Premature Ventricular Contractions Morphology Research Articles

Abstract Tu060: Unveiling Arrhythmogenic Right Ventricular Dysplasia In Pregnancy

Introduction: Arrhythmogenic right ventricular dysplasia (ARVD) is a rare autosomal dominant disease, caused by desmosomal gene mutations, and characterized by fibrofatty replacement of right ventricular (RV) myocardium with left ventricular (LV) involvement in advanced stages. It is mostly diagnosed between the second and forth decades of life and can present with ventricular tachycardia and arrhythmic sudden death. Here we present a case of ARVD diagnosis in a female in her forth pregnancy. Case description: A 28-year-old female, on her 27 th week of gestation (G4P3) was admitted to the hospital with preterm premature rupture of membranes. She also endorsed intermittent chest pressure, palpitations and shortness of breath. Her vital signs were stable, and electrocardiogram (ECG) revealed normal sinus rhythm with frequent premature ventricular contractions (PVCs) and T wave inversions in leads V1- V3. Laboratory studies showed normal troponin and D-dimer levels, and slightly elevated brain natriuretic peptide 240 pg/mL. Patient notably had frequent runs of monomorphic non-sustained ventricular tachycardia (NSVT) arising from RV apical territory, with left bundle branch morphology on telemetry. An echocardiogram revealed a dilated right atrium and RV with hypokinesis of RV; LV size and function were normal. Overall, patient met the revised task force diagnostic criteria for ARVD based on PVC morphology, abnormal ECG and dilated and hypokinetic RV. She had no sustained or hemodynamically unstable VT, no history of syncope or family history of sudden cardiac death and did not meet class I indication for implantable cardioverter defibrillator. She was started on oral metoprolol succinate 25 mg daily with which her arrhythmias significantly improved. She was recommended a cardiac magnetic resonance imaging and genetic testing for confirmation and to assess familial implications. Conclusion: Recognition of ARVD during pregnancy is challenging given the overlapping symptoms of normal pregnancy-related changes. Hormonal surge and sympathetic drive may have driven the increased frequency of NSVT in our patient and beta blocker was effective in managing these. Early recognition and tailored management are crucial to ensure the well-being of both the mother and the fetus. A close follow-up is necessary to understand the long-term implications for the patient and potential genetic predisposition in the family.

Electrocardiographic characteristics and catheter ablation of premature ventricular complex- mediated ventricular fibrillation

Abstract Background Premature ventricular contractions (PVCs) can trigger ventricular fibrillation (VF) in patients with/or without structural heart disease. There are limited data on coexisting electrocardiographic (ECG) features and catheter ablation outcomes in these patients which could suggest the concomitant presence of an abnormal electrical and structural substrate. Purpose We investigated ECG and electroanatomic characteristics and clinical outcomes in patents who underwent catheter ablation of PVCs triggering VF. Methods We analyzed data from a consecutive series of patients who underwent catheter ablation between 08/2019 and 04/2023 for PVCs triggering VF. On the 12-lead ECG, we assessed the following abnormalities: (a) Early repolarization (ER) pattern in either inferior or lateral leads (Figure 1), or (b) QRS Notching of either the native sinus beat or PVC (Figure 2). Post-ablation follow up outcomes were collected using a combination of ICD interrogation, remote transmission and clinical follow up. Results The cohort included 15 patients: age 52.1±16.8 years, 46.7% females, and 26.7% presenting with VF storm. On average, there were 3.8 HV shocks/per patient from an ICD prior to the index ablation procedure (range: 0-19 shocks). On the 12-lead ECG, the mean coupling interval of the PVC leading to VF was 204±82 ms, and an overall narrow PVC morphology with a mean QRS duration of 107±17 ms. We observed early repolarization (ER) in 6 (40%) of the cohort. In most patients (n=11; 73.3%), at least one of the 2 ECG abnormalities were present. An endocardial-only approach was adequate in all patients, and during catheter ablation, Purkinje potentials were targeted in 10 (66%) of the patients. Based on activation and pace-mapping, the PVCs were localized to the following sites: (a) left ventricular (LV) septum in 11 (73.3%), (b) papillary muscles in 2 (13.3%), and (c) other sites such as the Moderator band and right ventricular outflow tract in the remaining 2 (13.3%) patients. The ablation locations on the LV septum extended from basal to mid-septum. After an average of 1.7 ablation procedures targeting PVC-triggering VF, 12 (80%) patients remained free of sustained ventricular arrhythmias and ICD shocks, over a mean follow up of 479±395 days. Conclusion In most patients with PVCs-triggering VF, there was an evidence of an ECG abnormality either in the form of an ER pattern or notching of either the Sinus QRS or the PVC complex on pre-ablation ECG. During ablation, Purkinje potentials and PVCs were mapped to and ablated in the region of the LV interventricular septum and papillary muscles. Over long-term follow up, catheter ablation seemed durable and effective in reducing VF episodes and ICD shocks.Presence of Early Repolarization patternPresence of a notching pattern in the Si

