Cardiac arrhythmia classification using autoregressive modeling

Background  

Computer-assisted arrhythmia recognition is critical for the management of cardiac disorders. Various techniques have been utilized to classify arrhythmias. Generally, these techniques classify two or three arrhythmias or have significantly large processing times. A simpler autoregressive modeling (AR) technique is proposed to classify normal sinus rhythm (NSR) and various cardiac arrhythmias including atrial premature contraction (APC), premature ventricular contraction (PVC), superventricular tachycardia (SVT), ventricular tachycardia (VT) and ventricular fibrillation (VF).     

Life-threatening ventricular arrhythmia recognition by nonlinear descriptor

Background  

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are ventricular cardiac arrhythmia that could be catastrophic and life threatening. Correct and timely detection of VT or VF can save lives.     

Phospholamban cardiomyopathy: a Canadian perspective on a unique population

Introduction

Phospholamban cardiomyopathy is an inherited cardiomyopathy, characterised by a defect in regulation of the sarcoplasmic reticulum Ca²⁺ pump, often presenting with malignant arrhythmias and progressive cardiac dysfunction occurring at a young age.

Methods

Phospholamban R14del mutation carriers and family members were identified from inherited arrhythmia clinics at 13 sites across Canada. Cardiac investigations, including electrocardiograms, Holter monitoring (premature ventricular complexes, PVCs), and imaging results were summarised.

Results

Fifty patients (10 families) were identified (median age 30 years, range 3–71, 46% female). Mutation carriers were more likely to be older, have low-voltage QRS, T‑wave inversion, frequent PVCs, and cardiac dysfunction, compared to unaffected relatives. Increasing age, low-voltage QRS, T‑wave inversion, late potentials, and frequent PVCs were predictors of cardiac dysfunction (p < 0.05 for all). Older carriers (age ≥45 years) were more likely to have disease manifestations than were their younger counterparts, with disease onset occurring at an older age in Canadian patients and their Dutch counterparts.

Discussion

Among Canadian patients with phospholamban cardiomyopathy, clinical manifestations resembled those of their Dutch counterparts, with increasing age a major predictor of disease manifestation. Older mutation carriers were more likely to have electrical and structural abnormalities, and may represent variable expressivity, age-dependent penetrance, or genetic heterogeneity among Canadian patients.

     

The persistent sodium current blocker riluzole is antiarrhythmic and anti-ischaemic in a pig model of acute myocardial infarction

Background

The potential of the cardiac persistent sodium current as a target for protection of the myocardium from ischaemia and reperfusion injury is gaining increasing interest. We have investigated the anti-ischaemic and antiarrhythmic effects of riluzole, a selective INaP blocker, in an open chest pig model of infarction.

Methods and Principal Findings

The left anterior descending coronary artery (LAD) was ligated in 27 anesthetised pigs (landrace or large white, either sex, 20–35 kg) which had received riluzole (8 mg/kg IP; n = 6), lidocaine (2.5–12 mg/kg bolus plus 0.05–0.24 mg/kg/min; n = 11) or vehicle (n = 10) 50 min prior. Arrhythmias could be delineated into phase 1a (0 to 20 min), phase 1b (20 to 50 min) and phase 2 (from 50 min to termination at 180 min) and were classified as premature ventricular contractions (PVCs), non-sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) (spontaneously reverting within 15 s) or sustained VT or VF (ie. requiring cardioversion at 15 s). Riluzole reduced the average number of all arrhythmias in Phase 2 (PVCs from 484+/−119 to 32+/−13; non sustained arrhythmias from 8.9+/−4.4 to 0.7+/−0.5; sustained arrhythmias from 3.9+/−2.2 to 0.5+/−0.4); lidocaine reduced the average number of non-sustained and sustained arrhythmias (to 0.4+/−0.3 and 0.4+/−0.3 respectively) but not PVCs (to 390+/−234). Riluzole and lidocaine reduced the average number of sustained arrhythmias in phase 1b (from 1.8+/−0.4 to 0.17+/−0.13 (p<0.02) and to 0.55+/−0.26 (p = ns) respectively). Neither lidocaine or riluzole changed the ECG intervals: there was no statistical significance between groups at time zero (just before ligation) for any ECG measure. During the course of the 3 hour period of the ischaemia R-R, and P-R intervals shortened slightly in control and riluzole groups (not significantly different from each other) but not in the lidocaine group (significantly different from control). QRS and QTc did not change appreciably in any group Riluzole reduced the degree of histopathological tissue damage across the infarct zone considerably more than did lidocaine.

