein kinase II) activation, with AF susceptibility prevented by inactivation of Nlrp3. Cardiomyocytes isolated from Ldlr-/- mice with hematopoietic inactivation of Tet2 and fed a Western diet have impaired calcium release from the sarcoplasmic reticulum into the cytosol, contributing to atrial arrhythmogenesis. Abnormal sarcoplasmic reticulum calcium release was recapitulated in cocultures of cardiomyocytes with the addition of Tet2-deficient macrophages or cytokines IL-1β or IL-6. We identified a modest association between CHIP, particularly TET2 CHIP, and incident AF in the UK Biobank population. In a mouse model of AF resulting from hematopoietic-specific inactivation of Tet2, we propose altered calcium handling as an arrhythmogenic mechanism, dependent on Nlrp3 inflammasome activation. Our data are in keeping with previous studies of CHIP in cardiovascular disease, and further studies into the therapeutic potential of NLRP3 inhibition for individuals with TET2 CHIP may be warranted.

Case report: Para Hisian Atrial Tachycardia

Case report: Para Hisian Atrial Tachycardia

Thromboembolism prophylaxis practices of pediatric and congenital electrophysiologists during invasive electrophysiology studies: A PACES survey.

Thromboembolic events related to invasive electrophysiology studies, while rare, can have devastating consequences. Use of systemic anticoagulation for a pediatric or adult-congenital invasive electrophysiology study is recommended, however there is no established standard of practice in this population. To report on procedural practices for thromboembolism prophylaxis during invasive electrophysiology studies for pediatric patients and adults with congenital heart disease. An anonymous web-based survey was sent to the members of the Pediatric and Congenital Electrophysiology Society. The survey focused on pre-procedural, intra-procedural, and post-procedural thromboembolism prophylaxis practices during invasive electrophysiology studies. Significant practice variation was defined as <90% concordance among respondents. Survey was completed by 73 members; 52 (71%) practicing in the United States, 65 (89%) practicing in an academic institution, and 14 (19%) in an institution that performs more than 200 invasive electrophysiology procedures annually. Responses showed significant variation in practice. Prior to an invasive electrophysiology procedure, 25% discontinue aspirin while 47% discontinue anticoagulants. Heparin is given for all procedures by 32%. When heparin is administered, the first dose is given by 32% after sheaths are placed, 42% after crossing into the systemic atrium, and 26% just prior to systemic-side ablation. Most target an activated clotting time between 200-300 seconds. Post systemic-side ablation, 58% do not initiate a heparin infusion. Post-procedural oral agents were initiated on day of procedure by 34% of respondents and on post-procedure day 1 by 53%. If treating with aspirin, 74% use low-dose (3-5mg/kg or 81mg daily), and 68% treat for 4-6weeks. There is significant variation in thromboembolism prophylaxis for invasive EP studies among pediatric and congenital electrophysiologists. Further studies are needed to optimize the management of thromboembolism prophylaxis in this population.

Non‑synonymous polymorphisms in the HRC and ADRB1 genes may be associated with all‑cause death in patients with non‑ischemic heart failure.