Variable clinical expression of a novel FLNC truncating variant in a large family

BackgroundVariants in Filamin-C (FLNC) have been associated with various hereditary cardiomyopathies. Recent literature reports a prevalence of sudden cardiac death (SCD) of 13–25% among carriers of truncating-variants, with mean age of 42±15 years for first SCD event. This study reports two familial cases of SCD and the results of cascade screening of their large family. MethodsMolecular-autopsy of the SCD victims revealed a novel truncating-variant in the FLNC gene (chr 7:128496880 [hg19]; NM_001458.5; c.7467_7474del; p.(Ser2490fs)). We screened thirty-two family members following genetic counseling, and variant carriers underwent a comprehensive workup followed by consultation with a cardiologist with expertise in the genetics of cardiac diseases. ResultsSeventeen variant carriers were identified: ages between 9 and 85 (mean 47±26). Fifteen underwent clinical evaluation. To date, none of the identified carriers has had major adverse events. In evaluated patients, ECG showed right-axis deviation in 60% (n = 9). Holter recorded frequent premature ventricular contractions (PVCs) (991±2030 per 24 h) in 33% (n = 5) with 4 patients having polymorphic PVC morphology. Three carriers had echocardiographic evidence of mild left-ventricular (LV) systolic dysfunction and another with mild LV dilatation. Cardiac magnetic-resonance (CMR) exhibited late‑gadolinium-enhancement in 10 out of 11 exams, mainly in the mid-myocardium and sub-epicardium, frequently involving the septum and the inferior-lateral wall. ConclusionThis large FLNC truncating variant carrier family exhibits high cardiomyopathy penetrance, best diagnosed by CMR, with variable clinical expressions. These findings present a challenge in SCD prevention management and underscoring the imperative for better risk stratification measures.

Prognostic impact of morphology and duration of premature ventricular contractions in a population without structural heart disease.

Premature ventricular contractions (PVCs) are a common form of arrhythmia associated with an unfavorable prognosis in patients with structural heart disease. It is unclear whether PVCs site of origin and QRS-width has a prognostic significance in patients without structural heart disease. The aim of this study was to assess the prognostic importance of PVCs morphology and duration in this patient group. We included 511 consecutive patients without a history of previous heart disease. They were examined with echocardiography and exercise test with normal findings. We categorized the PVCs from a 12 lead ECG according to morphology and width of the QRS-complex and analyzed the outcome in terms of a composite endpoint of total mortality and cardiovascular morbidity. During a median follow-up time of 5.3 years, 19 patients (3.5%) died and 61 (11.3%) met the composite outcome. Patients with PVCs originating from the outflow tracts had a significantly lower risk for the composite outcome compared to patients with non-OT-PVCs. Similarly, patients with PVC originating from the right ventricle had a better outcome than patients with left ventricular PCVs. No difference in outcome depending on QRS-width during PVCs was noticed. In our cohort of consecutively included PVC patients without structural heart disease PVCs from the outflow tracts were associated with a better prognostic outcome than non-OT PVCs; the same was true for right ventricular PVCs when compared to left ventricular ones. The classification of the origin of the PVCs was based on 12-lead ECG morphology. QRS-width during PVC did not seem to have prognostic significance.

