Origin Of Tachycardia Research Articles

Systolic-dicrotic notch pressure difference can identify tachycardic patients with septic shock at risk of cardiovascular decompensation following pharmacological heart rate reduction

BackgroundDuring sepsis, heart rate (HR) reduction could be a therapeutic target, but identification of responders (non-compensatory tachycardia) and non-responders (compensatory for ‘fixed’ stroke volume [SV]) is challenging. We tested the ability of the difference between systolic and dicrotic pressure (SDPdifference), which reflects the coupling between myocardial contractility and a given afterload, in discriminating the origin of tachycardia. MethodsIn this post hoc analysis of 45 patients with septic shock with persistent tachycardia, we characterised features of haemodynamic response focusing on SDPdifference, classifying patients according to variations in arterial dP/dtmax after 4 h of esmolol administration to maintain HR <95 beats min−1. A cut-off value of 0.9 mm Hg ms−1 was used for group allocation. ResultsAfter reducing HR, arterial dP/dtmax remained above the cut-off in 23 patients, whereas it decreased below the cut-off in 22 patients (from 0.99 [0.37] to 0.63 [0.16] mm Hg ms−1; mean [SD], P<0.001). At baseline, patients with decreased dP/dtmax after esmolol had lower SDPdifference than those with higher dP/dtmax (40 [19] vs 53 [16] mm Hg, respectively; P=0.01). The SDPdifference remained unchanged after esmolol in the higher dP/dtmax group (49 [16] mm Hg), whereas it decreased significantly in patients with lower dP/dtmax (29 [11] mm Hg; P<0.001). In the latter, the HR reduction resulted in a significant cardiac output reduction with unchanged SV, whereas in patients with higher dP/dtmax SV increased (from 48 [12] to 67 [14] ml; P<0.001) with maintained cardiac output. ConclusionsA decrease in SDPdifference could discriminate between compensatory and non-compensatory tachycardia, revealing a covert loss of myocardial contractility not detected by conventional echocardiographic parameters and deteriorating after HR reduction with esmolol. Clinical trial registrationNCT02188888.

Atrial tachycardia eliminated at the ventricular side in patients with congenitally corrected transposition of the great arteries: Electrophysiological findings and anatomical concerns

The unique malformation of congenitally corrected transposition of the great arteries (cc-TGA) makes the pulmonary outflow tract (POT) a possible origin of atrial tachycardia (AT). The purpose of this study was to investigate the mapping characteristics of ATs successfully ablated at the POT in patients with cc-TGA. Patients with cc-TGA with AT eliminated at the POT were analyzed. Activation mapping of the atria and POT was performed under the guidance of a 3-dimensional electroanatomic mapping system. The activation pattern of these chambers was investigated, with the local activation time (LAT; using coronary sinus ostium as a reference) of the earliest activation site (EAS) being compared. AT eliminated at the POT was documented in 5 of 6 patients with cc-TGA. The EAS was at the right anteroseptal region with a LAT of 33 (21-120) ms in the right atrium and at the septal wall with a comparable LAT (26, 47, and 26 ms; P = .604) in the left atrium. The EAS of the POT was in the vicinity of the left-facing pulmonary sinus cusp in 3 cases and the nonfacing pulmonary sinus cusp in 2 cases, with a LAT of 106 (28-134) ms preceding both atria. Ablation at this site successfully eliminated AT in all 5 cases. AT arising adjacent to the POT is not an uncommon tachycardia in patients with situs solitus-type cc-TGA and can be safely eliminated by ablation targeting the EAS in the POT.