Sudden cardiac death (SCD) is an unpredictable and common mode of death in patients with heart failure (HF). Alterations in calcium handling may lead to malignant arrhythmias, resulting in SCD, and variants in calcium signaling-related genes have a significant association with SCD. Therefore, the aim of the present retrospective cohort study was to investigate the association of Ser96Ala [histidine-rich calcium-binding protein (HRC)], Ser49Gly [β1-adrenergic receptor (ADRB1)], Arg389Gly (ADRB1) and Gly1886Ser [ryanodine receptor 2 (RYR2)] polymorphisms with serious arrhythmic events and overall mortality in patients with HF with reduced left ventricular ejection fraction of non-ischemic etiology. In total, 136 patients with HF underwent physical examination, routine laboratory tests, non-invasive assessment of cardiac function and an invasive electrophysiological study. The primary outcome was the occurrence of serious arrhythmic events, set as either SCD or appropriate implantable cardioverter-defibrillator (ICD) therapy, and the secondary outcome was all-cause death. During a median follow-up of 37 months, arrhythmic events occurred in 26 patients (19%) and 41 patients (30%) died. Patients carrying the Ser allele of the Ser96Ala polymorphism in HRC had worse survival than those with the Ala/Ala genotype (log-rank P=0.043). Despite the difference in survival time, the Ala/Ala genotype was not associated with all-cause death in the regression analysis [unadjusted hazard ratio (HR)=0.17; 95% CI, 0.02-1.21]. Regarding the Ser49Gly and Arg389Gly polymorphisms in ADRB1, homozygosity for the major alleles at both sites (Ser49Ser and Arg389Arg) was associated with a two-fold increased risk of all-cause death compared with the other genotype combinations (unadjusted HR=1.98; 95% CI, 1.02-3.82). However, this association was lost after controlling for clinical covariates. No association was observed for the Gly1886Ser polymorphism in RYR2. Overall, the present findings are concurrent with the hypothesis that the Ser96Ala (HRC), Ser49Gly (ADRB1) and Arg389Gly (ADRB1) polymorphisms may be associated with HF prognosis. In particular, the Ser96Ala polymorphism might aid in risk stratification and patient selection for ICD implantation.

Atrial fibrosis heterogeneity is a risk for atrial fibrillation in pigs with ischaemic heart failure.

Atrial fibrillation (AF) is the most common arrhythmia and is associated with considerable morbidity and mortality. Ischaemic heart failure (IHF) remains one of the most common causes of AF in clinical practice. However, ischaemia-mediated mechanisms leading to AF are still incompletely understood, and thus, current treatment approaches are limited. To improve our understanding of the pathophysiology, we studied a porcine IHF model. In pigs, IHF was induced by balloon occlusion of the left anterior descending artery for 90 min. After 30 days of reperfusion, invasive haemodynamic measurements and electrophysiological studies were performed. Masson trichrome and immunofluorescence staining were conducted to assess interstitial fibrosis and myofibroblast activation in different heart regions. After 30 days of reperfusion, heart failure with significantly reduced ejection fraction (left anterior obique 30°, 34.78 ± 3.29% [IHF] vs. 62.03 ± 2.36% [control], p < .001; anterior-posterior 0°, 29.16 ± 3.61% vs. 59.54 ± 1.09%, p < .01) was observed. These pigs showed a significantly higher susceptibility to AF (33.90% [IHF] vs. 12.98% [control], p < .05). Histological assessment revealed aggravated fibrosis in atrial appendages but not in atrial free walls in IHF pigs (11.13 ± 1.44% vs. 5.99 ± .86%, p < .01 [LAA], 8.28 ± .56% vs. 6.01 ± .35%, p < .01 [RAA]), which was paralleled by enhanced myofibroblast activation (12.09 ± .65% vs. 9.00 ± .94%, p < .05 [LAA], 14.37 ± .60% vs. 10.30 ± 1.41%, p < .05 [RAA]). Correlation analysis indicated that not fibrosis per se but its cross-regional heterogeneous distribution across the left atrium was associated with AF susceptibility (r = .6344, p < .01). Our results suggest that left atrial cross-regional fibrosis difference rather than overall fibrosis level is associated with IHF-related AF susceptibility, presumably by establishing local conduction disturbances and heterogeneity.

Diagnostic accuracy of Apple Watch Series 6 recorded single-lead ECGs for identifying supraventricular tachyarrhythmias: a comparative analysis with invasive electrophysiological study.

