Papillary muscle ventricular ectopy ablation in a malignant mitral valve prolapse: Ablation in Malignant Mitral Valve Prolapse: Ablation in Malignant Mitral Valve Prolapse.

Patients with mitral valve prolapse (MVP) have a heterogeneous clinical spectrum, ranging from benign to severe clinical presentations such as sudden cardiac death (SCD). Some of the markers of "arrhythmic MVP" include inverted/biphasic T-waves, QT prolongation, and polymorphic premature ventricular contractions (PVCs) originating from the left ventricular outflow tract and papillary muscles (PMs). The genesis of arrhythmias in MVP recognizes the combination of the substrate (fibrosis) and the trigger (mechanical stretch). Therefore, ablation of ventricular arrhythmias originating from PMs in a patient with MVP can be considered an adjunctive strategy to lower the arrhythmic burden and reduce the risk of ICD shocks.

How to evaluate premature ventricular beats in the athlete: critical review and proposal of a diagnostic algorithm.

Although premature ventricular beats (PVBs) in young people and athletes are usually benign, they may rarely mark underlying heart disease and risk of sudden cardiac death during sport. This review addresses the prevalence, clinical meaning and diagnostic/prognostic assessment of PVBs in the athlete. The article focuses on the characteristics of PVBs, such as the morphological pattern of the ectopic QRS and the response to exercise, which accurately stratify risk. We propose an algorithm to help the sport and exercise physician manage the athlete with PVBs. We also address (1) which athletes need more indepth investigation, including cardiac MRI to exclude an underlying pathological myocardial substrate, and (2) which athletes can remain eligible to competitive sports and who needs to be excluded.

Magnetic resonance imaging abnormalities in the basal interventricular septum of patients with left ventricular outflow tract arrhythmias.

INTRODUCTION: Concealed structural abnormalities were detected by delayed enhancement - magnetic resonance imaging (DE-MRI) in patients with apparently idiopathic tachycardia of left ventricular (LV) origin. Basal septal fibrosis was evaluated as a potential arrhythmia substrate in patients with left ventricular outflow tract (LVOT) arrhythmias. METHODS AND RESULTS: A total of 22 patients with LVOT arrhythmias, including frequent monomorphic premature ventricular complexes (PVCs) in 15 patients and ventricular tachycardia (VT) in 7 patients, underwent catheter ablation and DE-MRI. A total of 19 patients with frequent PVCs and 17 patients with idiopathic VT of other origin served as a control group. Basal septal intramural fibrosis as thin strip-shaped intramyocardial DE or as marked intramyocardial DE involving >25% of wall thickness was detected more frequently in patients with LVOT arrhythmias (41% and 32%) than in patients with non LVOT arrhythmias (14% and 3%). After successful ablation, 4/16 patients with basal septal intramural fibrosis and LVOT PVCs (n = 3) or LVOT VT (n = 1) compared with no patient without basal septal fibrosis experienced episodes of sustained VT with similar or different QRS morphology resulting in ICD therapy in three patients. Follow-up DE-MRI after PVC ablation (17 ± 7 months) revealed an increase in LV ejection fraction from 49 ± 5% to 56 ± 5% (n = 9) but the amount of septal DE remained unchanged. CONCLUSIONS: Basal septal intramural fibrosis may serve as the arrhythmia substrate in a substantial part of patients with premature ventricular complexes (PVCs) and VT originating from the LVOT and identifies patients with continued risk for VT recurrence after initially successful ablation of LVOT arrhythmias.

Influence of myocardial scar on the response to frequent premature ventricular complex ablation.