Focal atrial tachycardia – The localization differences between men and women – a study of 487 consecutive patients

Objective:The preferential sites for focal atrial tachycardia (FAT) are mainly in the right atrium in both sexes. However, a limited number of studies have indicated that sex differences in the localization of FAT. This study investigated possible sex differences in the distribution of FAT in a large cohort of patients referred for ablation.Methods:From 2004 to 2019, 487 patients (298 women) were referred to our institution for ablation of FAT. A standard electrophysiological study was conducted, and isoproterenol or atropine was given when needed. Conventional catheter mapping, electroanatomic contact mapping, and noncontact mapping were used to assess the origin of ectopic atrial tachycardia.Results:Overall, 451 foci were successfully ablated in 436 patients (90%). Although the foci located along the crista terminalis were more common in women than in men (42% vs. 29%; p=0.023), the opposite were found in the foci located along the tricuspid annulus (5% vs. 11%; p=0.032) and the right atrial appendage (RAA) (1% vs. 3%; p=0.032). Other locations were similarly distributed in men and women. In addition, the presence of persistent FAT was more frequent in men than in women (22% vs. 5%; p<0.001). Finally, the difference in the induction pattern of FAT was also remarkable between sexes.Conclusion:The distribution of FAT in women and men is different. In addition, persistent FAT seems more often in men than in women. The different distribution, persistency, and induction pattern of FAT should be considered in the successful management of this type of tachycardia. (Anatol J Cardiol 2020; 24: 405-9)

478 A rare case of right ventricular ischaemia and ventricular tachycardia in neonate caused by intermittent occlusion of origin of the right coronary artery by an echogenic mass

Abstract OnBehalf Cornwall A term neonate with poor condition at birth was noted to be markedly bradycardic when crying. ECG showed first degree heart block. Echocardiogram demonstrated poor bi-ventricular function. He was treated for Hypoxic ischemic encephalopathy (HIE). In the next few hours he developed short episodes of ventricular tachycardia with left bundle branch block and non-conducted P waves suggesting an origin of tachycardia from the right ventricle. His repeat ECHO suggested that he had right ventricular infarction due to a very rare finding of intermittent occlusion of the origin of the right coronary artery by an echogenic mass. He was transferred for emergency cardiac surgery to remove a clot of 1.6cm, occluding the right coronary artery. Histology findings were in keeping with a thrombus. Thrombophilia screen for both parents and infant were negative. MRI Brain did not show evidence of HIE suggesting his poor condition at birth was secondary to intermittent coronary ischemia. Discussion: Myocardial infarction (MI) in neonates is a rarely encountered and potentially life-threatening condition, with mortality rate as high as 90%. We present one of the first reported cases of successful surgical management of an acute right coronary artery thrombosis after an early diagnosis. The cause of thrombosis remains unclear in our patient. They were born in poor condition with initial pH 6.9 and lactate of 10, but with a structurally normal heart and negative thrombophilia screen. Perinatal asphyxia is a potential cause; however there is doubt that this may be a symptom rather than cause of the right coronary artery occlusion. Early diagnosis was key in management after a high level of clinical suspicion. He made significant recovery with near normal RV function, and is currently on captopril and carvedilol post-surgery. This is one of the first cases to document near full return of cardiac function following ischaemia to the right ventricle Abstract 478 Figure. 5

Mapping the Heart

Andrea Natale, MD, FACC, FHRS, Consulting EditorView Large Image Figure ViewerDownload Hi-res image Download (PPT)Cardiac mapping is simply the correlation of the electrical activity of the heart to the underlying anatomy. In its simplest form, placement of multipolar intracardiac catheters and induction of sustained arrhythmias are a form of mapping to determine the location of an accessory pathway or the site of origin of ventricular tachycardia, and such. Since interventional electrophysiology began in the 1980s, more and more sophisticated cardiac mapping tools as well as electrophysiologic concepts have been developed to pinpoint the mechanisms and the exact anatomic localization of susceptible arrhythmic substrates. Cardiac mapping has not been fully automated, but requires detailed electrophysiology study, the use of electrophysiologic maneuvers, and deductive reasoning. Dr Shenasa has been active for over 2 decades in summarizing the advancements in cardiac mapping periodically. His current book, Cardiac Mapping is in its fifth edition. We are grateful to Drs Shenasa and Al-Ahmad for their effort of providing a summary of contemporary issues of interest in cardiac mapping for the clinical electrophysiology community. They have assembled an international panel of experts to discuss everything from anatomical considerations in mapping, the fundamentals of cardiac mapping, and unipolar mapping, all the way to the comparative advantages of the commercially available mapping systems. This issue contains useful information for electrophysiology fellows, associated professionals in electrophysiology as well as the practicing electrophysiologist. We hope the readership will find this issue useful and informative.