The advancements in wearable technology have made the detection of arrhythmias more accessible. While smartwatches are commonly used to detect patients with atrial fibrillation, their effectiveness in the differential diagnosis of supraventricular tachycardias (SVT) lacks consensus. A study was conducted on 47 patients with documented SVTs on a 12-lead ECG. All patients in the cohort underwent electrophysiology study with induction of SVT. A 6th generation Apple Watch was used to record ECG tracings during baseline sinus rhythm and during induced SVT. Cardiology residents and attending cardiologists evaluated these recordings to diagnose the differential diagnosis of SVT. The evaluation revealed 27 cases of typical atrioventricular nodal reentrant tachycardia (AVNRT), 11 cases of atrioventricular reentrant tachycardia (AVRT), and 9 cases of atrial tachycardia/atrial flutter (AT/AFL) among the induced tachycardias. Attending physicians achieved an accuracy of 66.0 to 76.6%, and residents demonstrated accuracy rates between 68.1 and 74.5%. Interrater reliability was assessed using Fleiss's Kappa method, resulting in a moderate level of agreement between residents (Kappa = 0.465, p < 0.001, 95% CI 0.30-0.63) and attendings (Kappa = 0.519, p < 0.001, 95% CI 0.35-0.68). The overall Kappa value was 0.417 (p < 0.001, 95% CI 0.34-0.49). Smartwatch recordings demonstrate moderate feasibility in diagnosing SVT when following a pre-specified algorithm. However, this diagnostic performance was lower than the accuracy obtained from 12-lead ECG tracings when blinded to procedure outcomes.

Abstract 15963: A Novel SGK1 Inhibitor (SGK1-I), Prevents Obesity-Related Atrial Fibrillation

Introduction: Obesity is an important risk factor for atrial fibrillation. We have previously demonstrated the protective effect of genetic SGK1 inhibition in a mouse model of obesity-related atrial fibrillation (AF). SGK1-I is a novel and potent SGK1 inhibitor that has been shown to reduce late sodium current and has currently entered clinical trials as a potential treatment of long QT syndrome. Hypothesis: We sought to assess the efficacy of pharmacologic SGK1 inhibition in a mouse model of obesity-related AF. Methods: Wild type C57/Bl6 mice were fed a high fat diet containing 60% cholesterol (by calories) compounded with (HFD-SGK1i) or without (HFD) SGK1-I for 10 weeks. After feeding, the mice were assayed with invasive electrophysiology studies (EPS), optical mapping, and biochemical assays. Results: There were no significant differences in rate of weight gain, final body weight, fasting glucose, glucose tolerance, or tail-cuff blood pressure between the two groups of mice throughout the study. During EPS, there were no differences in nodal (sinus and atrio-ventricular) function or tissue (atrial/ventricular) refractory periods. However, HFD-SGK1i mice were significantly protected from obesity-related inducible AF during EPS, with a lower rate of AF inducibility (5.7% versus 1.5%, p&lt;0.0001) and a lower total AF burden (35±54 versus 5.5±10.7 s, p=0.04). Optical mapping revealed abbreviated right (RA), but not left (LA), atrial action potential duration (APD) and attenuated inter-atrial APD differences in HFD-SGK1i mice as compared to HFD mice. In this context, Western blotting data demonstrated greater RA (versus LA) SGK1 activity/expression resulting from HFD, suggesting that SGK1 signaling may contribute to inter-atrial heterogeneity caused by HFD. Finally, protein expression of NLRP3 inflammasome components, Caspase-1 and ASC, as well as TGF-β expression were decreased in the SGK1-1 group; consistent with anti-inflammatory and anti-fibrotic signaling resulting from SGK1-I treatment. Conclusion: SGK1-I protects mice from obesity-related AF. These data further highlight SGK1 and its inhibition as a compelling target in cardiac arrhythmogenesis.

Hypertrophic Cardiomyopathy and Ventricular Preexcitation in the Young: Cause and Accessory Pathway Characteristics.

