Premature Ventricular Complexes Burden Research Articles

Clinical significance of myocardial scar in patients with frequent premature ventricular complexes undergoing catheter ablation

Frequent premature ventricular complexes (PVCs) can result in PVC-induced cardiomyopathy (PICM). Scarring has been described in patients with frequent PVCs in the absence of apparent heart disease and in patients with known cardiomyopathy. The purpose of this study was to determine the impact of focal myocardial scarring as detected by cardiac magnetic resonance imaging (CMR) on PICM, procedural outcomes, and recovery of left ventricular function in patients with frequent PVCs. A total of 351 consecutive patients (181 men; age 53 ± 15 years; ejection fraction [EF] 51% ± 12%) with frequent PVCs referred for ablation were included. CMR was performed in all patients before the ablation procedure. A ≥10% increase in EF or normalization of a previously abnormal EF was defined as evidence of PICM. Myocardial scarring was present in 134 of 351 patients (38%); 66 of 134 patients (49%) with scarring and 54 of 217 patients (25%) without scarring had improvement or normalization of EF after ablation. The presence of myocardial scarring, PVC burden >22%, male sex, asymptomatic status, and PVC QRS width >150 ms were associated with PICM by univariate analysis (P <.01 for all). The presence of scar was independently associated with PICM (odds ratio 2.2; 95% confidence interval 1.3-3.7; P <.005). The success rate of PVC ablation was lower in patients with scarring than in patients without focal scarring (mean 70% vs 82%; P <.01). Focal scar defined by CMR is independently associated with PICM. Although ablation outcomes are worse in the presence of scarring, EF recovery can occur in most of these patients after ablation.

Risk Factors for Left Ventricle Enlargement in Children With Frequent Ventricular Premature Complexes

We aimed to assess the risk factors for left ventricle (LV) enlargement in children with idiopathic frequent ventricular premature complexes (VPC) and discuss the clinical features and treatment strategies. Children diagnosed with idiopathic frequent VPC at Xinhua Hospital affiliated to the Shanghai Jiao Tong University during 2013 to 2019 were retrospectively evaluated. Gender, age, body mass index, weight, number and sources of frequent VPC, and changes in the LV structure were analyzed and compared. A total of 29 patient showed changes in LV enlargement at diagnosis [age 7.3 ± 4.0 years, 8 (24.1%) had symptoms such as syncope, palpitations, fatigue, and dizziness], whereas 220 showed a normal LV structure [age 7.2 ± 4.5 years, 77 (32.3%) with symptoms]. Patients with LV enlargement showed a higher percentage of VPC on Holter recordings (30.2 ± 10.7 versus 9.4 ± 6.9, p < 0.05), higher prevalence of ventricular tachycardia [22 (75.9%) vs 36 (16.4%), p < 0.0001], higher number of couplets [26 (96.7%) vs 132 (60.0%), p = 0.002], higher number of trigeminy[27 (97.8%) vs 133 (83.2%), p < 0.001], higher QRS wave width [80.0 ± 5.9 vs 77.8 ± 6.8, p = 0.021], and higher incidence of right bundle branch block [11 (37.9%) vs 2 (0.9%), p < 0.001]. Multivariate analysis suggested that right bundle branch block (Odds Ratio = 143.9 p <0.001) and VPC burden (>20%) (Odds Ratio = 132.6, p <0.001) were the risk factors for LV enlargement in children with idiopathic frequent VPC. In conclusion, frequent VPC can induce prominent enlargement or LV dysfunction in children. LV enlargement are reversible after catheter ablation or medication.