Conclusions

At the doses used, riluzole was at least as effective as lidocaine at reducing the number of episodes of ischaemic VT or VF in pigs, and much more effective at reducing the number of PVCs. We propose that this is related to the ability of riluzole to block cardiac persistent sodium current.     

Unique features of epicardial ventricular arrhythmias/premature ventricular complexes ablated from coronary venous system in veteran population

IntroductionVentricular arrhythmias/premature ventricular complexes (VA/PVCs) that can be ablated from within the coronary venous system (CVS) have not been described in the United States Veterans Health Administration (VHA) population. We retrospectively studied the VA/PVCs ablations that were performed in the VHA population.MethodsData from 42 consecutive patients who underwent VA/PVCs ablation at Veterans Affairs Hospital, Indianapolis, IN, with 44 VA/PVCs was included in the study. Patients were divided into two groups (CVS group [n = 10], and non-CVS group [n = 32]) based on where the earliest pre-systolic activation was seen with >95% pacematch.ResultsThe mean age in CVS group was 65 ± 8 years versus 64 ± 12 years (p = 0.69) in non-CVS group. Overall there was a statistically significant reduction in PVC burden post ablation (27.7% (pre-ablation) versus 4.7% (post-ablation). In the 10 patients in the CVS group, either ablation or catheter-related mechanical trauma resulted in complete (n = 6 [60%]) or partial (n = 4 [40%]) long-term suppression of VA/PVCs. Right bundle branch block-type VA/PVC (9/11: 82%) was the most common morphology in the CVS group, whereas in the non-CVS group, this type was seen in only 3/33 (9%). The CVS group (25% of total VA/PVCs) had shorter activation time compared to non CVS group.ConclusionIn our experience VA/PVCs with electrocardiograms suggestive of epicardial origin can often be safely and successfully ablated within the coronary venous system. These arrhythmias have unique features in Veterans patient population.     

Susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic rat heart

Diabetic heart is suggested to exhibit either increased or decreased resistance to ischemic injury. Ischemic preconditioning suppresses arrhythmias in the normal heart, whereas relatively little is known about its effects in the diseased myocardium. Our objective was to investigate whether development of diabetes mellitus modifies the susceptibility to ischemia-induced arrhythmias and affects preconditioning in the rat heart. Following 1 and 9 weeks of streptozotocin-induced (45 mg/kg, i.v.) diabetes, the hearts were Langendorff-perfused at constant pressure of 70 mm Hg and subjected to test ischemia induced by 30 min occlusion of the left anterior descending (LAD) coronary artery. Preconditioning consisted of one cycle of 5 min ischemia and 10 min reperfusion, prior to test ischemia. Susceptibility to ischemia-induced arrhythmias was lower in 1-week diabetics: only 42 % of diabetic hearts exhibited ventricular tachycardia (VT) and 16 % had short episodes of ventricular fibrillation (VF) as compared to VT 100 % and VF 70 % (including sustained VF 36 %) in the non-diabetics (P<0.05). Development of the disease was associated with an increased incidence of VT (VT 92 %, not significantly different from non-diabetics) and longer total duration of VT and VF at 9-weeks, as compared to 1-week diabetics. Preconditioning effectively suppressed arrhythmias in the normal hearts (VT 33 %, VF 0 %). However, it did not provide any additional antiarrhythmic protection in the acute diabetes. On the other hand, in the preconditioned 9-weeks diabetic hearts, the incidence of arrhythmias tended to decrease (VT 50 %, transient VF 10 %) and their severity was reduced. Diabetic rat hearts are thus less susceptible to ischemia-induced arrhythmias in the acute phase of the disease. Development of diabetes attenuates increased ischemic tolerance, however, diabetic hearts in the chronic phase can benefit more from ischemic preconditioning, due to its persisting influence.     