The cause of hypertrophic cardiomyopathy (HCM) in the young is highly varied. Ventricular preexcitation (preexcitation) is well recognized, yet little is known about the specificity for any cause and the characteristics of the responsible accessory pathways (AP). Retrospective cohort study of patients <21 years of age with HCM/preexcitation from 2000 to 2022. The cause of HCM was defined as isolated HCM, storage disorder, metabolic disease, or genetic syndrome. Atrioventricular AP (true AP) were distinguished from fasciculoventricular fibers (FVF) using standard invasive electrophysiology study criteria. AP were defined as high risk if any of the following were <250 ms: shortest preexcited RR interval in atrial fibrillation, shortest paced preexcited cycle length, or anterograde AP effective refractory period. We identified 345 patients with HCM and 28 (8%) had preexcitation (isolated HCM, 10/220; storage disorder, 8/17; metabolic disease, 5/19; and genetic syndrome, 5/89). Six (21%) patients had clinical atrial fibrillation (1 with shortest preexcited RR interval <250 ms). Twenty-two patients underwent electrophysiology study which identified 23 true AP and 16 FVF. Preexcitation was exclusively FVF mediated in 8 (36%) patients. Five (23%) patients had AP with high-risk conduction properties (including ≥1 patient in each etiologic group). Multiple AP were seen in 8 (36%) and AP plus FVF in 10 (45%) patients. Ablation was acutely successful in 13 of 14 patients with recurrence in 3. One procedure was complicated by complete heart block after ablation of a high-risk midseptal AP. There were significant differences in QRS amplitude and delta wave amplitude between groups. There were no surface ECG features that differentiated AP from FVF. Young patients with HCM and preexcitation have a high likelihood of underlying storage disease or metabolic disease. Nonisolated HCM should be suspected in young patients with large QRS and delta wave amplitudes. Surface ECG is not adequate to discriminate preexcitation from a benign FVF from that secondary to potentially life-threatening AP.

Shared Decision Making and Cardioneuroablation Allow Discontinuation of Permanent Pacing in Patients with Vagally Mediated Bradycardia.

Safe discontinuation of pacemaker therapy for vagally mediated bradycardia is a dilemma. The aim of the study was to present the outcomes of a proposed diagnostic and therapeutic process aimed at discontinuing or not restoring pacemaker therapy (PPM) in patients with vagally mediated bradycardia. The study group consisted of two subgroups of patients with suspected vagally mediated bradycardia who were considered to have PPM discontinued or not to restore their PPM if cardioneuroablation (CNA) would successfully treat their bradycardia. A group of 3 patients had just their pacemaker explanted but reimplantation was suggested, and 17 patients had preexisting pacemakers implanted. An invasive electrophysiology study was performed. If EPS was negative, extracardiac vagal nerve stimulation (ECVS) was performed. Then, patients with positive ECVS received CNA. Patients with an implanted pacemaker had it programmed to pace at the lowest possible rate. After the observational period and control EPS including ECVS, redo-CNA was performed if pauses were induced. The decision to explant the pacemaker was obtained based on shared decision making (SDM). After initial clinical and electrophysiological evaluation, 17 patients were deemed eligible for CNA (which was then performed). During the observational period after the initial CNA, all 17 patients were clinically asymptomatic. The subsequent invasive evaluation with ECVS resulted in pause induction in seven (41%) patients, and these patients underwent redo-CNA. Then, SDM resulted in the discontinuation of pacemaker therapy or a decision to not perform pacemaker reimplantation in all the patients after CAN. The pacemaker was explanted in 12 patients post-CNA, while in 2 patients explantation was postponed. During a median follow-up of 18 (IQR: 8-22) months, recurrent syncope did not occur in the CNA recipients. Pacemaker therapy in patients with vagally mediated bradycardia could be discontinued safely after CNA.

A Concept for Myocardial Current Density Estimation with Magnetoelectric Sensors

Abstract In this paper we present a novel noninvasive approach to estimate current densities in the heart from magnetocardiography. The proposed algorithm uses nested optimization to model current densities in equally-sized voxels of myocardial tissue. First-order Thiran all-pass filters are used to describe the propagation between voxels.We demonstrate feasibility of the algorithm for a noise-free single-layer simulation. However, challenges remain, such as addressing measurement noise and optimizing propagation velocity. Overall, this approach has the potential to complement or replace invasive catheter-based electrophysiological studies for localization of arrhythmogenic tissue.