125Manual vs. automatic local activation time annotation for guiding premature ventricular complex ablation procedures (MANIaC - PVC study)

Abstract Funding Acknowledgements Financial support was provided in form of a research grant from Biosense Webster Introduction The use of an algorithmic method (wavefront, WF) based on automatic annotation of the maximal negative slope of the unipolar electrogram (uni-EGM) within the window demarcated by the bipolar EGM (bi-EGM) may accurately identify the earliest activation site (EAS) during premature ventricular complex (PVC) ablation procedures. Purpose To assess the potential benefits of a local activation time (LAT) automatic acquisition protocol using WF plus an automatic algorithm for ECG pattern matching recognition (AUT-arm) instead of a manual LAT annotation plus ECG visual inspection (MAN-arm) during premature ventricular complexes (PVCs) ablation procedures. Methods Prospective, randomized, controlled and international multicenter study (NCT03340922). 69 consecutive patients with indication for PVC ablation were enrolled and randomized to AUT (n = 34) or MAN (n = 35) annotation protocols using the CARTO3 navigation system. The primary endpoint was mapping success, defined as complete PVC abolition after a maximum of 2 radiofrequency (RF) applications or up to 90 seconds at the identified EAS, considered the site of origin (SOO). Complete PVC abolition was considered as the procedure success, whereas clinical success was defined as the PVC-burden reduction of &amp;gt;80% in the 24-h Holter at least 1 month after the procedure. Concordance analysis of the maps obtained with both methods was performed. Results Mean age was 69 ± 15, 58% men. The mean baseline PVC burden was 26 ± 13%, mean LVEF 55 ± 12%. Baseline characteristics were similar between groups. The most frequent PVC-SOO were RVOT (41%), LV (25%; being the summit the most frequent location), and LVOT (16%), with no MAN-AUT differences. Total mapping time, number of RF applications, RF time, and procedure time were similar for both groups. The AUT-arm had a higher number of mapping points acquired (164 vs. 61; p = 0.002). There was a delayed detection of LAT at the EAS in the AUT-arm (mean 23 ± 13 ms), being more significant in left-sided PVCs (30 ± 12 vs. 15 ± 9 ms, p &amp;lt; 0.001). The 10-ms isochronal area was significantly bigger in the MAN-arm (1.95 ± 2.7 vs. 1.0 ± 1.0; p = 0.05). The median (interquartile range) distance between AUT-EAS and MAN-EAS was 4 (0–6.8) mm. Mapping success was similar for AUT (65%) and MAN (63%) (p = 1.0). Procedure success was significantly better for the AUT-arm (100% AUT vs. 86% MAN; p = 0.04), but without differences in clinical success (87% AUT vs. 82% MAN; p = 0.7). There were no procedure-related complications. Conclusions The use of a complete automatic protocol for LAT annotation (WF + ECG pattern matching) during PVC ablation procedures is feasible and safe, allowing to achieve equivalent procedural and clinical endpoints as compared to manual procedures carried out by expert operators.