Morning Surge of Ventricular Arrhythmias in a New Arrhythmogenic Canine Model of Chronic Heart Failure Is Associated with Attenuation of Time-Of-Day Dependence of Heart Rate and Autonomic Adaptation,and Reduced Cardiac Chaos

Patients with chronic heart failure (CHF) exhibit a morning surge in ventricular arrhythmias, but the underlying cause remains unknown. The aim of this study was to determine if heart rate dynamics, autonomic input (assessed by heart rate variability (HRV)) and nonlinear dynamics as well as their abnormal time-of-day-dependent oscillations in a newly developed arrhythmogenic canine heart failure model are associated with a morning surge in ventricular arrhythmias. CHF was induced in dogs by aortic insufficiency & aortic constriction, and assessed by echocardiography. Holter monitoring was performed to study time-of-day-dependent variation in ventricular arrhythmias (PVCs, VT), traditional HRV measures, and nonlinear dynamics (including detrended fluctuations analysis α1 and α2 (DFAα1 & DFAα2), correlation dimension (CD), and Shannon entropy (SE)) at baseline, as well as 240 days (240d) and 720 days (720d) following CHF induction. LV fractional shortening was decreased at both 240d and 720d. Both PVCs and VT increased with CHF duration and showed a morning rise (2.5-fold & 1.8-fold increase at 6 AM-noon vs midnight-6 AM) during CHF. The morning rise in HR at baseline was significantly attenuated by 52% with development of CHF (at both 240d & 720d). Morning rise in the ratio of low frequency to high frequency (LF/HF) HRV at baseline was markedly attenuated with CHF. DFAα1, DFAα2, CD and SE all decreased with CHF by 31, 17, 34 and 7%, respectively. Time-of-day-dependent variations in LF/HF, CD, DFA α1 and SE, observed at baseline, were lost during CHF. Thus in this new arrhythmogenic canine CHF model, attenuated morning HR rise, blunted autonomic oscillation, decreased cardiac chaos and complexity of heart rate, as well as aberrant time-of-day-dependent variations in many of these parameters were associated with a morning surge of ventricular arrhythmias.     

Increased ventricular repolarization heterogeneity in patients with ventricular arrhythmia vulnerability and cardiomyopathy: a human in vivo study

Increased repolarization heterogeneity can provide the substrate for reentrant ventricular arrhythmias in animal models of cardiomyopathy. We hypothesized that ventricular repolarization heterogeneity is also greater in patients with cardiomyopathy and ventricular arrhythmia vulnerability (inducible ventricular tachycardia or positive microvolt T wave alternans, VT/TWA) compared with a similar patient population without ventricular arrhythmia vulnerability (no VT/TWA). Endocardial and epicardial repolarization heterogeneity was measured in patients with (n = 12) and without (n = 10) VT/TWA by using transvenous 26-electrode catheters placed along the anteroseptal right ventricular endocardium and left ventricular epicardium. Local activation times (AT), activation-recovery intervals (ARI), and repolarization times (RT) were measured from unipolar electrograms. Endocardial RT dispersion along the apicobasal ventricle was greater (P < 0.005) in patients with VT/TWA than in those without VT/TWA because of greater ARI dispersion (P < 0.005). AT dispersion was similar between the two groups. Epicardial RT dispersion along the apicobasal ventricle was greater (P < 0.05) in patients with VT/TWA than in those without VT/TWA because of greater ARI dispersion (P < 0.05). AT dispersion was similar between the two groups. A plot of AT as a function of ARI revealed an inverse linear relationship for no VT/TWA such that progressively later activation was associated with progressively shorter ARI. The AT-ARI relationship was nonlinear in VT/TWA. In conclusion, patients with cardiomyopathy and VT/TWA have greater endocardial and epicardial repolarization heterogeneity than those without VT/TWA without associated conduction slowing. The steep repolarization gradients in VT/TWA may provide the substrate for functional conduction block and reentrant ventricular arrhythmias.     

Left Atrial Appendage Dysfunction in a Patient with Premature Ventricular Contractions - A Risk Factor for Stroke?