OBJECTIVE: This study aims to evaluate the influence of myocardial scar after premature ventricular complexes (PVC) ablation in patients with left ventricular (LV) dysfunction. METHODS: 70 consecutive patients (58±11 years, 58 (83%) men, 23% (18-32) mean PVC burden) with LV dysfunction and frequent PVCs submitted for ablation were included. A late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) was performed prior to the ablation and a quantitative and qualitative analysis of the scar was done. RESULTS: Left ventricular ejection fraction progressively improved from 34.3%±9% at baseline to 44.4%±12% at 12 months (p<0.01) and 48 (69%) patients were echocardiographic responders. New York Heart Association class improved from 1.96±0.9 points at baseline to 1.36±0.6 at 12 months (p<0.001). Brain natriuretic peptide decreased from 120 (60-284) to 46 (23-81) pg/mL (p=0.04). Twenty-nine (41%) patients showed scar in the preprocedural LGE-CMR with a mean scar mass of 10.4 (5-20) g. Mean scar mass was significantly smaller in responders than in non-responders (0 (0-4.7) g vs 2 (0-14) g, respectively, p=0.017). PVC burden reduction (OR 1.09 (1.01-1.16), p=0.02) and scar mass (OR 0.9 (0.81-0.99), p=0.04) were independent predictors of response, but the former showed a higher accuracy. CONCLUSIONS: Presence of myocardial scar modulates, but does not preclude, the probability of response to PVC ablation in patients with LV dysfunction.

Genome-wide association study and meta-analysis identify loci associated with ventricular and supraventricular ectopy.

The genetic basis of supraventricular and ventricular ectopy (SVE, VE) remains largely uncharacterized, despite established genetic mechanisms of arrhythmogenesis. To identify novel genetic variants associated with SVE/VE in ancestrally diverse human populations, we conducted a genome-wide association study of electrocardiographically identified SVE and VE in five cohorts including approximately 43,000 participants of African, European and Hispanic/Latino ancestry. In thirteen ancestry-stratified subgroups, we tested multivariable-adjusted associations of SVE and VE with single nucleotide polymorphism (SNP) dosage. We combined subgroup-specific association estimates in inverse variance-weighted, fixed-effects and Bayesian meta-analyses. We also combined fixed-effects meta-analytic t-test statistics for SVE and VE in multi-trait SNP association analyses. No loci reached genome-wide significance in trans-ethnic meta-analyses. However, we found genome-wide significant SNPs intronic to an apoptosis-enhancing gene previously associated with QRS interval duration (FAF1; lead SNP rs7545860; effect allele frequency = 0.02; P = 2.0 × 10-8) in multi-trait analysis among European ancestry participants and near a locus encoding calcium-dependent glycoproteins (DSC3; lead SNP rs8086068; effect allele frequency = 0.17) in meta-analysis of SVE (P = 4.0 × 10-8) and multi-trait analysis (P = 2.9 × 10-9) among African ancestry participants. The novel findings suggest several mechanisms by which genetic variation may predispose to ectopy in humans and highlight the potential value of leveraging pleiotropy in future studies of ectopy-related phenotypes.

Feasibility of Performing Radiofrequency Catheter Ablation and Endomyocardial Biopsy in the Same Setting.

In patients with unexplained cardiomyopathy, electroanatomical mapping can identify abnormal tissue to target during electrophysiology-guided endomyocardial biopsy (EP-guided EMB). The objective of this study is to determine whether catheter ablation performed in the same setting as EP-guided EMB increases procedural risk. Sixty-seven patients (mean age 54.4 ± 13.8, 57% male) undergoing EP-guided EMB were included. Radiofrequency catheter ablation was performed in 17 patients (25%) for ventricular arrhythmias and in 2 (3%) for typical atrial flutter. Femoral arterial access was obtained in 90% ablation patients and 40% biopsy-only patients; vascular access complications were more common in the ablation group than in the EMB-only group (p = 0.02). There were no significant differences in rate of tricuspid regurgitation, thromboembolism, or pericardial effusion, whether procedural anticoagulation was used. In conclusion, catheter ablation and procedural anticoagulation can be combined with EP-guided EMB with an increased risk of vascular access complications, but no significant increase in intracardiac complications.