Abstract 15433: Very Late Recurrence After Successful Ablation of Premature Ventricular Contractions in Patients Without Structural Heart Disease

Background: Earlier studies have shown the superiority of catheter ablation over pharmacological therapy in eliminating premature ventricular contractions (PVC) in patients without structural heart disease. We investigated very late recurrences after successful PVC ablation in this cohort. Methods: Consecutive patients undergoing clinically indicated radiofrequency ablation for symptomatic idiopathic PVCs, documented by standard ECG, were included in the analysis and prospectively followed up. Those with history of structural heart disease were excluded. For all patients, 12-lead ECGs were reviewed to assess PVC morphology. During the index procedure, all PVC morphologies were targeted for ablation. Standardized RF power settings (40-50 W) were used during the procedure. Ablation was performed using 4-mm irrigated tip catheter guided by 3-D mapping system and intra-cardiac echocardiography. Patients were followed up with remote monitoring as well as ICD interrogations and office visits every 6 months for 4 years. Long-term success was defined as absence of previously targeted PVCs or any new PVC morphology on 12-lead ECG or device interrogation during all follow-up visits. Results: In total, 638 patients were included (mean age 59.2±5.6 years, 69.75% male, LVEF 54±12%). At the index ablation, PVCs were detected to be localized in the right ventricular outflow tract in 268 (42%), left ventricular outflow tract in 299 (46.8%) and multiple sites of origin in 71 (11.2%) patients. Non-inducibility was achieved in all patients at the end of the index procedure. At 4 years, 585 (91.7%) patients remained arrhythmia-free. Remaining 53 patients (8.1%) experiencing recurrence underwent repeat procedure. Median time to recurrence was 29±6.2 months. At the redo, new PVC morphologies were detected and ablated in 46/53 (86.8%) patients. One year after the repeat ablation, 50/53 (94.3%) were arrhythmia-free. Conclusion: In this prospective single-center series, very late recurrence following index PVC ablation in patients with no structural heart disease was mostly associated with new PVC morphologies that were amenable to be successfully ablated at the repeat procedure.

Abstract 13613: Prevalence of Atrial Fibrillation and Procedure-Outcome in Patients Undergoing Catheter Ablation for Premature Ventricular Contractions

Introduction: Atrial fibrillation (AF) and premature ventricular contractions (PVC) are common arrhythmias encountered in clinical practice. Theoretically, retrograde atrial conduction can occur in the presence of PVC, causing atrial ectopy. However, the clinical significance of this association is not defined yet. Hypothesis: We investigated the prevalence of AF in patients with PVC and its impact on PVC ablation. Methods:: Consecutive patients undergoing PVC ablation at our institution between 2016 and 2019 were included in this analysis. Patients with structural heart disease, hyperthyroidism, malignancy, alcoholism and advanced renal or hepatic disease were excluded. For all patients, 12-lead ECG was used to diagnose AF and assess PVC morphology. During the index procedure, all PVC morphologies were targeted for ablation. Patients were followed up with remote monitoring as well as ICD interrogations and office visits every 6 months for 2 years. Detection of any PVC in the electrogram was considered as recurrence. Results: A total of 394 patients undergoing PVC ablation were included of which 96 (24%) had the documented evidence of AF. Baseline characteristics of the study population without (group 1, n=298) versus with AF (group 2, n=96) is provided in table 1. Clinical parameters were comparable between the groups except age, which was higher in group 2. PVCs with multiple (≥2) morphology were detected at the index procedure in 41 (13.7%) and 58 (60.4%) patients in group 1 and 2 respectively (p <0.001). At 2 years of follow-up, recurrence rate following PVC-ablation was significantly higher in group 2 compared to group 1 (17 (18%) vs 27 (9%), p=0.026). Conclusions: In this consecutive series, AF was documented in 1/4 th of the population undergoing PVC ablation and presence of AF was associated with lower procedural success at long term, which could be attributed to older age and significantly higher prevalence of multiple morphology’ PVCs in the group 2 population.

Speckle Tracking Echocardiography in Pediatric Patients with Premature Ventricular Contractions.