A 16-year-old female with ventricular dysfunction and frequent ventricular arrhythmia presented with a cardioembolic stroke. Prior electrophysiology study and ablation was performed for ventricular tachycardia (VT). For remaining ventricular ectopy, the patient was maintained on carvedilol and mexiletine. After one year on this regimen, she presented with an acute stroke. Transesophageal echocardiography revealed no evidence of an intracardiac or ventricular thrombus but demonstrated markedly decreased left atrial appendage (LAA) flow velocity worsened during frequent premature ventricular contractions (PVC). In the absence of atrial fibrillation (AF), the LAA dysfunction was considered secondary to the frequent PVCs and was thought to be the underlying cause for the stroke. We present this case to highlight a potential under recognized association between LAA dysfunction and ventricular arrhythmia, similar to that observed with atrioventricular dyssynchronous pacing.     

Ablation of Premature Ventricular Complexes Triggering Ventricular Fibrillation in a Patient with Long QT Syndrome

We describe the case of a patient with long QT syndrome and recurrent ventricular fibrillation, triggered by premature ventricular complexes (PVCs) with a left bundle branch block pattern and inferior axis of the QRS. Activation mapping demonstrated the origin of the PVCs to be in the right ventricular outflow tract. Ventricular fibrillation (VF) was successfully treated by catheter ablation of the triggering PVCs and there has been no recurrence of VF during a follow-up period of 14 months.     

Sequential algorithm for life threatening cardiac pathologies detection based on mean signal strength and EMD functions

Background  

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most serious cardiac arrhythmias that require quick and accurate detection to save lives. Automated external defibrillators (AEDs) have been developed to recognize these severe cardiac arrhythmias using complex algorithms inside it and determine if an electric shock should in fact be delivered to reset the cardiac rhythm and restore spontaneous circulation. Improving AED safety and efficacy by devising new algorithms which can more accurately distinguish shockable from non-shockable rhythms is a requirement of the present-day because of their uses in public places.     

SPEAR Trial: Smartphone Pediatric ElectrocARdiogram Trial

Objectives

Smartphone-enabled ECG devices have the potential to improve patient care by enabling remote ECG assessment of patients with potential and diagnosed arrhythmias. This prospective study aimed to assess the usefulness of pediatric ECG tracings generated by the AliveCor device (Oklahoma City, OK) and to assess user satisfaction.

Study Design

Enrolled pediatric patients with documented paroxysmal arrhythmia used the AliveCor device over a yearlong study period. Pediatric electrophysiologists reviewed all transmitted ECG tracings. Patient completed surveys were analyzed to assess user satisfaction.

Results

35 patients were enrolled with the following diagnoses: supraventricular tachycardia (SVT, 57%), atrial fibrillation (AF, 11%), ectopic atrial tachycardia (EAT, 6%), atrial tachycardia (AT, 3%), and ventricular tachycardia (VT, 23%). A total of 238 tracings were received from 20 patients, 96% of which were of diagnostic quality for sinus rhythm, sinus tachycardia, SVT, and AF. 126 patient satisfaction surveys (64% from parents) were completed. 98% of the survey responses indicated that it was easy to obtain tracings, 93% found it easy to transmit the tracings, 98% showed added comfort in managing arrhythmia by having the device, and 93% showed interest in continued use of the device after the study period ended.

Conclusions

Smartphone-enabled ECG devices can generate tracings of diagnostic quality in children. User satisfaction was extremely positive. Use of the device to manage certain patients with AF and SVT showcases the future role of remote ECGs in the successful outpatient management of arrhythmias in children by potentially reducing Emergency Department visits and healthcare costs.     

Premature ventricular contractions of the right ventricular outflow tract: is there an incipient underlying disease? New insights from a speckle tracking echocardiography study

ContextPremature ventricular contractions (PVCs) originating in the right ventricular outflow tract (RVOT) are traditionally considered idiopathic and benign. Echocardiographic conventional measurements are typically normal.AimsTo assess whether right ventricle longitudinal strain, determined by two-dimensional speckle tracking echocardiography, differ between RVOT PVCs patients (treated with catheter ablation) and healthy controls.MethodsWe retrospectively selected patients with PVCs from the RVOT who underwent electrophysiological study and catheter ablation between 2016 and 2019. Patients with documented structural heart disease were excluded. Transthoracic echocardiography was performed and right ventricle global longitudinal strain (RV-GLS), free wall longitudinal strain (RVFW-LS) and left ventricle global longitudinal strain (LV-GLS) were determined as well as conventional ultrasound measurements of RV and LV function.ResultsWe studied 21 patients with RVOT PVCs and 13 controls. Patients with PVCs from the RVOT had lower values of RV-GLS and RVFW-LS compared with the control group (?19.4% versus ?22.5%, P = 0.015 and ?22.1% versus ?25.5, P = 0.041, respectively). They also had lower values of LV-GLS, although still within the normal range (?19.1% versus ?20.9%, P = 0.047). Regarding RVOT PVCs patients only, RV-GLS and RVFW-LS had no correlation with the PVCs burden prior to catheter ablation and they did not differ between the patients in whom the catheter ablation was successful and those in whom it was not. RV-GLS also had a positive correlation with RVOT proximal diameter (r = 0.487, P = 0.025).ConclusionsIn this group of RVOT PVCs patients, we found worse RV longitudinal strain values (and therefore sub-clinical myocardial dysfunction) when compared to healthy controls.     