Activation of ß1-adrenoceptors may not be involved in arrhythmogenesis in ischemic heart disease.

Although ischemic heart disease is invariably associated with marked activation of sympathetic nervous system, elevated levels of circulating catecholamines and lethal ventricular arrhythmias, the mechanisms of arrhythmogenesis due to myocardial ischemia are not fully understood. Since catecholamines are known to produce stimulatory effects in the heart mainly by acting on ß1-adrenoceptors, this study was undertaken to test the involvement of these receptors in the development of arrhythmias due to myocardial infarction (MI) induced upon occluding the left coronary artery in rats for a period of 2 h. The animals were treated with or without atenolol (20 mg/kg; daily), a selective ß1-adrenoceptors blocker, for 14 days before inducing MI. No alterations in the number of MIinduced episodes and incidence or duration of different types of arrhythmias were observed. In fact, the incidence of trigemines and reversible ventricular fibrillation due to MI were significantly increased in the atenolol-treated animals. These observations support the view that the activation of ß;1-adrenoceptors may not be exclusively involved in the development of arrhythmias during the occurrence of ischemic heart disease and other mechanisms can underlie the electric instability of such damaged heart.

Stochastic spontaneous calcium release events and sodium channelopathies promote ventricular arrhythmias.

Premature ventricular complexes (PVCs), the first initiating beats of a variety of cardiac arrhythmias, have been associated with spontaneous calcium release (SCR) events at the cell level. However, the mechanisms underlying the degeneration of such PVCs into arrhythmias are not fully understood. The objective of this study was to investigate the conditions under which SCR-mediated PVCs can lead to ventricular arrhythmias. In particular, we sought to determine whether sodium (Na+) current loss-of-function in the structurally normal ventricles provides a substrate for unidirectional conduction block and reentry initiated by SCR-mediated PVCs. To achieve this goal, a stochastic model of SCR was incorporated into an anatomically accurate compute model of the rabbit ventricles with the His-Purkinje system (HPS). Simulations with reduced Na+ current due to a negative-shift in the steady-state channel inactivation showed that SCR-mediated delayed afterdepolarizations led to PVC formation in the HPS, where the electrotonic load was lower, conduction block, and reentry in the 3D myocardium. Moreover, arrhythmia initiation was only possible when intrinsic electrophysiological heterogeneity in action potential within the ventricles was present. In conclusion, while benign in healthy individuals SCR-mediated PVCs can lead to life-threatening ventricular arrhythmias when combined with Na+ channelopathies.

Empiema intraventricular piogénico por Veillonella parvula en un recién nacido prematuro / Pyogenic intraventricular empyema owing to Veillonella parvulain a preterm infant

No disponible

Remodeling of repolarization and arrhythmia susceptibility in a myosin-binding protein C knockout mouse model.

Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiac diseases and among the leading causes of sudden cardiac death (SCD) in the young. The cellular mechanisms leading to SCD in HCM are not well known. Prolongation of the action potential (AP) duration (APD) is a common feature predisposing hypertrophied hearts to SCD. Previous studies have explored the roles of inward Na+ and Ca2+ in the development of HCM, but the role of repolarizing K+ currents has not been defined. The objective of this study was to characterize the arrhythmogenic phenotype and cellular electrophysiological properties of mice with HCM, induced by myosin-binding protein C (MyBPC) knockout (KO), and to test the hypothesis that remodeling of repolarizing K+ currents causes APD prolongation in MyBPC KO myocytes. We demonstrated that MyBPC KO mice developed severe hypertrophy and cardiac dysfunction compared with wild-type (WT) control mice. Telemetric electrocardiographic recordings of awake mice revealed prolongation of the corrected QT interval in the KO compared with WT control mice, with overt ventricular arrhythmias. Whole cell current- and voltage-clamp experiments comparing KO with WT mice demonstrated ventricular myocyte hypertrophy, AP prolongation, and decreased repolarizing K+ currents. Quantitative RT-PCR analysis revealed decreased mRNA levels of several key K+ channel subunits. In conclusion, decrease in repolarizing K+ currents in MyBPC KO ventricular myocytes contributes to AP and corrected QT interval prolongation and could account for the arrhythmia susceptibility.NEW & NOTEWORTHY Ventricular myocytes isolated from the myosin-binding protein C knockout hypertrophic cardiomyopathy mouse model demonstrate decreased repolarizing K+ currents and action potential and QT interval prolongation, linking cellular repolarization abnormalities with arrhythmia susceptibility and the risk for sudden cardiac death in hypertrophic cardiomyopathy.