IDIOPATHIC VENTRICULAR TACHYCARDIA: A MENACE

SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Majority of VTs of chronic ischemic disease are subendocardial in origin, though up to 12-17% of VTs can originate from an epicardial focus. Prevalence can be as high as 25-35% in dilated nonischemic cardiomyopathy. CASE PRESENTATION: 80 year old male with no significant cardiac history presented with worsening dyspnea (NYHA I to NYHA III) over a period of 3 months with episodic dizziness. He underwent Holter monitoring, which showed 7% episodes of monomorphic non-sustained VT coinciding with symptoms. Echocardiogram showed preserved left and right ventricular systolic function. Stress testing to rule out ischemia revealed a possible of reversible posterior basal ischemia but cardiac catheterization was negative for obstructive coronary artery disease. His symptoms did not improve with long acting beta blockers. On a follow up visit, he was again noted to have long runs of slow NSVT and admitted for initiation of medical cardioversion with amiodarone which was discontinued due to prolonged QTc interval. On close inspection of EKG by electrophysiologists, it was determined that the source of his VT was epicardial as against the more commonly seen endocardial focus. Cardiac MRI was negative for structural abnormalities or scars. Patient opted for a trial of medical therapy with sotalol instead of radiofrequency ablation. Since discharge, he was admitted 3 more times with VT storm before he agreed for a successful VT ablation. DISCUSSION: Epicardial VT can be identified on an EKG, even though no single finding is considered gold standard. When initial activation starts at an epicardial site, there is an intramyocardial delay in the activation of the His Purkinje system which is reflected as initial slurring of QRS complex and is referred to as the “pseudo delta” wave. A pseudo delta wave of >34 msec and an intrinsicoid deflection time >85 msec in lead V2 has >90% specificity in predicting the epicardial origin of VT. Other parameters include a maximum deflection index (MDI) >0.55msec, Q waves in lead 1, shortest RS complex duration >121 msec. Theoretically, there may be a difference in the effectiveness of antiarrhythmic pharmacological therapy as there are differences in action potential characteristics between endo and epicardium, but no difference in efficacy has been found in studies. Epicardial radiofrequency ablation is the treatment of choice and is deemed immediately successful in 76% of patients, with about a quarter having recurrent VT by the end of a year. CONCLUSIONS: Epicardial VTs are more common than thought, tend to be idiopathic and are mostly not a risk factor for sudden cardiac death. Consider looking for it on EKG in a patient with no underlying ischemic disease or with a failed endocardial radiofrequency ablation. Reference #1: Epicardial ventricular tachycardia :Turk Kaardiyol Dem Arg-Arch Turk Soc Cardiol 2013;41(8); 746-754 Electrocardiocardiographic Recognition of the epicardial origin of ventricular tachycardia; circulation, 2004;109;1842-1847 Reference #2: How to recognize epicardial origin of ventricular tachycardia? CURRENT Cardiology Reviews, 2014,10,246-256 DISCLOSURES: No relevant relationships by Raghav Chaudhary, source=Web Response no disclosure on file for Ritu Kathuria

Sequential Factorized Autoencoder for Localizing the Origin of Ventricular Activation From 12-Lead Electrocardiograms.