Radiofrequency ablation of premature ventricular contractions originating from uncommon sites of right ventricle

Premature Ventricular Contraction (PVC)/ventricular tachycardia (VT) with left bundle branch block (LBBB) morphology and inferior axis has been described classically to originate from the right ventricular outflow tract (RVOT). Some uncommon sites of idiopathic ventricular arrhythmia (VA) origins have been revealed including tricuspid annulus (TA) and right ventricular (RV) inflow free wall region. We present a series of two cases who have undergone electrophysiological study and successful radiofrequency ablation of frequent monomorphic PVCs with LBBB pattern originating from relatively uncommon sites of RV – TA and RV inflow free wall region.     

Catheter Ablation of Idiopathic Premature Ventricular Contractions and Ventricular Tachycardias Originating from Right Ventricular Septum

Background

Idiopathic premature ventricular contractions (PVCs) and ventricular tachycardias (IVTs) originating from the subtricuspid septum and near the His bundle have been reported. However, little is known about the prevalence, distribution, electrocardiographic characteristics and the efficacy of radiofrequency catheter ablation (RFCA) for the ventricular arrhythmias arising from the right ventricular (RV) septum. This study aimed to investigate electrocardiographic characteristics and effects of RFCA for patients with symptomatic PVCs/IVTs, originating from the different portions of the RV septum.

Methodology/Principal Findings

Characteristics of body surface electrocardiogram and electrophysiologic recordings were analyzed in 29 patients with symptomatic PVCs/IVTs originating from the RV septum. Among 581 patients with PVCs/IVTs, the incidence of ventricular arrhythmias originating from the RV septum was 5%. Twenty (69%) had PVCs/IVTs from the septal portion of the tricuspid valvular RV region (3 from superoseptum, 15 from midseptum, 2 from inferoseptum), and 9 (31%) from the septal portion of the basal RV (1 from superoseptum, 4 from midseptum, 4 from inferoseptum). There were different characteristics of ECG of PVCs/VT originating from the different portions of the RV septum. Twenty-seven of 29 patients with PVCs/IVTs arising from the RV septum were successfully ablated (93.1% acute success).

Conclusions/Significance

ECG characteristics of PVCs/VTs originating from the different portions of the RV septum are different, and can help regionalize the origin of these arrhythmias. The septal portion of the tricuspid valvular RV region was the preferential site of origin. RFCA was effective and safe for the PVCs/IVTs arising from the RV septum.     

Effects of HNS-32, a novel antiarrhythmic drug,on ventricular arrhythmias induced by coronary artery occlusion and reperfusion in anesthetized rats