Premature ventricular contractions (PVCs) in pediatric patients without structural heart disease and normal left ventricular systolic function rarely require therapy, though it is unknown whether these patients have subclinical cardiac dysfunction. Speckle tracking echocardiography is an additional means of evaluating cardiac function in asymptomatic pediatric PVC patients with normal standard measures of left ventricular (LV) function. Asymptomatic pediatric patients (< 21years) without congenital heart disease, LV ejection fraction (LVEF) ≥ 55% and PVC burden ≥ 5% on 24-h Holter monitor were included. Demographic information, exercise stress test results, standard echocardiographic measures of LV systolic function and PVC morphology by 12-lead ECG were collected. Peak global systolic longitudinal strain (GLS) from apical four-chamber view was analyzed offline. 29 patients were identified (mean age 11.7 ± 5.8years, 49.2 ± 25.3kg, 59% male). Mean PVC burden was 12.0 ± 7.0% (range 5-37.5%). 14/29 (48%) had exercise stress testing with evidence of PVCs; 9/14 (64%) had PVC suppression at a mean heart rate (HR) of 160 ± 23bpm and 5/14 (36%) did not suppress at a mean maximum HR of 188 ± 9bpm. All patients had normal strain values by speckle tracking echocardiography (mean LV GLS - 22.5 ± 2.0%, LV global circumferential strain - 25.3 ± 3.9 and RV GLS - 24.1 ± 3.0%). There was no correlation between PVC burden and cardiac function parameters. Asymptomatic pediatric patients without structural heart disease, preserved LVEF/shortening fraction and PVC burden ≥ 5% demonstrated normal cardiac function including strain patterns indicating no evidence of subclinical cardiac dysfunction. Larger scale studies and longitudinal evaluation of left ventricular function using speckle tracking echocardiography is warranted in this population.

P95412 lead Holter monitoring in Brugada syndrome

Abstract Background 12 lead-Holter monitoring is commonly used for the assessment of type 1 Brugada repolarization"s burden. However, data considering the prevalence and morphology of premature ventricular contractions (PVC) in these patients is lacking. Purpose. We investigated the prevalence of PVCs in subjects with Brugada syndrome (BRs) phenotype during 24-hour 12 lead-Holter monitoring (12-L Holter), trying to identify their origin according to morphology. Methods. From January 2013 to September 2018, a total of 156 patients with type 1 BRs phenotype (spontaneous or drug induced) were screened for PVCs. In these patients we placed the right precordial leads at the second (V1-V2) and the forth (V3-V4) intercostal spaces. Results. 83 subjects (53%) displayed PVCs. Their mean age was 50 years (range 21-73) and 63 (76%) were male. 14 subjects (17%) had a spontaneous type 1 repolarization whereas 69 (83%) presented a drug induced type 1. One patient had implanted an ICD as secondary prevention after an aborted sudden cardiac death. The others were mostly asymptomatic as only five of them (6%) had history of suspected cardiac syncope. 17 subjects (20%) had performed an electrophysiological study, which resulted positive in 3 cases (4%). The population without PVCs had similar baseline characteristics. In 59 (71%) patients PVCs were monomorphic, in the other 29% we analyzed the prevalent morphology. PVCs were classified according to their morphology as follows (i) left bundle branch block (LBBB)/inferior axis suggesting an origin from the right ventricular outflow tract (RVOT), that was shown in 40 (48%) subjects; (ii) right bundle branch block (RBBB)/left axis suggesting an origin close to the posterior fascicle of the left bundle branch in 36 (43%). The other 7 patients presented several morphologies. According to their number during the 24-hour monitoring, PVCs were arbitrarily classified as follows: (i) 1-59,present in 62 patients (75%); (ii) 60-749, present in 16 patients (19%); (iii) 750-9000, present in 4 patients (5%); (iv) &amp;gt;9000, in only one patient (1%). Conclusions. In our population of subjects with BRs phenotype the prevalence of PCVs is similar to that of the general population. Their morphologies suggest an origin from the RVOT or close to the posterior fascicle of the left bundle branch.

Arrhythmias from the Right Ventricular Moderator Band: Diagnosis and Management.