P933Novel missense variant in DPP6 in familial ventricular fibrillation

Abstract Funding Acknowledgements This work was supported by an ESC Research Grant to A.R., and by The Netherlands CardioVascular Research Initiative (CVON PREDICT2), Den Haag, The N Background The DPP6 gene, encoding dipeptidyl aminopeptidase-like protein-6, has been associated with familial ventricular fibrillation (VF) and early repolarization. The DPP6 protein is part of the macromolecular Ito-channel complex and functionally expressed in ventricular myocytes (VM) and Purkinje cells (PC). Here we report a novel missense variant in DPP6 identified in a family with sudden cardiac death/arrest due to VF. Purpose To examine the consequences of the novel DPP6 variant c.821G &amp;gt; A, p.(R274H) for cardiac Ito and their potential contribution to a VF substrate. Methods: Clinical Co-segregation of DPP6-R274H with major adverse cardiac events in the family members was investigated. Ambulatory ECGs, echocardiograms, exercise tests and ICD recordings were systematically analyzed. Cellular Chinese hamster ovary cells were transiently transfected with Ito α and β subunits in order to mimic the VM (Kv4.3 + KChIP2) or the PC phenotype (Kv4.3 + NCS1). Additionally, DPP6 wild type (WT) or variant was transfected. Ito was assessed by patch clamping. Results: Clinical DPP6-R274H, affecting a conserved region in the extracellular protein domain segregated with an autosomal dominant pattern of inheritance. The female index patient experienced first VF at 17 years, and subsequent ICD therapy, after her brother had died suddenly at 13 years. Both carriers were also known with mitral-valve prolapse (MVP), but otherwise without structural heart disease. A third sibling without arrhythmia, but with mild MVP, did not carry the DPP6 variant. No other pathogenic mutations were found by next generation sequencing in the index patient. ECGs of the index patient revealed dynamic early repolarization, U waves with varying amplitudes and pause-dependent prominence, and &amp;gt;8000/24 h superimposed premature ventricular complexes (PVCs) and (non)sustained VT. PVCs (QRS duration 120 ms) displayed both a left posterior (80%) and anterior (20%) fascicular origin. PVC burden was higher during daytime and exercise, with pause-dependent occurrence. Cellular In the PC model DPP6-R274H markedly decreased Ito density (at +30 mV: 291 pA/pF vs 995 pA/pF in WT; p &amp;lt; 0.001), whereas it did not in the VM model. In VM, but not in PC, Ito inactivation was slowed by the variant (Tau at 0 mV: 91 ms vs 49 ms in WT; p &amp;lt; 0.001). Conclusions The novel DPP6 variant R274H has differential effects on Ito in cellular models of VM versus PC. Our main finding of a loss-of-function in the PC model combined with a slowed Ito inactivation in the VM phenotype may exaggerate electrical heterogeneity, especially at the PC-VM junction. Ito loss in PC would prolong action-potential duration and promote early afterdepolarizations, consistent with the dynamic patterns of T-U-dispersion and (fascicular) ectopy in the index case. Mechano-electric influences by the MVP further promote arrhythmogenesis.

673Bipolar radiofrequency ablation supported by non-ionic catheter irrigation

Abstract Introduction Bipolar radiofrequency catheter ablation (Bi-RFCA) or irrigation of ablation catheter (AC) using non-ionic coolant, such as dextrose-5 in water (D5W), are novel ways to improve lesion formation in case of arrhythmia refractoriness. Combination of these two methods has not yet been described. Puprose To determine feasibility and effectiveness of Bi-RFCA additionally supported by non-ionic catheter irrigation for treatment of refractory premature ventricular complexes (PVC) or ventricular tachycardia (VT). Methods Consecutive patients after failed extensive Bi-RFCA or D5W-irrigated ablation for symptomatic PVCs or non-sustained VT (nsVT) underwent Bi-RFCA supported with D5W coolant. Results We ultimately enrolled 2 patients (2 males, age 64 ± 12 years) after failed extensive ablations for the left ventricular summit PVCs and nsVT to undergo Bi-RFCA supported with D5W irrigation of both AC and intracardiac return electrode (IRE). Previous pharmacological antiarrhythmic treatment consisting of at least one drug and catheter ablation failed in both patients. Bi-RFCA was delivered between earliest activation sites located in the left/right aortic commissure and the left pulmonic cusp (Figure). Efforts were made to achieve safe distance from coronary arteries, AC, and IRE. Bipolar RFCA (35 ± 7W power, 8 ± 4 applications, 199 ± 166s RF time) led to acute elimination of PVCs in both patients. Baseline impedance oscillated around 250Ω and initial 50-70Ω impedance drop was observed during first 20s of bipolar applications, followed by impedance rise up to 350-450Ω. No steam pop occurred and there were no complications during procedures. All antiarrhythmic drugs were discontinued. Follow-up lasted 8 ± 2 months, there was no nsVT recurrence and 90,4% PVC burden reduction was achieved: from 30000 to 3100 PVC/day in patient #1 and from 39000 to 3500 PVC/day in patient #2. Both patients remained symptom-free. Conclusion Bi-RFCA can be additionally supported using non-ionic D5W coolant. Such approach is feasible and can be safe and effective. More data on impedance imbalance during D5W-supported bipolar RF applications is warranted. Abstract Figure. Fluoroscopic view and 12-lead ECG