This work presents a novel approach to handle the inter-subject variations existing in the population analysis of ECG, applied for localizing the origin of ventricular tachycardia (VT) from 12-lead electrocardiograms (ECGs). The presented method involves a factor disentangling sequential autoencoder (f-SAE) - realized in both long short-term memory (LSTM) and gated recurrent unit (GRU) networks - to learn to disentangle the inter-subject variations from the factor relating to the location of origin of VT. To perform such disentanglement, a pair-wise contrastive loss is introduced. The presented methods are evaluated on ECG dataset with 1012 distinct pacing sites collected from scar-related VT patients during routine pace-mapping procedures. Experiments demonstrate that, for classifying the origin of VT into the predefined segments, the presented f-SAE improves the classification accuracy by 8.94% from using prescribed QRS features, by 1.5% from the supervised deep CNN network, and 5.15% from the standard SAE without factor disentanglement. Similarly, when predicting the coordinates of the VT origin, the presented f-SAE improves the performance by 2.25 mm from using prescribed QRS features, by 1.18 mm from the supervised deep CNN network and 1.6 mm from the standard SAE. These results demonstrate the importance as well as the feasibility of the presented f-SAE approach for separating inter-subject variations when using 12-lead ECG to localize the origin of VT. This work suggests the important research direction to deal with the well-known challenge posed by inter-subject variations during population analysis from ECG signals.

Accuracy of cardiac ablation catheter guidance by means of a single equivalent moving dipole inverse algorithm to identify sites of origin of cardiac electrical activation.

We have developed a system that could potentially be used to identify the site of origin of ventricular tachycardia (VT) and to guide a catheter to that site to deliver radio-frequency ablation therapy. This system employs the Inverse Solution Guidance Algorithm based upon Single Equivalent Moving Dipole (SEMD) localization method. The system was evaluated in in vivo swine experiments. Arrays consisting of 9 or 16 bipolar epicardial electrodes and an additional mid-myocardial pacing lead were sutured to each ventricle. Focal tachycardia was simulated by applying pacing pulses to each epicardial electrode at multiple pacing rates during breath hold at the end-expiration phase. Surface potentials were recorded from 64 surface electrodes and then analyzed using the SEMD method to localize the position of the pacing electrodes. We found a close correlation between the locations of the pacing electrodes as measured in computational and real spaces. The reproducibility error of the SEMD estimation of electrode location was 0.21 ± 0.07cm. The vectors between every pair of bipolar electrodes were computed in computational and real spaces. At 120bpm, the lengths of the vectors in the computational and real space had a 95% correlation. Computational space vectors were used in catheter guidance simulations which showed that this method could reduce the distance between the real space locations of the emulated catheter tip and the emulated arrhythmia origin site by approximately 72% with each movement. We have demonstrated the feasibility of using our system to guide a catheter to the site of the emulated VT origin.

Dynamics of Pivoting Electrical Waves in a Cardiac Tissue Model.

Through a detailed mathematical analysis we seek to advance our understanding of how cardiac tissue conductances govern pivoting (spiral, scroll, rotor, functional reentry) wave dynamics. This is an important problem in cardiology since pivoting waves likely underlie most reentrant tachycardias. The problem is complex, and to advance our methods of analysis we introduce two new tools: a ray tracing method and a moving-interface model. When used in combination with an ionic model, they permit us to elucidate the role played by tissue conductances on pivoting wave dynamics. Specifically we simulate traveling electrical waves with an ionic model that can reproduce the characteristics of plane and pivoting waves in small patches of cardiac tissue. Then ray tracing is applied to the simulated pivoting waves in a manner to expose their real displacement. In this exercise we find loci with special characteristics, as well as zones where a part of a pivoting wave quickly transitions from a regenerative to a non-regenerative propagation mode. The loci themselves and the monitoring of the ionic model state variables in this zone permit to elucidate several aspects of pivoting wave dynamics. We then formulate the moving-interface model based on the information gathered with the above-mentioned analysis. Equipped with a velocity profile v(s), s: distance along of the pivoting wave contour and the steady- state action potential duration (APD) of a plane wave during entrainment, APDss(T), at period T, this simple model can predict: shape, orbit of revolution, rotation period, whether a pivoting wave will break up or not, and whether the tissue will admit pivoting waves or not. Because v(s) and APDss(T) are linked to the ionic model, dynamical analysis with the moving-interface model conveys information on the role played by tissue conductances on pivoting wave dynamics. The analysis conducted here enables us to better understand previous results on the termination of pivoting waves. We surmise the method put forth here could become a means to discover how to alter tissue conductances in a manner to terminate pivoting waves at the origin of reentrant tachycardias.