HNS-32 (N¹,N¹-dimethyl-N²-(2-pyridylmethyl)-5-isopropyl-3, 8-dimethylazulene-1-carboxamidine: CAS 186086-10-2) is a newly synthesized compound, and possesses antiarrhythmic properties with vasodilator action in dog hearts. The aim of this study was to investigate the dose-dependent effects of HNS-32 on ischemia- and/or reperfusion-induced ventricular arrhythmias in anesthetized rats in vivo and compared with those of mexiletine. Saline or drugs were administered intravenously 5 min prior to coronary artery occlusion. On the ischemia-induced ventricular arrhythmias, HNS-32 showed dose-dependent reduction of total number of premature ventricular complexes (PVC) from 2091 ± 225 to 656 ± 116 and 286 ± 69 beats/30 min (p < 0.05), the ventricular tachycardia (VT) duration from 183 ± 33 to 28 ± 9 and 4 ± 2 sec (p < 0.05), the incidence of VT from 100 to 90 (n.s.) and 40% (p < 0.05), and the incidence of ventricular fibrillation (VF) from 50 to 0 and 0% (p < 0.05) with 3 and 5 mg/kg, respectively. Mexiletine also reduced these parameters to 936 ± 159 beats/30 min (p < 0.05), 39 ± 22 sec (p < 0.05), 90% (n.s.) and 10% (n.s.), respectively. HNS-32 completely suppressed the late reperfusion-induced arrhythmias, however mexiletine did not affect them. On the early reperfusion-induced ventricular arrhythmias, HNS-32 showed dose-dependent reduction of VT duration from 126 ± 34 to 37 ± 12 and 3 ± 2 sec (p < 0.05), incidence of VT from 100 to 90 (n.s.) and 40% (p < 0.05), incidence of VF from 100 to 10 and 0% (p < 0.05), and mortality rate from 90 to 0 and 0% (p < 0.05), with 3 and 5 mg/kg, respectively. Mexiletine also reduced these parameters to 16 ± 9 sec (p < 0.05), 80 (n.s.), 50 (p < 0.05), and 10% (p < 0.05), respectively. HNS-32 significantly reduced the heart rate in a dose-dependent manner, from 399 ± 14 to 350 ± 8 and 299 ± 10 beats/min (p < 0.05) with 3 and 5 mg/kg, respectively. The antiarrhythmic effects of HNS-32 were more potent than that of the similar dose of mexiletine against occlusion-induced and reperfusion-induced arrhythmias in in vivo rats.     

A mobile one-lead ECG device incorporated in a symptom-driven remote arrhythmia monitoring program. The first 5,982 Hartwacht ECGs

Background

In recent years many mobile devices able to record health-related data in ambulatory patients have emerged. However, well-organised programs to incorporate these devices are sparse. Hartwacht Arrhythmia (HA) is such a program, focusing on remote arrhythmia detection using the AliveCor Kardia Mobile (KM) and its algorithm.

Objectives

The aim of this study was to assess the benefit of the KM device and its algorithm in detecting cardiac arrhythmias in a real-world cohort of ambulatory patients.

Methods

All KM ECGs recorded in the HA program between January 2017 and March 2018 were included. Classification by the KM algorithm was compared with that of the Hartwacht team led by a cardiologist. Statistical analyses were performed with respect to detection of sinus rhythm (SR), atrial fibrillation (AF) and other arrhythmias.

Results

5,982 KM ECGs were received from 233 patients (mean age 58 years, 52% male). The KM algorithm categorised 59% as SR, 22% as possible AF, 17% as unclassified and 2% as unreadable. According to the Hartwacht team, 498 (8%) ECGs were uninterpretable. Negative predictive value for detection of AF was 98%. However, positive predictive value as well as detection of other arrhythmias was poor. In 81% of the unclassified ECGs, the Hartwacht team was able to provide a diagnosis.

Conclusions

This study reports on the first symptom-driven remote arrhythmia monitoring program in the Netherlands. Less than 10% of the ECGs were uninterpretable. However, the current performance of the KM algorithm makes the device inadequate as a stand-alone application, supporting the need for manual ECG analysis in HA and similar programs.

     

Normal pacing function with normal impedance trends despite evident lead fracture in an implantable defibrillator – What is the mechanism?

A 63-year-old lady with a high-grade atrioventricular (AV) block and a structurally normal heart underwent permanent pacemaker implantation (dual chamber, Medtronic Ltd) 8 years back. On follow up, she had a recurrence of syncope after 3 years. The device interrogation at that time had revealed ventricular tachycardia (VT) for which she underwent implantable cardioverter defibrillator (ICD, Medtronic Ltd, Egida DR, DF1) upgradation at another center (electrograms not available). Now, she presents with episodes of presyncope after another 5 years. The Echocardiography was unremarkable. The ICD was interrogated & there was a stored ventricular fibrillation (VF) episode. But the electrograms suggested noise over a true VF electrogram noted in both near and far-field. In all probability, the VF was not a true one which might have arisen from some lead noise or from an electromagnetic interference (EMI). Fluoroscopy revealed an evident lead fracture near the superior vena cava (SVC) coil. The stored electrogram (EGM) characteristics also suggested possible lead noise rather than a true VF. She was advised for lead revision. Interestingly, all pacing parameters were normal along with normal impedance despite the evident lead fracture. This happened due to the ICD lead arrangements as there are separate electrodes for the SVC/RV coil and pacing. While the SVC coil was damaged, the pacing electrodes remained unaffected. Since the patient has no episode of true VT/NSVT and the echocardiography was normal, she was managed temporarily by changing the pacemaker to asynchronous (DOO) mode.     