133Bipolar ablation of refractory ventricular arrhythmias originating from the close proximity of His bundle

Abstract Introduction Biophysics of bipolar radiofrequency catheter ablation (Bi-RFCA) suggest more condensed and selective lesion formation when compared to conventional-unipolar approach. Whether more selective Bi-RFCA can result in safe and effective ablation of arrhythmic substrates in close proximity of His bundle has not been investigated so far. Purpose To determine feasibility and effectiveness of Bi-RFCA in His bundle area. Methods Consecutive patients after failed unipolar ablation for symptomatic premature ventricular complexes (PVC) or ventricular tachycardia (VT) originating from the vincity of His bundle underwent Bi-RFCA. Results We ultimately enrolled 8 patients (2 females, age 60 ± 15 years) to undergo Bi-RFCA of PVC/VT. Previous pharmacological treatment consisting of at least one antiarrhythmic drug and conventional catheter ablation failed in all. Bi-RFCA using open-irrigated and non-irrigated ablation catheters (AC) was delivered from two earliest PVC/VT activation sites located in the vincity of His bundle (Figure, panels A-B). A total number of 93 bipolar applications were delivered (mean bipolar RF time 508 ± 565s, mean power 35 ± 13W, mean impedance 163 ± 18Ω). Transient conduction disturbances occurred in 2 patients and were associated with mechanical compression of conduction system. No persistent conduction disturbances occurred. Bipolar RFCA led to acute elimination of PVC/VT in 6 (75%) patients. Follow up lasted 11 ± 5 months: two patients underwent repeat procedure using dual-irrigated Bi-RFCA, there was no VT recurrence and 72% PVC burden reduction was achieved (16200 ± 11600 pre-ablation vs 4500 ± 6200 post-ablation PVC/day, p = 0,035) (Figure, panel C). Conclusion Bi-RFCA performed in proximity of His bundle can be safe and effective in majority of patients. Abstract Figure. Bipolar ablation of parahisian PVC/VT

Evaluation and Management of Premature Ventricular Complexes.

Premature ventricular complexes (PVCs) are extremely common, found in the majority of individuals undergoing long-term ambulatory monitoring. Increasing age, a taller height, a higher blood pressure, a history of heart disease, performance of less physical activity, and smoking each predict a greater PVC frequency. Although the fundamental causes of PVCs remain largely unknown, potential mechanisms for any given PVC include triggered activity, automaticity, and reentry. PVCs are commonly asymptomatic but can also result in palpitations, dyspnea, presyncope, and fatigue. The history, physical examination, and 12-lead ECG are each critical to the diagnosis and evaluation of a PVC. An echocardiogram is indicated in the presence of symptoms or particularly frequent PVCs, and cardiac magnetic resonance imaging is helpful when the evaluation suggests the presence of associated structural heart disease. Ambulatory monitoring is required to assess PVC frequency. The prognosis of those with PVCs is variable, with ongoing uncertainty regarding the most informative predictors of adverse outcomes. An increased PVC frequency may be a risk factor for heart failure and death, and the resolution of systolic dysfunction after successful catheter ablation of PVCs demonstrates that a causal relationship can be present. Patients with no or mild symptoms, a low PVC burden, and normal ventricular function may be best served with simple reassurance. Either medical treatment or catheter ablation are considered first-line therapies in most patients with PVCs associated with symptoms or a reduced left ventricular ejection fraction, and patient preference plays a role in determining which to try first. If medical treatment is selected, either β-blockers or nondihydropyridine calcium channel blockers are reasonable drugs in patients with normal ventricular systolic function. Other antiarrhythmic drugs should be considered if those initial drugs fail and ablation has been declined, has been unsuccessful, or has been deemed inappropriate. Catheter ablation is the most efficacious approach to eradicate PVCs but may confer increased upfront risks. Original research remains necessary to identify individuals at risk for PVC-induced cardiomyopathy and to identify preventative and therapeutic approaches targeting the root causes of PVCs to maximize effectiveness while minimizing risk.