Regional modulation of action potential duration and arrhythmias by ß1- and ß2-adrenergic receptor stimulation in the porcine right ventricle

The right ventricular outflow tract (RVOT) is the main origin of idiopathic ventricular tachycardia (IVTs). Sympathetic stimulation is involved in IVTs but mechanisms underlying this preferential origin remain unknown. To determine the role of ß1- and ß2-adrenergic receptors (ß1-AR, ß2-AR) in the regional modulation of right ventricular (RV) electrophysiological properties and arrhythmias. Porcine RVs were isolated and perfused via both right and left coronary arteries. Epicardial (EPI) electrical activity was optically mapped (di-4-ANEPPS 20 μM) and APD measured at 80% repolarization (APD80) in the RVOT and posterior RV free wall region (RVFW). Regional mRNA and protein expression for ß1-AR and ß2-AR was determined respectively by RT-PCR and Western-Blot. Combined ß1- and ß2-AR stimulation (50 nM isoprenaline, ISO) shortened APD80 EPI with a larger effect in the RVFW than the RVOT. Interestingly, isolated ß2-AR stimulation (10–25 μM salbutamol, SALBU with 4 μM metoprolol, METO) only decreased APD80 significantly in the RVOT EPI ( P < 0.05). ß2-AR stimulation did not affect APD80 in the RVOT endocardium leading to a larger transmural APD gradient in this region ( P < 0.01). ß1-AR expression was lower in the RVOT than in the RVFW EPI at the mRNA and protein levels. Conversely, ß2-AR protein expression was greater in the RVOT EPI ( P < 0.05). ISO (1.8 nM–1 μM) led to a significant increase in spontaneous arrhythmias while isolated ß2-AR did not (SALBU 10–50 μM). At higher concentrations (500nM-1 μM) ISO triggered VT episodes that originated from the RVOT or the anterior RV. ß2-AR blockade (ICI 118,551 100 nM) accelerated while ß1-AR blocker METO (4 μM) slowed or abolished VT. Conlcusion These results suggest a ß2-AR specific regulation of RVOT electrophysiology but its role in the triggering of arrhythmias in this region requires further studies.

Characteristics of ventricular intracardiac electrograms of ventricular tachycardias originating from the epicardia in patients with an implantable cardioverter defibrillator.

While characteristic waveforms of 12-lead electrocardiograms have been reported to predict the epicardial origin of ventricular tachycardia (VT), it has not been fully examined whether ventricular intracardiac electrograms (VEGMs) recorded from the implantable cardioverter defibrillator (ICD) via telemetry can determine the origin of VT or not. The aim of this study was to investigate the VEGM characteristics of VT originating from the epicardia. Intracardiac VEGMs of the induced VTs, with detected sites of origin during the VT study, were recorded in 15 (23 VTs) of the 46 patients. The characteristics of the 23 VTs were evaluated using far-field and near-field VEGMs recorded via telemetry. Five of 23 VTs were found to be focused on the epicardial site (epi group) and 18 VTs were focused on the endocardium (endo group). VTs of the epi group had longer VEGM duration in far-field EGM than those of the endo group (epi group: 240 ± 49 ms vs endo group: 153 ± 45 ms; P = 0.002) and the duration from the onset to the peak of VEGM was also longer than that of the endo group (epi group: 153 ± 53 ms vs endo group: 63 ± 28 ms; P < 0.001). There was no difference in the V wave duration in tip-ring EGM between both groups (epi group: 122 ± 52 ms vs endo group: 98 ± 6 ms; P = 0.377). Evaluation of intracardiac VEGM before VT ablation may be helpful to predict the epicardial origin of VT in patients with an ICD.