Exclusion of alternative exon 33 of CaV1.2 calcium channels in heart is proarrhythmogenic.

Alternative splicing changes the CaV1.2 calcium channel electrophysiological property, but the in vivo significance of such altered channel function is lacking. Structure-function studies of heterologously expressed CaV1.2 channels could not recapitulate channel function in the native milieu of the cardiomyocyte. To address this gap in knowledge, we investigated the role of alternative exon 33 of the CaV1.2 calcium channel in heart function. Exclusion of exon 33 in CaV1.2 channels has been reported to shift the activation potential -10.4 mV to the hyperpolarized direction, and increased expression of CaV1.2Δ33 channels was observed in rat myocardial infarcted hearts. However, how a change in CaV1.2 channel electrophysiological property, due to alternative splicing, might affect cardiac function in vivo is unknown. To address these questions, we generated mCacna1c exon 33-/--null mice. These mice contained CaV1.2Δ33 channels with a gain-of-function that included conduction of larger currents that reflects a shift in voltage dependence and a modest increase in single-channel open probability. This altered channel property underscored the development of ventricular arrhythmia, which is reflected in significantly more deaths of exon 33-/- mice from ß-adrenergic stimulation. In vivo telemetric recordings also confirmed increased frequencies in premature ventricular contractions, tachycardia, and lengthened QT interval. Taken together, the significant decrease or absence of exon 33-containing CaV1.2 channels is potentially proarrhythmic in the heart. Of clinical relevance, human ischemic and dilated cardiomyopathy hearts showed increased inclusion of exon 33. However, the possible role that inclusion of exon 33 in CaV1.2 channels may play in the pathogenesis of human heart failure remains unclear.

JPH-2 interacts with Cai-handling proteins and ion channels in dyads: Contribution to premature ventricular contraction-induced cardiomyopathy.

BACKGROUND: In a canine model of premature ventricular contraction-induced cardiomyopathy (PVC-CM), Cav1.2 is downregulated and misplaced from transverse tubules (T tubules). Junctophilin-2 (JPH-2) is also downregulated. OBJECTIVES: The objectives of this study were to understand the role of JPH-2 in PVC-CM and to probe changes in other proteins involved in dyad structure and function. METHODS: We quantify T-tubule contents (di-8-ANEPPS fluorescence in live myocytes), examine myocyte ultrastructures (electron microscopy), probe JPH-2-interacting proteins (co-immunoprecipitation), quantify dyad and nondyad protein levels (immunoblotting), and examine subcellular distributions of dyad proteins (immunofluorescence/confocal microscopy). We also test direct JPH-2 modulation of channel function (vs indirect modulation through dyad formation) using heterologous expression. RESULTS: PVC myocytes have reduced T-tubule contents but otherwise normal ultrastructures. Among 19 proteins examined, only JPH-2, bridging integrator-1 (BIN-1), and Cav1.2 are highly downregulated in PVC hearts. However, statistical analysis indicates a general reduction in dyad protein levels when JPH-2 is downregulated. Furthermore, several dyad proteins, including Na/Ca exchanger, are missing or shifted from dyads to the peripheral surface in PVC myocytes. JPH-2 directly or indirectly interacts with Cai-handling proteins, Cav1.2 and KCNQ1, although not BIN-1 or other scaffolding proteins tested. Expression in mammalian cells that do not have dyads confirms direct JPH-2 modulation of the L-type Ca channel current (Cav1.2/voltage-gated Ca channel ß subunit 2) and slow delayed rectifier current (KCNQ1/KCNE1). CONCLUSION: JPH-2 is more than a "dyad glue": it can modulate Cai handling and ion channel function in the dyad region. Downregulation of JPH-2, BIN-1, and Cav1.2 plays a deterministic role in PVC-CM. Dissecting the hierarchical relationship among the three is necessary for the design of therapeutic interventions to prevent the progression of PVC-CM.