Abstract P3149: Effect Of SGLT2 Inhibitors On Atrial Fibrillation Susceptibility In Diabetic Mice

Background: Diabetes mellitus (DM) and heart failure (HF) are independent risk factors for atrial fibrillation (AF), the commonest clinical arrhythmia. A new class of drugs - sodium glucose cotransporter 2 inhibitors (SGLT2i) have beneficial effect in DM and HF and are now part of the guideline directed therapy for HF. However, conflicting evidence exists regarding their role and effect on cardiac arrhythmias including AF independent of their effect on HF and their exact mechanism(s) of action on the heart. Objective: Here we tested the effect of two commonly used SGLT2i on AF susceptibility in a type 2 DM (T2D) mouse model. Methods and Results: We used a T2D mouse model (high fat diet + low dose streptozocin) and a cohort of T2D mice were treated with SGLT2i - Empagliflozin (30mg/kg/d) or Dapagliflozin (5mg/kg/d) for 10 weeks in drinking water. We performed invasive electrophysiologic studies (EPS) to assess AF susceptibility by a rapid atrial burst pacing protocol in male mice aged 5 months at the time of EPS. T2D mice had increased AF susceptibility compared with non-diabetic littermate controls (normal chow diet + citrate buffer) [78% (14/18) vs. 28% (5/18), p &lt; 0.01]. T2D mice treated with Empagliflozin were protected from increased AF susceptibility (22% (3/18) [p &lt; 0.01]) while T2D mice treated with Dapagliflozin were not protected from increased AF susceptibility (58% (11/19) [p = 0.29]). Both Empagliflozin and Dapagliflozin treated T2D mice had normalization of their blood glucose levels to comparable levels with the non-diabetic control mice. T2D mice had mild LV dysfunction compared with non-diabetic controls (EF - 66% vs 81%, p &lt; 0.01) and treatment with either Empagliflozin or Dapagliflozin attenuated the degree of LV dysfunction (EF - 71% in both groups). Conclusion: Taken together, our data support the concept that SGLT2i decrease AF susceptibility in hyperglycemia primed AF, in addition to attenuating LV dysfunction in T2D. However, the effect on AF was only observed with Empagliflozin but not Dapagliflozin treatment independent of their effect on hyperglycemia and LV dysfunction. Further investigations are necessary to determine if there is a class effect of SGLT2i on AF susceptibility and the specific mechanisms of action modulating this effect.

Melatonin induced Ventricular Arrhtymias

Abstract Idiopathic ventricular arrhythmias are frequently encountered in clinical practices. Melatonin is a frequently used medication for treating insomnia. Melatonin is usually considered a safe option among the drugs used to control insomnia. Here, we report a patient with ventricular ectopics induced by melatonin. The patient’s ventricular ectopics and symptoms disappeared on stopping melatonin. This case illustrates the importance of history taking specifically all medication history in clinching the etiology before proceeding for invasive electrophysiological studies.

Invasive electrophysiology study guided loop recorder implantation in myotonic dystrophy type 1: a prospective single-center study