Premature ventricular contraction detection for long-term monitoring in an implantable cardiac monitor.

Premature ventricular complexes (PVCs) are an important therapeutic target in symptomatic patients and in the setting of PVC-induced cardiomyopathy; however, measuring burden and therapeutic response is challenging. We developed and validated an algorithm for continuous long-term monitoring of PVC burden in an insertable cardiac monitor (ICM). A high-specificity PVC detection algorithm was developed using real-world ICM data and validated using simultaneous Holter data and real-world ICM data. The PVC algorithm uses long-short-long RR interval sequence and morphology characteristics for three consecutive beats to detect the occurrence of single PVC beats. Data are expressed as gross incidence, patient average, and generalized estimating equation estimates, which were used to determine sensitivity, specificity, positive and negative predictive value (PPV, NPV). The PVC detection algorithm was developed on eighty-seven 2-min EGM strips recorded by an ICM to obtain a sensitivity and specificity of 75.9% and 98.8%. The ICM validation data cohort consisted of 787 ICM recorded ECG strips 7-16 min in duration from 134 patients, in which the algorithm detected PVC beats with a sensitivity, specificity, PPV, and NPV of 75.2%, 99.6%, 75.9%, and 99.5%, respectively. In the Holter validation dataset with continuous 2-h snippets from 20 patients, the algorithm sensitivity, specificity, PPV, and NPV were 74.4%, 99.6%, 68.8%, and 99.7%, respectively, for detecting PVC beats. The PVC detection algorithm was able to achieve a high specificity with only 0.4% of the normal events being incorrectly identified as PVCs, while detecting around three of four PVCs on a continuous long-term basis in ICMs.

Novel risk calculator performance in athletes with arrhythmogenic right ventricular cardiomyopathy

Disease progression and ventricular arrhythmias (VAs) in arrhythmogenic right ventricular cardiomyopathy (ARVC) are correlated with physical exercise, and clinical detraining and avoidance of competitive sport practice are suggested for ARVC patients. An algorithm assessing primary arrhythmic risk in ARVC patients was recently developed by Cadrin-Tourigny etal. Data regarding its transferability to athletes are lacking. The purpose of this study was to assess the reliability of the Cadrin-Tourigny risk prediction algorithm in a cohort of athletes with ARVC and to describe the impact of clinical detraining on disease progression. All athletes undergoing clinical detraining after ARVC diagnosis at our institution were enrolled. Baseline and follow-up clinical characteristics and data on VA events occurring during follow-up were collected. The Cadrin-Tourigny algorithm was used to calculate the a priori predicted VA risk, which was compared with the observed outcomes. Twenty-five athletes (age 36.1 ± 14.0 years; 80% male) with definite ARVC who were undergoing clinical detraining were enrolled. Over median (interquartile range) follow-up of 5.3 (3.2-6.6) years, a reduction in premature ventricular complex (PVC) burden (P = .001) was assessed, and 10 VA events (40%) were recorded. The a priori algorithm-predicted risk seemed to fit with the observed cohort arrhythmic risk [mean observed-predicted risk difference over 5 years -0.85% (interquartile range -4.8% to +3.1%); P = .85]. At 1-year follow-up, 11 patients (44%) had an improved stress ECG response, and no significant changes in right ventricular ejection fraction were observed. Clinical detraining is associated with PVC burden reduction in athletes with ARVC. The novel risk prediction algorithm does not seem to require any correction for its application to ARVC athletes.