SEARCH OF THE STRESS INDUSED VENTRICULAR TACHICARDIA REASONS — THE METABOLIC THERAPY OPPORTUNITIES

A clinical case of a 56-year-old man is presented in which only ventricular tachycardia without clinical and ECG criteria of myocardial ischemia is recorded on the exercise test. The ventricular tachycardia was the only reason for stopping the test. This clinical case demonstrates all the difficulties in determining the genesis of ventricular arrhythmias induced by exercise. The purpose of the work was to show all the difficulties in determining the genesis of exercise-induced ventricular arrhythmia. The literature references related to the exercise-induced ventricular arrhythmia differentiation is rather poor. It is only known that if a patient develops and progresses ventricular arrhythmia, a tredmill test is considered questionable. Exerciseinduced ventricular arrhythmias especially ventricular tachycardia, are the most dangerous. Therefore, additional diagnostic methods were used to reveal the main disease as the background of ventricular tachycardia. Results of pharmacological test with nitroglycerine were the indication of the ischemic origin of ventricular tachycardia. Coronary angiography did not reveal coronary artery stenoses. Positron emission tomography revealed coronary microcirculation disturbance after which a decision about metabolic therapy with Mexicor was made. The correct choice of the drug (Mеxisor) was confirmed by the results of control studies — improvement of metabolism and antiarrhythmic effect. The article concludes that the choice of the treatment exercise-induced ventricular arrhythmia in patients with stable coronary artery disease should be individual and pathogenetic.

Validation and Opportunities of Electrocardiographic Imaging: From Technical Achievements to Clinical Applications.

Electrocardiographic imaging (ECGI) reconstructs the electrical activity of the heart from a dense array of body-surface electrocardiograms and a patient-specific heart-torso geometry. Depending on how it is formulated, ECGI allows the reconstruction of the activation and recovery sequence of the heart, the origin of premature beats or tachycardia, the anchors/hotspots of re-entrant arrhythmias and other electrophysiological quantities of interest. Importantly, these quantities are directly and non-invasively reconstructed in a digitized model of the patient’s three-dimensional heart, which has led to clinical interest in ECGI’s ability to personalize diagnosis and guide therapy. Despite considerable development over the last decades, validation of ECGI is challenging. Firstly, results depend considerably on implementation choices, which are necessary to deal with ECGI’s ill-posed character. Secondly, it is challenging to obtain (invasive) ground truth data of high quality. In this review, we discuss the current status of ECGI validation as well as the major challenges remaining for complete adoption of ECGI in clinical practice. Specifically, showing clinical benefit is essential for the adoption of ECGI. Such benefit may lie in patient outcome improvement, workflow improvement, or cost reduction. Future studies should focus on these aspects to achieve broad adoption of ECGI, but only after the technical challenges have been solved for that specific application/pathology. We propose ‘best’ practices for technical validation and highlight collaborative efforts recently organized in this field. Continued interaction between engineers, basic scientists, and physicians remains essential to find a hybrid between technical achievements, pathological mechanisms insights, and clinical benefit, to evolve this powerful technique toward a useful role in clinical practice.

Electrocardiographic criteria of epicardial ventricular tachycardia with anterior origin.

ECG criteria for identifying an epicardial origin of ventricular tachycardia (VT) have mainly been described for VTs with basal-superior and lateral origin. The aim of this study was to determine ECG criteria for epicardial VTs with anterior origin as a guide for trans-pericardial ablation. Among 22 patients undergoing successful ablation of VTs from the anterior myocardial wall, 14 patients underwent endocardial ablation and 8 patients underwent epicardial ablation. VTs with anterior origin ablated epicardially had widened QS complexes in precordial leads with staircase-shaped notching and slowing of the descent to the nadir of S. In comparison, endocardial VTs with anterior origin usually had narrower QS complexes with a smooth and fast downstroke to the nadir of S. The duration of the negative pseudodelta wave was longer in epicardial VTs (55 ± 12ms) compared to endocardial VTs (22 ± 12ms). The interval "time to the nadir of S" in patients with anterior VT origin was longer in epicardial VTs (121 ± 16ms) than in endocardial VTs (80 ± 22ms). The QRS duration was also longer in patients with epicardial origin (212 ± 19ms) than with endocardial VT origin (166 ± 30ms). Epicardial origin of VTs arising from the anterior myocardial wall produces a slowing, widening and staircase-shaped notching in the initial VT-QS complex. Thus, the morphology of the initial part of the QS complex in precordial leads can be used as a guide for trans-pericardial ablation of VTs with anterior origin.