A Computational Study of the Factors Influencing the PVC-Triggering Ability of a Cluster of Early Afterdepolarization-Capable Myocytes.

Premature ventricular complexes (PVCs), which are abnormal impulse propagations in cardiac tissue, can develop because of various reasons including early afterdepolarizations (EADs). We show how a cluster of EAD-generating cells (EAD clump) can lead to PVCs in a model of cardiac tissue, and also investigate the factors that assist such clumps in triggering PVCs. In particular, we study, through computer simulations, the effects of the following factors on the PVC-triggering ability of an EAD clump: (1) the repolarization reserve (RR) of the EAD cells; (2) the size of the EAD clump; (3) the coupling strength between the EAD cells in the clump; and (4) the presence of fibroblasts in the EAD clump. We find that, although a low value of RR is necessary to generate EADs and hence PVCs, a very low value of RR leads to low-amplitude EAD oscillations that decay with time and do not lead to PVCs. We demonstrate that a certain threshold size of the EAD clump, or a reduction in the coupling strength between the EAD cells, in the clump, is required to trigger PVCs. We illustrate how randomly distributed inexcitable obstacles, which we use to model collagen deposits, affect PVC-triggering by an EAD clump. We show that the gap-junctional coupling of fibroblasts with myocytes can either assist or impede the PVC-triggering ability of an EAD clump, depending on the resting membrane potential of the fibroblasts and the coupling strength between the myocyte and fibroblasts. We also find that the triggering of PVCs by an EAD clump depends sensitively on factors like the pacing cycle length and the distribution pattern of the fibroblasts.

Development of new anatomy reconstruction software to localize cardiac isochrones to the cardiac surface from the 12 lead ECG.

Non-invasive electrocardiographic imaging (ECGI) of the cardiac muscle can help the pre-procedure planning of the ablation of ventricular arrhythmias by reducing the time to localize the origin. Our non-invasive ECGI system, the cardiac isochrone positioning system (CIPS), requires non-intersecting meshes of the heart, lungs and torso. However, software to reconstruct the meshes of the heart, lungs and torso with the capability to check and prevent these intersections is currently lacking. Consequently the reconstruction of a patient specific model with realistic atrial and ventricular wall thickness and incorporating blood cavities, lungs and torso usually requires additional several days of manual work. Therefore new software was developed that checks and prevents any intersections, and thus enables the use of accurate reconstructed anatomical models within CIPS. In this preliminary study we investigated the accuracy of the created patient specific anatomical models from MRI or CT. During the manual segmentation of the MRI data the boundaries of the relevant tissues are determined. The resulting contour lines are used to automatically morph reference meshes of the heart, lungs or torso to match the boundaries of the morphed tissue. Five patients were included in the study; models of the heart, lungs and torso were reconstructed from standard cardiac MRI images. The accuracy was determined by computing the distance between the segmentation contours and the morphed meshes. The average accuracy of the reconstructed cardiac geometry was within 2mm with respect to the manual segmentation contours on the MRI images. Derived wall volumes and left ventricular wall thickness were within the range reported in literature. For each reconstructed heart model the anatomical heart axis was computed using the automatically determined anatomical landmarks of the left apex and the mitral valve. The accuracy of the reconstructed heart models was well within the accuracy of the used medical image data (pixel size <1.5mm). For the lungs and torso the number of triangles in the mesh was reduced, thus decreasing the accuracy of the reconstructed mesh. A novel software tool has been introduced, which is able to reconstruct accurate cardiac anatomical models from MRI or CT within only a few hours. This new anatomical reconstruction tool might reduce the modeling errors within the cardiac isochrone positioning system and thus enable the clinical application of CIPS to localize the PVC/VT focus to the ventricular myocardium from only the standard 12 lead ECG.