Abstract Funding Acknowledgements Type of funding sources: None. Introduction In one third of the patients with myotonic dystrophy type 1 (DMT1) the cause of death is of cardiac origin. The most common cardiac manifestations are arrhythmias and conduction disturbances. Purpose Due to its extreme long monitoring properties, implantable loop recorders (ILRs) are highly suitable to detect rare cardiac arrhythmias. To date, there are only limited data using ILRs in DMT1. We aimed to evaluate the role of the invasive electrophysiology study (EPS)-guided loop recorder implantation in patients with DMT. Methods In our prospective study 18 genetically confirmed DMT1 patients underwent non-invasive cardiac examination including transthoracic echocardiography, 24-hour Holter monitoring and surface ECG. In addition, EPS was performed in all cases to evaluate the risk of sudden cardiac death and infra-Hisian conduction properties. Based on the performed non-invasive diagnostic evaluation and EPS findings, patients were divided into low, intermediate and high-risk groups. For patients with normal investigation results and normal HV interval (&amp;lt;55 ms) only annual cardiac follow-up visits were planned (low-risk group). Patients with increased PR interval (&amp;gt;240 ms), QRS duration (&amp;gt;120 ms), or slightly prolonged HV interval (55-70 ms) underwent implantable loop recorder (ILR) implantation (intermediate-risk group). Permanent pacemaker (PM) or implantable cardiac defibrillator (ICD) was implanted in patients with 2nd/3rd degree atrioventricular block (AVB), significantly prolonged HV interval (&amp;gt;100 ms) or if sustained ventricular tachyarrhythmia could be induced during EPS. All patients were followed for at least 3 years. Results According to our study criteria, 8 patients could be categorized as "intermediate risk", 7 of them received implantable loop recorder (ILR). 1 ILR had to be removed 3 weeks after implantation due to skin infarction. During three-years of follow-up, 2 patients had many asymptomatic atrial high-rate episodes, but no 2nd or 3rd degree AVB, significant asystole or malignant ventricular arrhythmia were detected. Conclusions Our single-center prospective study examined the EPS-guided ILR implantation for the risk stratification of DMT1 patients for the first time. A more extensive, multicenter study is warranted to define optimal management of DMT1 patients with slightly impaired infrahisian conduction.

P450 ADVANCED ATRIOVENTRICULAR BLOCK AT LOOP RECORDER MONITORING IN A YOUNG PATIENT WITH BRUGADA SYNDROME AND CONDUCTION ABNORMALITIES: CAUSE OF SYNCOPE OR INCIDENTAL FINDING?

Abstract A 32–year–old man healthy man presented to the emergency department because of remittent fever. His past medical history, physical examination and chest X–ray were unremarkable except for a body temperature of 39 Celsius degrees. Laboratory exams showed a marked elevation of transaminases, cholestasis markers and C–reactive protein, while an abdomen ultrasound revealed hepatomegaly and diffuse hyperechogenicity of the liver. He was diagnosed with acute hepatitis and admitted to the Gastroenterology Unit. Due to the persistent hyperpyrexia despite antipyretics and antibiotics, he was successfully treated with intravenous diclofenac, resulting in temporary remission of fever. First electrocardiogram during apyrexia showed sinus rhythm, first–degree atrioventricular block (PR interval 240 milliseconds), and non–specific intraventricular conduction delay. In the following days, liver and cholestasis markers improved, but he underwent two syncopal episodes without prodromes, the former while he was walking and the latter during meal. A new electrocardiogram revealed a type 1 Brugada pattern. At the time of its recording, however, his body temperature was 38.6 Celsius degrees. He was then admitted to the Cardiology Unit for monitoring and further investigations. 2D–echocardiogram and cardiac magnetic resonance imaging were unremarkable. Telemetry monitoring showed nocturnal episodes of marked sinus bradycardia (up to 35 beats per minute), but no ventricular arrhythmias were documented. He also underwent an invasive electrophysiological study with programmed ventricular stimulation, but again no ventricular arrhythmias were induced. Recording of His bundle electrogram, however, revealed the prolongation of both AH and HV interval (190 and 76 milliseconds respectively). Given the syncopal episodes, an implantable cardioverter defibrillator implantation was proposed, but the patient refused, so he underwent an implantable loop recorder implantation. After three months, at remote monitoring, a nocturnal episode of complete atrioventricular block with a pause of 15 seconds was recorded, thus he was again admitted to the Cardiology Unit. This time he was apyretic, but his electrocardiogram showed a spontaneous type 1 Brugada pattern with “high arrhythmic risk” features as first–degree atrioventricular block and a prominent S wave in lead I. He then underwent a successful implantable cardioverter defibrillator implantation with still an uneventful follow up.