P4841To the root of the matter: better long-term success of para-Hisian atrial tachycardias ablated from the aortic root than any other origin of atrial tachycardia

P4841To the root of the matter: better long-term success of para-Hisian atrial tachycardias ablated from the aortic root than any other origin of atrial tachycardia

Determinants of slowed conduction in premature ventricular beats induced during programmed stimulations in perfused guinea-pig heart.

What is the central question of this study? Is the slowed conduction upon premature ventricular activations during clinical electrophysiological testing attributable to the prolonged activation latency, or increased impulse propagation time, or both? What is the main finding and its importance? Prolonged activation latency at the stimulation site is the critical determinant of conduction slowing and associated changes in the ventricular response intervals in premature beats initiated during phase 3 repolarization in perfused guinea-pig heart. These relations are likely to have an effect on arrhythmia induction and termination independently of the presence of ventricular conduction defects or the proximity of the stimulation site to the re-entrant circuit. During cardiac electrophysiological testing, slowed conduction upon premature ventricular activation can limit the delivery of the closely coupled impulses from the stimulation site to the region of tachycardia origin. In order to examine the contributing factors, in this study, cardiac conduction intervals and refractory periods were determined from left ventricular (LV) and the right ventricular (RV) monophasic action potential recordings obtained in perfused guinea-pig hearts. A premature activation induced immediately after the termination of the refractory period was associated with conduction slowing. The latter was primarily accounted for by the markedly increased (+54%) activation latency at the LV stimulation site, with only negligible changes (+12%) noted in the LV-to-RV delay. The prolonged activation latency was acting to limit the shortest interval at which two successive action potentials can be induced in the LV and RV chambers. The prolongation of the activation latency in premature beats was accentuated upon an increase in the stimulating current intensity, or during hypokalaemia. This change was related to the reduced ratio of the refractory period to the action potential duration, which allowed extrastimulus capture to occur earlier during phase 3 repolarization. Flecainide, a Na+ channel blocker, prolonged both the activation latency and the LV-to-RV delay, without changing their relative contributions to conduction slowing. In summary, these findings suggest that the activation latency is the critical determinant of conduction slowing and associated changes in the ventricular response intervals upon extrastimulus application during phase 3 of the action potential.

A QRS axis–based algorithm to identify the origin of scar-related ventricular tachycardia in the 17-segment American Heart Association model

Previously proposed algorithms to predict the ventricular tachycardia (VT) exit site have been based on diverse left ventricular models, but none of them identify the precise region of origin in the electroanatomic map. Moreover, no electrocardiographic (ECG) algorithm has been tested to predict the region of origin of scar-related VTs in patients with nonischemic cardiomyopathy. The purpose of this study was to validate a simple ECG algorithm to identify the segment of origin (SgO) of VT relative to the 17-segment American Heart Association model in patients with structural heart disease (SHD). The study included 108 consecutive patients with documented VT and SHD [77 (71%) with coronary artery disease]. A novel frontal plane axis-based ECG algorithm (highest positive or negative QRS voltage) together with the polarity in leads V3 and V4 was used to predict the SgO of VT. The actual SgO of VT was obtained from the analysis of the electroanatomic map during the procedure. Conventional VT mapping techniques were used to identify the VT exit. In total, 149 12-lead ECGs of successfully ablated VT were analyzed. The ECG-suggested SgO matched with the actual SgO in 122 of the 149 VTs (82%). In 21 of the 27 mismatched ECG-suggested SgOs (77.8%), the actual SgO was adjacent to the segment suggested by the ECG. There were no differences in the accuracy of the algorithm based on the SgO or the type of SHD. This novel QRS axis-based algorithm accurately identifies the SgO of VT in the 17-segment American Heart Association model in patients with SHD.