Predictors of adverse outcome in patients with frequent premature ventricular complexes: The ABC-VT risk score

No independently validated score currently exists for risk stratification of patients with frequent premature ventricular complexes (PVCs). The purpose of this study was to develop a risk score to predict adverse events in patients with frequent PVCs. We analyzed consecutive patients between 2012 and 2017 undergoing 14-day continuous monitoring with frequent PVCs (>5%) and concurrent echocardiography. We performed binary logistic regression to determine multivariate predictors of adverse left ventricular remodeling (left ventricular ejection fraction [LVEF] <45% or left ventricular end-diastolic volume index >75 mL/m2). A risk score was created using the log(odds ratio (OR)) of these predictors and validated prospectively to determine the risk of future adverse events in those with baseline LVEF >45%. An adverse event was defined as LVEF decline by 10%, heart failure hospitalization, or cardiovascular mortality. Two validation cohorts were used: follow-up from the original derivation cohort (cohort 1) and an independent Korean PVC registry (cohort 2). The derivation cohort comprised 206 patients with a mean PVC burden of 11.6% ± 6.2% and considerable daily fluctuation (minimum burden 7.3% ± 6.2% vs maximum 17.9% ± 8.0%). Independent predictors of adverse remodeling were as follows: superiorly directed PVC axis (OR 2.7; 1 point), PVC burden 10%-20% (OR 3.5; 2 points) and >20% (OR 4.4; 3 points), PVC coupling interval >500 ms (OR 4.7; 4 points), nonsustained ventricular tachycardia (OR 5.3; 4 points), which form the ABC-VT risk score. This score predicted future adverse events in both validation cohorts: cohort 1, hazard ratio 1.43; 95% confidence interval 1.19-1.73; P< .001 and cohort 2, hazard ratio 1.22; 95% confidence interval 1.05-1.42; P = .01. The ABC-VT score is a simple tool that predicts adverse left ventricular remodeling and future clinical deterioration in patients with frequent PVCs.

Influence of baseline QRS on the left ventricular ejection fraction recovery after frequent premature ventricular complex ablation

Frequent premature ventricular complexes (PVCs) can induce or worsen left ventricular systolic dysfunction. We aimed to investigate the influence of the baseline QRS in the response after PVC ablation in patients with depressed left ventricular ejection fraction (LVEF). Two hundred and fifteen [59 ± 13 years old, 152 (71%) men] consecutive patients with left ventricular (LV) systolic dysfunction and frequent PVCs referred for ablation were included and followed-up for 12 months. Echocardiographic response was defined as an improvement of at least five absolute points in LVEF. Clinical, electrocardiogram, and electrophysiological characteristics were analysed. Mean baseline QRS duration was 110 ms [97-140]. Premature ventricular complex burden significantly decreased after ablation from 23% [16-33] at baseline to 1% [0-8] at 12 months, P < 0.001. Mean PVC burden reduction was 18 [8-30] points. There was a significant improvement of LVEF from 35% [29-40] at baseline to 44% [35-55] at 12 months, P < 0.001. One hundred and thirty (61%) patients were considered as echocardiographic responders. Baseline QRS duration (ms) [odds ratio (OR) 0.98 (0.97-0.99), P = 0.01] was an independent predictor of echocardiographic response. Mean LVEF improvement was 16 [10-21] points when the baseline QRS duration was <90 ms; 12 [4-20] when it was 90-110 ms; 5 [0-15] when it was 110 ± 130 ms; and 0 [0-6] points when it was >130 ms. In patients with LV systolic dysfunction, intrinsic QRS duration is inversely related to the probability and the degree of echocardiographic response after frequent PVC ablation. Patients with a QRS duration >130 ms at baseline have the poorer response after ablation.

The Ubiquitous Premature Ventricular Complex.