The moderator band in the right ventricle is being increasingly recognised as a source for arrhythmias in the absence of identifiable structural heart disease. Because it carries part of the conduction system from the right ventricle septum to the free wall, it is a source of Purkinje-mediated ventricular arrhythmias that manifest as premature ventricular contractions (PVC) or repetitive ventricular tachycardia. More importantly, short coupled PVCs triggering polymorphic ventricular tachycardia and VF have been localised to the moderator band and ablation of these Purkinje mediated PVCs can effectively prevent recurrent VF. The exact mechanism of arrhythmogenesis is still debated but stretch, fibrosis and ion channel alterations might be responsible. Arrhythmias originating in this region of the right ventricle may thus be another cause for idiopathic VF that is potentially treatable with catheter-based ablation techniques. Recognition of the typical PVC morphology can point to the moderator band as the source of idiopathic VF and an opportunity for timely intervention. The available data on the anatomy, electrophysiology and management options are reviewed.

Long-term mode and timing of premature ventricular complex recurrence following successful catheter ablation.

Catheter ablation of premature ventricular contractions (PVCs) is highly successful and has become the hallmark treatment for symptomatic or highly prevalent cases. However, few studies exist that evaluate the outcomes of ablation and likely mechanisms of PVC recurrence beyond 1year of follow-up. This study is a retrospective analysis of patients who underwent catheter ablation for symptomatic PVCs with acute procedural success and had clinical follow-up ≥ 12months. Forty-four patients (24 women; age 53.5 ± 4.8years) following acutely successful PVC ablation with long-term follow-up were studied. At a mean of 36 ± 6months, overall long-term ablation success was 75% (33/44 patients). Notably, recurrence of the targeted PVC focus was low (6.8%, 3/44 patients); the majority of recurrences were from a new source location (18.2%, 8/44 patients). The time course for targeted versus de novo PVC recurrences was significantly different: recurrence of a PVC similar to the targeted PVC morphology occurred at a mean of 5.0 ± 2.0months, while recurrence of a PVC different from the index case occurred at a mean of 35.8 ± 17.1months (p = 0.01). Non-ischemic cardiomyopathy was associated with increased risk of PVC recurrence (odds ratio [OR] 14.50 (95% confidence interval [CI] 1.92-109.33, p = 0.01)) and was a significant negative prognostic factor in multivariate analysis for PVC recurrence survival (hazard ratio [HR] 4.63, 95% CI 1.03-20.74, p = 0.04). The majority of long-term PVC recurrences occur late in follow-up, at locations remote from the targeted PVC source or sources. Such sites may represent ongoing substrate evolution; additional work is required to determine the precise substrate alterations which promote such arrhythmogenic changes.

Coupling interval variability of premature ventricular contractions in patients with different underlying pathology: an insight into the arrhythmia mechanism

PurposeCoupling interval (CI) variability of premature ventricular contractions (PVCs) is influenced by the underlying arrhythmia mechanism. The aim of this study was to compare CI variability of PVCs in different myocardial disease entities, in order to gain insight into their arrhythmia mechanism.MethodsSixty-four patients with four underlying pathologies were included: idiopathic (n = 16), non-ischemic dilated cardiomyopathy (NIDCM) (n = 16), familial cardiomyopathy (PLN/LMNA) (n = 16), and post-MI (n = 16)-associated PVCs. The post-MI group was included as a reference, on account of its known re-entry mechanism. On Holter registrations, the first 20 CIs of the dominant PVC morphology were measured manually after which median ΔCI and mean SD of CI/√R-R (= CI of PVC corrected for underlying heart rate) were obtained. Two observers independently measured PVC CIs on pre-selected Holter registrations in order to determine inter- and intra-observer reliability.ResultsThe largest ΔCI was seen in the PLN/LMNA group (220 ms (120–295)), the lowest in the idiopathic group (120 ms (100–190)). The ΔCI in the PLN/LMNA group was significantly larger than the post-MI group (220 ms (120–295) vs 130 ms (105–155), p = 0.023). Mean SD of CI/√R-R in the PLN/LMNA group was also significantly higher than in the post-MI group (p = 0.044). Inter- and intra-observer reliability was good (ICC = 0.91 vs 0.86 and 0.96 vs 0.77, respectively).ConclusionsLow ΔCI and SD of CI/√R-R of idiopathic and NIDCM PVCs suggest that the underlying arrhythmia mechanisms might be re-entry or triggered activity. Abnormal automaticity or modulated parasystole are unlikely mechanisms. High CI variability in PLN/LMNA patients suggests that the re-entry and triggered activity are less likely mechanisms in this group.