9) Idiopathic Ventricular Tachycardia in an Adolescent Female

Introduction: Idiopathic ventricular tachycardia is defined as an arrhythmia without evidence of a predisposing factor such as structural heart disease or a secondary medical cause. Pharmacologic management may differ based on the anatomic origin of the tachycardia. This case highlights the management of an adolescent patient with idiopathic ventricular tachycardia and a brief review of current literature. Case Report: A previously healthy 13 year old female presented with the sensation of palpitations after soccer practice. Initial EKG demonstrated a wide QRS ventricular tachycardia at 195 beats per minute with a left …

An electrocardiographic diagnostic model for differentiating left from right ventricular outflow tract tachycardia origin.

Although several electrocardiographic (ECG) algorithms have been proposed for differentiating the origins of outflow tract ventricular arrhythmias, the most optimal one has not been agreed on. The purpose of this study was to establish an ECG diagnostic model based on the previous ECG algorithms. The following ECG diagnostic model, Y=-1.15×( TZ )-0.494×(V2S/V3R), was developed by standard 12-lead ECG algorithms in 488 patients with idiopathic premature ventricular contractions or ventricular tachycardia with a left bundle branch block pattern and inferior axis QRS morphology. Binary logistic regression analysis was performed to establish the ECG diagnostic model. The ECG diagnostic model consisted of two ECG algorithms-the transition zone (TZ) index and V2S/V3R index. The area under the curve by receiver operating characteristic curve analysis for the ECG diagnostic model was 0.88, with a cut-off value of ≥ -0.76 predicting a left ventricular outflow tract (LVOT) origin with a sensitivity of 82% and a specificity of 86%, which was higher than other ECG algorithms in this study. The predictive accuracy of the ECG diagnostic model was also the best among all ECG algorithms in patients with a lead V3 precordial transition. This model was tested prospectively in 207 patients with a sensitivity of 90%, a specificity of 87%, and Youden index of 0.77. A highly accurate ECG diagnostic model for correctly differentiating LVOT origin from right ventricular outflow tract origin was developed.

Regional β-adrenergic regulation of action potential duration and arrhythmias in the pig right ventricle

The right ventricular outflow tract (RVOT) is the main origin of idiopathic ventricular tachycardia (VT). Although these arrhythmias appear to be cAMP-dependent, the actual mechanisms leading to VT remain uncertain. Here we studied β-adrenergic regulation of action potential duration (APD) in the healthy pig right ventricle (RV). To determine regional β-adrenergic regulation of APD and arrhythmias in the RVOT. The RV of 4 pig hearts were isolated and perfused via both the coronary arteries. Epicardial electrical activity was optically mapped (di-4-ANEPPS 20 μM) and APD measured at 80% repolarization (APD80) in the RVOT and posterior RV free wall region (RVFW). Regional mRNA and protein expression of β-adrenergic receptors was determined respectively by RT-PCR and Western-Blot. The expression of β1-adrenergic receptor (β1-AR) was lower in the RVOT at the mRNA level ( P < 0.05) but remained unchanged at the protein level compared to the RVFW while β2-adrenergic receptor (β2-AR) expression remained similar in both regions. At lower concentrations (0.6–10 nM), isoprenaline (ISO) led to a prolongation of APD80 in the RVOT and the RVFW. Higher ISO concentrations (500 nM–1 μM) led to a larger APD80 shortening in the RVOT than in the RVFW and triggered VT episodes that originated from the RVOT or the anterior RV. β2-AR blockade (ICI 118,551 100 nM) accelerated while β1-AR blocker Metoprolol (4 μM) slowed or abolished VT. Similar ISO concentrations triggered bursts of Ca2+ transients in RVOT myocytes that stopped upon ISO washout while these events remained rare in RVFW myocytes. β-adrenergic stimulation differentially regulates APD80 in the RVOT and RVFW. Although β1-AR expression was similar in the 2 regions, ISO preferentially shortened APD and triggered arrhythmia in the RVOT. These results suggest the presence of a high sensitivity of RVOT electrophysiology to β-adrenergic stimulation.