The quantification of the QT-RR interaction in ECG signal using the detrended fluctuationanalysis and ARARX modelling.

In this paper, the detrended fluctuation analysis DFA is used to investigate and quantify the QT-RR interaction in different pathologic cases in order to distinguish between them. The study is carried out on the ECG signals of MIT-BIH universal database. Different ECG signals related to cardiac pathological cases are concerned with this study. These are: Premature Ventricular Contraction (PVC) (9 cases), Right Bundle Branch Block (RBBB) (4 cases), Left Bundle Branch Block (LBBB) (2 cases), Atrial Premature Beat (APB) (4 cases), Paced Beat (PB) (4 cases), and other pathologic cases with different severity (10 cases). All this cases are compared to the 15 normal cases. The obtained results show that the DFA can identify the healthy subject from the pathologic cases according to the values of the scaling exponent α. The results indicate that α varies between 0.5 and 1 in all cases which means that there is a long range correlation in RR and QT series. The QT and RR series are also modelled using the ARARX model. The parameters of the model are then extracted. The power spectral density (PSD) is estimated by using these parameters in order to provide further information about the causal interactions within the signals and also to determine the power scaling exponent ß. This scaling exponent confirms the relationship between RR and QT intervals in all the studied cases except in APB and PB cases where the behaviour is similar to that of the white noise. The QT variability degrees are calculated and the DFA is applied on it. The obtained results show a long range correlation between RR and QT intervals in all cases and an ambiguity in the APB case. The DFA is compared to the Poincaré method in order to evaluate the algorithm performance using the Fuzzy Sugeno classifier is used for this purpose.

Effects of Nardostachys chinensis on spontaneous ventricular arrhythmias in rats with acute myocardial infarction.

OBJECTIVES: To investigate the effects and mechanisms of Nardostachys chinensis (NC) on spontaneous ventricular arrhythmias in rats with hyper-acute myocardial infarction (AMI). METHODS: Seventy-two rats were randomly divided into the control group (n = 24), metoprolol group (n = 24), and the NC group (n = 24). Premature ventricular contractions (PVCs), ventricular tachycardias (VTs), ventricular fibrillations (VFs), and blood pressure were monitored for 4 hours after coronary artery ligation. The connexin 43 (Cx43) expression in ventricular myocardium was measured by immunohistochemistry, Western blot, and real-time RT-PCR. RESULTS: Compared with the control, metoprolol and NC decreased the VF incidence (50% vs. 4.2%, P < 0.001, and 50% vs. 12.5%, P = 0.005, respectively). There was a steady decrease in the cumulative number of PVCs and VTs within 4 hours from ligating in 3 groups. Compared with the control, metoprolol and NC reduced the cumulative number of VTs and PVCs. Compared with control, metoprolol and NC decreased the infarct size of the left ventricular tissue (55.98% ± 6.20% vs. 39.13% ± 4.53%, P < 0.001, and 55.98% ± 6.20% vs. 42.39% ± 3.44%, P < 0.001, respectively). The results from immunohistochemistry, Western blot, and real-time RT-PCR showed that the protein expression of Cx43 in the control group was significantly lower than that in the metoprolol and NC groups in the infarcted zone. CONCLUSIONS: NC decreased the incidence of spontaneous ventricular arrhythmias (especially VF), reduced Cx43 degradation, and improved Cx43 redistribution in myocardial infarcted zone in rats with hyper-AMI. The data of the present study indicated that NC may be a promising drug in the future to prevent patients with AMI from lethal ventricular arrhythmias in prehospital setting.