The Different Substrate Characteristics of Arrhythmogenic Triggers in Idiopathic Right Ventricular Outflow Tract Tachycardia and Arrhythmogenic Right Ventricular Dysplasia: New Insight from Noncontact Mapping

BackgroundThe aim of this study was to investigate the different substrate characteristics of repetitive premature ventricular complexed (PVC) trigger sites by the non-contact mapping (NCM).MethodsThirty-five consecutive patients, including 14 with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC) and 21 with idiopathic right ventricular outflow tract tachycardia (RVOT VT), were enrolled for electrophysiological study and catheter ablation guided by the NCM. Substrate and electrogram (Eg) characteristics of the earliest activation (EA) and breakout (BO) sites of PVCs were investigated, and these were confirmed by successful PVC elimination.ResultsOverall 35 dominant focal PVCs were identified. PVCs arose from the focal origins with preferential conduction, breakout, and spread to the whole right ventricle. The conduction time and distance from EA to BO site were both longer in the ARVC than the RVOT group. The conduction velocity was similar between the 2 groups. The negative deflection of local unipolar Eg at the EA site (EA slope_3,5,10ms values) was steeper in the RVOT, compared to ARVC patients. The PVCs of ARVC occurred in the diseased substrate in the ARVC patients. More radiofrequency applications were required to eliminate the triggers in ARVC patients.Conclusions/InterpretationThe substrate characteristics of PVC trigger may help to differentiate between idiopathic RVOT VT and ARVC. The slowing and slurred QS unipolar electrograms and longer distance from EA to BO in RVOT endocardium suggest that the triggers of ARVC may originate from mid- or sub-epicardial myocardium. More extensive ablation to the trigger site was required in order to create deeper lesions for a successful outcome.     

Protective role of protein kinase C epsilon activation in ischemia-reperfusion arrhythmia

PURPOSE: Ischemic heart disease carries an increased risk of malignant ventricular tachycardia (VT), fibrillation (VF), and sudden cardiac death. Protein kinase C (PKC) epsilon activation has been shown to improve the hemodynamics in hearts subjected to ischemia/reperfusion. However, very little is known about the role of epsilon PKC in reperfusion arrhythmias. Here we show that epsilon PKC activation is anti-arrhythmic and its inhibition is pro-arrhythmic. METHOD: Langendorff-perfused isolated hearts from epsilonPKC agonist (epsilonPKC activation), antagonist (epsilonPKC inhibition) transgenic (TG), and wild-type control mice were subjected to 30 min stabilization period, 10 min global ischemia, and 30 min reperfusion. Action potentials (APs) and calcium transients (CaiT) were recorded simultaneously at 37 degrees C using optical mapping techniques. The incidence of VT and VF was assessed during reperfusion. RESULTS: No VT/VF was seen in any group during the stabilization period in which hearts were perfused with Tyrode's solution. Upon reperfusion, 3 out of the 16 (19%) wild-type mice developed VT but no VF. In epsilonPKC antagonist group, in which epsilonPKC activity was downregulated, 10 out of 13 (76.9%) TG mice developed VT, of which six (46.2%) degenerated into sustained VF upon reperfusion. Interestingly, in epsilonPKC agonist mice, in which the activity of epsilonPKC was upregulated, no VF was observed and only 1 out of 12 mice showed only transient VT during reperfusion. During ischemia and reperfusion, CaiT decay was exceedingly slower in the antagonist mice compared to the other two groups. CONCLUSION: Moderate in vivo activation of epsilonPKC exerts beneficial antiarrhythmic effect vis-a-vis the lethal reperfusion arrhythmias. Abnormal CaiT decay may, in part, contribute to the high incidence of reperfusion arrhythmias in the antagonist mice. These findings have important implications for the development of PKC isozyme targeted therapeutics and subsequently for the treatment of ischemic heart diseases.