Premature ventricular complexes (PVCs) are one of the most commonly encountered arrhythmias and are ubiquitous in clinical practice, both in the outpatient and inpatient settings. They are often discovered incidentally in asymptomatic patients, however, can cause myriad symptoms acutely and chronically. Long thought to be completely benign, PVCs have been historically disregarded without pursuing any further evaluation. Newer data have revealed that a high burden of PVCs with specific characteristics can significantly increase a patient's risk of developing PVC-induced cardiomyopathy. The aim of this literature review is to provide further clarification on the identification of high-risk PVCs, subsequent workup, and the currently available treatment options. PVCs arise from an ectopic focus within the ventricles. Patients with PVCs can be either asymptomatic or have severe disabling symptoms. The diagnostic workup for PVCs includes electrocardiogram (ECG) and 24-h Holter monitor to assess the QRS morphology and its frequency. A transthoracic echocardiogram (TTE) is done to look for structural heart disease and cardiomyopathy. Management of PVCs should be focused on identifying and treating the underlying causes, such as electrolyte abnormalities, substance use, and underlying structural heart disease. Beta-blockers are first-line therapy for symptomatic PVCs. Nondihydropyridine calcium channel blockers, classic antiarrhythmic agents, and amiodarone can be considered as second-line agents. Patients who are unable to tolerate medical therapy should undergo catheter ablation of the PVC focus to prevent PVC-induced cardiomyopathy. PVCs are common in clinical practice, and it is vital to identify patients at higher risk for PVC-induced cardiomyopathy to facilitate early intervention. Patients with no evidence of structural heart disease and infrequent PVCs should be monitored closely, while those who are symptomatic should be treated medically. For those who have failed medical therapy, catheter ablation of the PVCs focus is recommended. Catheter ablation has been shown to reduce PVCs burden and improve left ventricular ejection fraction (LVEF) in those with PVC-induced cardiomyopathy.

Premature ventricular complexes: diagnostic and therapeutic considerations in clinical practice : A state-of-the-art review by the American College of Cardiology Electrophysiology Council.

Premature ventricular complexes (PVCs) are common arrhythmias in the clinical setting. PVCs in the structurally normal heart are usually benign, but in the presence of structural heart disease (SHD), they may indicate increased risk of sudden death. High PVC burden may induce cardiomyopathy and left ventricular (LV) dysfunction or worsen underlying cardiomyopathy. Sometimes PVCs may be a marker of underlying pathophysiologic process such as myocarditis. Identification of PVC burden is important, since cardiomyopathy and LV dysfunction can reverse after catheter ablation or pharmacological suppression. This state-of-the-art review discusses pathophysiology, clinical manifestations, how to differentiate benign and malignant PVCs, PVCs in the structurally normal heart, underlying SHD, diagnostic procedures (physical examination, electrocardiogram, ambulatory monitoring, exercise testing, echocardiography, cardiac magnetic resonance imaging, coronary angiography, electrophysiology study), and treatment (lifestyle modification, electrolyte imbalance, medical, and catheter ablation).

Prognostic significance of premature ventricular complex burden on hospitalized patients with heart failure.

BackgroundThe clinical significance of premature ventricular complexes (PVCs) in heart failure (HF) remains unclear. We aimed to clarify the associations of PVC burden with re‐hospitalization and cardiac death in HF patients.MethodsWe studied 435 HF patients (271 men, mean age 65 years). All patients were hospitalized for worsening HF. After optimal medications, echocardiography, 24 hours Holter monitoring and cardiopulmonary exercise testing were performed before discharge. The clinical characteristics and outcomes of the HF patients were investigated.ResultsDuring a median follow‐up period of 2.3 years, there were 125 (28.7%) cardiac events (re‐hospitalization due to worsening HF, fatal arrhythmias, or cardiac death). The patients with cardiac events had higher PVC burden compared to those without (median 0.374%/d [interquartile range 0.013‐1.510] vs median 0.026%/d [interquartile range 0.000‐0.534], P < .001). We examined cutoff value of PVC burden for predicting cardiac events. Receiver‐operating characteristic analysis showed PVC burden (>0.145%/d) to be a predictive factor of cardiac events (area under the curve: 0.64). Kaplan‐Meier analysis demonstrated that cardiac events were more frequent in patients with high‐PVC burden (>0.145%/d, n = 194) compared to those with low‐PVC burden (≤0.145%/d, n = 241). Furthermore, the high‐PVC burden patients had left ventricular (LV) and atrial dilatation, reduced LV ejection fraction, and impaired exercise capacity, compared to the low‐PVC burden patients. In Cox proportional hazards analysis, high‐PVC burden was significantly associated with cardiac events with a hazard ratio of 2.028 (95% confidence interval: 1.418‐2.901, P < .001).ConclusionThese results suggest that PVC burden is an important predictor of cardiac events in HF patients.