ECG morphology of premature ventricular contractions predicts the presence of myocardial fibrotic substrate on cardiac magnetic resonance imaging in patients undergoing ablation.

The most likely origin of premature ventricular contractions (PVCs) may be deduced from surface electrocardiogram (ECG) analysis while planning an electrophysiological study (EPS). Apart from purely benign forms of increased ventricular ectopy, myocardial substrate (e.g., regional fibrosis) may be present in certain cases, which will significantly impact the ablation approach. Cardiac magnetic resonance (CMR) imaging can reliably identify fibrotic target lesions and, hence, may assist in adequate patient selection and procedural planning. We analyzed 101 patients (59% males, mean age 57.15 ± 15.5 years, mean PVC count 19,801 ± 14,021 per 24 hours) referred for ablation of PVCs. The CMR (1.5T, Philips Ingenia, Best, The Netherlands) protocol included cine and three-dimensional-delayed enhancement imaging using standard cardiac geometries. On surface, ECG right bundle branch block (RBBB) morphology was present in 43% of patients. Twenty-one patients showed the fibrotic substrate on CMR. On univariate analysis, both RBBB morphology (P<0.001) and presence of multiple PVC morphologies (≥2) significantly predicted the presence of fibrotic substrate (P=0.01), which various baseline characteristics including left ventricular ejection fraction (45.7 ± 12.6% vs. 50.6 ± 11.0%, P=0.08) failed to do. CMR-identified fibrosis was associated with the site of origin of the clinical PVCs during EPS and was successfully treated by radiofrequency ablation in 93% (PVC reduction>95%). In patients with RBBB morphology and/or multiple PVC patterns, CMR imaging before ablation may be helpful due to the increased prevalence of fibrotic lesions with regard to patient stratification and periprocedural management.

Characteristics of premature ventricular contractions in healthy children and their impact on left ventricular function

There are few data regarding the characteristics of premature ventricular contractions (PVCs) in healthy children and their impact on left ventricular (LV) function. The purpose of this study was to assess the prevalence of LV systolic dysfunction in children with frequent PVCs (≥10%) and determine whether it is associated with PVC characteristics (e.g., proportion, coupling interval, width, and/or morphology). We conducted a single-center cohort study of children with structurally normal hearts and PVC burden ≥10% by 24-hour Holter monitoring performed between 2008 and 2012. Clinical, arrhythmic, and echocardiographic data were reviewed at baseline and during follow-up. A total of 47 children (22 female [47%], mean age 8.2 ± 6.5 years) had a mean PVC burden of 20.9 ± 11.9% at baseline. The PVC coupling interval averaged 430 ± 110 ms, with a PVC width of 118 ± 27 ms. PVCs were monomorphic in 44 patients (94%). Although no patient had severe cardiomyopathy, 7 (15%) had reduced shortening fraction (Z-score <-2). A strong association was observed between PVC coupling interval and LV shortening fraction Z-score <-2.0 (area under the curve 0.95 ± 0.03, P <.001). A cutoff value <365 ms yielded the greatest discriminatory ability (Youden J-statistic 0.72, sensitivity 85.7%, specificity 86.5%). PVC proportion, width, and morphology were not significantly associated with LV shortening fraction. During 4.0 ± 2.8 years of follow-up, the PVC burden decreased from a median of 18% to 1.5% (P<.001). PVCs in children with structurally normal hearts are associated with a relatively benign course, with spontaneous resolution in most children. Mild LV systolic dysfunction, observed in 15%, is strongly correlated with a shorter coupling interval (<365 ms).

Better outcome of ablation for sustained outflow-tract ventricular tachycardia when tachycardia is inducible.