Sodium current reduction unmasks a structure-dependent substrate for arrhythmogenesis in the normal ventricles.

BACKGROUND: Organ-scale arrhythmogenic consequences of source-sink mismatch caused by impaired excitability remain unknown, hindering the understanding of pathophysiology in disease states like Brugada syndrome and ischemia. OBJECTIVE: We sought to determine whether sodium current (INa) reduction in the structurally normal heart unmasks a regionally heterogeneous substrate for the induction of sustained arrhythmia by premature ventricular contractions (PVCs). METHODS: We conducted simulations in rabbit ventricular computer models with 930 unique combinations of PVC location (10 sites) and coupling interval (250-400 ms), INa reduction (30 or 40% of normal levels), and post-PVC sinus rhythm (arrested or persistent). Geometric characteristics and source-sink mismatch were quantitatively analyzed by calculating ventricular wall thickness and a newly formulated 3D safety factor (SF), respectively. RESULTS: Reducing INa to 30% of its normal level created a substrate for sustained arrhythmia induction by establishing large regions of critical source-sink mismatch (SF<1) for ectopic wavefronts propagating from thin to thick tissue. In the same simulations but with 40% of normal INa, PVCs did not induce reentry because the volume of tissue with SF<1 was >95% smaller. Likewise, when post-PVC sinus activations were persistent instead of arrested, no ectopic excitations initiated sustained reentry because sinus activation breakthroughs engulfed the excitable gap. CONCLUSION: Our new SF formulation can quantify ectopic wavefront propagation robustness in geometrically complex 3D tissue with impaired excitability. This novel methodology was applied to show that INa reduction precipitates source-sink mismatch, creating a potent substrate for sustained arrhythmia induction by PVCs originating near regions of ventricular wall expansion, such as the RV outflow tract.

[Preferential conduction to right ventricular outflow track leads to left bundle-branch block morphology in patient with premature ventricular contraction originating from the aortic sinus cusp].

OBJECTIVE: The purpose of this study was to explore the relationship between originate and breakout and radiofrequency catheter ablation strategy in patients undergoing radiofrequency ablation for premature ventricular contractions originating from the aortic sinus cusp (ASC) using 3-dimensional electro anatomic mapping. METHODS: This study included 21 consecutive patients (10 male) underwent ablation for frequent PVCs originating from ASC in our hospital between May 2009 and February 2012. Electro anatomic mapping and ablation of right ventricular outflow track (RVOT) and left ventricular outflow track (LVOT) were performed with the 7F 4-mm-tip ablation catheter from right femoral vein and artery. Activation mapping and pacing mapping were performed in all patients. RESULTS: Ablation was successful in all 21 patients successful ablation target in left coronary sinus cusp (LCC, n = 17), in right coronary sinus cusp (RCC, n = 2) and in noncoronary sinus cusp (NCC, n = 2). Seven patients showed a RBBB morphology (group A) and 14 patients showed a LBBB morphology (group B). In group A, earliest ventricular activation (EVA) was recorded 22 - 34 (27.4 ± 4.6) ms earlier before QRS at the site of catheter ablation in ASC. In group B, EVA was later in RVOT than that in ASC in 5 patients and EVA at the site of catheter ablation in RVOT and ASC was 22 - 28 (25.2 ± 2.7) ms and 26 - 40 (32.8 ± 5.2) ms, respectively (t = -3.6, P = 0.024) while EVA was earlier in the remaining 9 patients and EVA recorded in RVOT and ASC was 22 - 38 (28.7 ± 5.9) ms and 18 - 28 (22.7 ± 3.6) ms, respectively (t = 3.8, P = 0.005). CONCLUSION: Patients with premature ventricular contractions originating from the ASC often show preferential conduction to the RVOT, which may explain the LBBB morphology of ECG in these patients.