In patients presenting with spontaneous sustained ventricular tachycardia (VT) from the outflow-tract region without overt structural heart disease ablation may target premature ventricular contractions (PVCs) when VT is not inducible. We aimed to determine whether inducibility of VT affects ablation outcome. Data from 54 patients (31 men; age, 52 ± 13 years) without overt structural heart disease who underwent catheter ablation for symptomatic sustained VT originating from the right- or left-ventricular outflow region, including the great vessels. A single morphology of sustained VT was inducible in 18 (33%, SM group) patients, and 11 (20%) had multiple VT morphologies (MM group). VT was not inducible in 25 (46%) patients (VTni group). After ablation, VT was inducible in none of the SM group and in two (17%) patients in the MM group. In the VTni group, ablation targeted PVCs and 12 (48%) patients had some remaining PVCs after ablation. During follow-up (21 ± 19 months), VT recurred in 46% of VTni group, 40% of MM inducible group, and 6% of the SM inducible group (P = 0.004). Analysis of PVC morphology in the VTi group further supported the limitations of targeting PVCs in this population. Absence of inducible VT and multiple VT morphologies are not uncommon in patients with documented sustained outflow-tract VT without overt structural heart disease. Inducible VT is associated with better outcomes, suggesting that attempts to induce VT to guide ablation are important in this population.

The Burden and Morphology of Premature Ventricular Contractions and their Impact on Clinical Outcomes in Patients Receiving Biventricular Pacing in the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT).

Premature ventricular contractions (PVCs) frequently occur in patients with left ventricular dysfunction. However, there are limited data regarding the burden and morphologic characteristics of PVCs in patients receiving cardiac resynchronization therapy. Patients enrolled in the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT) with >5000 PVCs on a predevice implant 12-lead, 24-hour Holter were identified. The putative PVC site of origin for the most dominant PVC was characterized and their effects on clinical outcomes were evaluated. A total of 146 patients were identified to have >5000 PVCs on Holter of which 75 (51%) had PVCs originating from a non-outflow tract site. Other sites included the left ventricular outflow tract (LVOT), right ventricular outflow tract (RVOT), and the sinus of Valsalva. In multivariate analysis, the risk for HF/Deatd was similar in patients with Outflow tract PVCs when compared to patients with Non-outflow tract PVCs (HR 1.4, 95% CI 0.7-2.8, P = 0.3). The degree of echocardiographic reverse remodeling was similar in patients with outflow tract versus Non-outflow tract PVCs. One-third of patients with nonischemic cardiomyopathy were found to have PVCs originating from the RVOT. In patients with mild symptoms of heart failure, there is no difference in the risk of HF or death in patients with outflow versus non-outflow tract PVCs. One-third of patients with NICM have frequent PVCs originating from the RVOT.

A Novel, Minimally-Invasive Surgical Approach for Ablation of Ventricular Tachycardia Originating Near the Proximal Left Anterior Descending Coronary Artery

Idiopathic ventricular tachycardia (VT) arising from the left ventricular (LV) summit can be challenging for catheter-based percutaneous ablation. We present a patient in whom endocardial and percutaneous epicardial ablations were not successful in eliminating VT. Subsequently, a minimally invasive surgical approach with robotic-assisted mapping, followed by minithoracotomy and cryoablation of the myocardium near the region of the proximal left anterior descending (LAD) coronary artery, was successful in eliminating arrhythmia. A 54-year-old man with a medical history significant for hypertension and sleep apnea presented with exertional palpitations associated with lightheadedness. Holter monitoring revealed frequent premature ventricular contractions (PVCs) and nonsustained VT. β-blockers were started (metoprolol 100 mg BID), but sustained VT was demonstrated on exercise stress testing performed while on β-blockers. Physical examination and laboratory evaluation were unremarkable. Coronary angiography documented normal epicardial coronary vessels with a normal LV ejection fraction (64%). Cardiac magnetic resonance imaging revealed mild LV hypertrophy without fibrosis or other structural abnormalities. Despite optimal dose of β-blockers (metoprolol 100 mg BID) and calcium channel blockers (diltiazem CD 120 mg QD), the patient continued to have symptoms of lightheadedness and presyncope and was subsequently brought to the electrophysiology laboratory for further evaluation and treatment. On 12-lead ECG, the morphology of spontaneous PVCs was predominantly positive in the inferior leads with early precordial transition (V2). The ratio of QS complexes in aVL/aVR was <1, suggestive of origin from the inaccessible region of the LV summit.1 (Figure 1) Figure 1. Surface 12-lead ECG showing premature ventricular contractions with inferior axis, early transition suggesting site of origin near the anterosuperior …

Idiopathic Mitral Annular PVCs with Multiple Breakouts and Preferential Conduction Unmasked by Radiofrequency Catheter Ablation

A 39-year-old man with idiopathic monomorphic premature ventricular contractions (PVCs), exhibiting a right bundle branch block and inferior axis QRS morphology, underwent electrophysiological testing. After a radiofrequency (RF) application to the anterior mitral annulus (MA) eliminated the spontaneous PVC morphology, a second PVC morphology occurred. Pacing from the first ablation site exhibited an excellent match to the second PVCs with a long stimulus to QRS interval. An RF application delivered near the first lesion eliminated all PVCs. The MA PVCs in this case exhibited a single origin with multiple breakouts and preferential conduction that were unmasked by RF ablation.

Differential effects of cardiac sodium channel mutations on initiation of ventricular arrhythmias in patients with Brugada syndrome

Premature ventricular contractions (PVCs) do not occur frequently but can induce ventricular fibrillation (VF) in patients with Brugada syndrome. The effect of SCN5A mutation on the onset of ventricular arrhythmias is unknown. The purpose of this study was to evaluate PVC morphology and onset of VF in patients with Brugada syndrome. Morphology of PVCs was evaluated by 12-lead ECG in 32 patients with Brugada syndrome. Patients had spontaneous ventricular arrhythmia (n = 17) or sodium channel blocker-induced ventricular arrhythmia (n = 19). Patients were classified into two groups according to the existence of SCN5A mutation (22 mutation negative, 10 mutation positive). Patients without mutation often had PVCs of left bundle branch block (LBBB) morphology (82%), especially with inferior axis (77%). Patients with mutation had PVCs of both right bundle branch block (36%) and LBBB (64%) morphologies. Only two patients with mutation had PVCs of LBBB, inferior-axis morphology. Patients without SCN5A mutation often had PVCs of LBBB, inferior-axis morphology, suggesting a right ventricular outflow tract origin. Patients with SCN5A mutations had PVCs that originated from both the right and left ventricles.

Efficacy of electroanatomic mapping in the catheter ablation of premature ventricular contractions originating from the right ventricular outflow tract

Mapping of premature ventricular contractions (PVCs) originating from the right ventricular outflow tract (RVOT) sometimes is not easy because of an unstable incidence and multiple foci of the PVCs. The aim of this study was to evaluate the effectiveness of electroanatomic mapping in catheter ablation of those PVCs. One hundred patients with 134 RVOT origin PVCs were randomly allotted to undergo either conventional (group I; 50 patients with 65 PVCs) or electroanatomic mapping (group II; 50 patients with 69 PVCs). In group II, electroanatomic mapping of the RVOT was performed using auto-freeze maps in patients with frequent PVCs, and pace mapping was performed marking the pacing sites on the remap which was made by extracting the anatomic frame out of the baseline map during sinus rhythm in patients with infrequent PVCs. Successful ablation was achieved in 44 (88%) group I patients and 48 (96%) group II patients (p = 0.14). The fluoroscopy and procedure times and those per PVC morphology were all significantly shorter in group II than group I overall (p < 0.0001 for all comparisons), and in each patient group with infrequent PVCs, frequent PVCs or unstable PVCs (p < 0.05-0.0001). The number of RF applications and that per PVC was significantly smaller in group II than group I (5.3 +/- 1.8 vs 6.2 +/- 2.4, and 4.4 +/- 1.2 vs 5.2 +/- 2.1; p < 0.05). The use of electroanatomic mapping may reduce the fluoroscopy and procedure times in the ablation of RVOT PVCs, but there is no evidence that it improves the overall efficacy of the procedure.