P5703The anterior interventricular crux: anatomic basis for ablation below the left sinus of valsalva (LSOV) of varied ECG morphology PVCs

Abstract Background Outflow tract premature ventricular complexes (PVCs) may be ablated at sites where the local electrogram is early. We describe ablation of PVCs of varying morphology at a cruciate structure extending from the inflection of the great cardiac vein to the junction of the distal RVOT and from the left ventricular (LV) inflow myocardium through the aortic mitral continuity (AMC) to the right coronary sinus of Valsalva centered below LSOV, termed the LV crux. Purpose Evaluate a novel target for ablation of PVCs with varied QRS morphologies. Methods A series of 51 patients undergoing ablation for PVCs between 2013–2018 was identified. In all cases, ICE-guided ablation occurred at the center of the LV crux. Results All patients had high PVC burden &gt;20% (28±8%); EF&lt;50% in 40/51 (78%). QRS morphology of PVCs is summarized in Table 1. 50% had prior ablation attempted at early sites. Mapping and ICE-guided ablation at the LV crux (Figure 1 A-B) revealed early activation with near-field ventricular or fascicular signal in 31 (61%), while others had early sites at extensions of the crux. PVCs were eliminated in 50/51 (98%) with continued suppression at 3-months. EF normalized in all 51. Table 1. ECG charactaeristics ECG characteristics Number of patients (%) Inferior morphology 51/51 (100%) Lead I morphology Monophasic R 8/51 (16%) Rs 9/51 (18%) rS 34/51 (66%) Precordial transition Positive across precordium 40 (78%) V2 transition 7 (14%) V3 transition 4 (8%) Maximum deflection index &lt;0.55 37 (73%) &gt;0.55 14 (27%) Figure 1. Mapping and ablation Conclusions A cruciate interventricular multidimensional crux centered below the LSOV is a site for successful ablation of varied PVC morphologies and should be considered for detailed mapping and ablation, particularly when multiple morphologies are present or prior ablation at early sites is unsuccessful. Ventricular myocardial architecture along with conduction system remnants may be the basis for this phenomenon.

The effect of idiopathic premature ventricular complexes on left ventricular ejection fraction.

AimCurrent literature lacks a definitive threshold of idiopathic premature ventricular complex (PVC) burden for predicting cardiomyopathy (CMP). The main objective of the present study was to evaluate relationship between the PVC burden and left ventricular ejection fraction (LVEF).MethodThis multicenter, cross‐sectional study included 341 consecutive patients with more than 1,000 idiopathic PVC in 24 hr of Holter monitoring admitted to the cardiology clinics between January 2019 and May 2019 in the nineteen different centers. The primary outcome was the LVEF measured during the echocardiographic examination.ResultOverall, the median age was 50 (38–60) and 139 (49.4%) were female. Percentage of median PVC burden was 9% (IQR: 4%–17.4%). Median LVEF was found 60% (55–65). We used proportional odds logistic regression method to examine the relationship between continuous LVEF and candidate predictors. Increase in PVC burden (%) (regression coefficient (RE) −0.644 and 95% CI −1.063, –0.225, p < .001), PVC QRS duration (RE‐0.191 and 95% CI −0.529, 0.148, p = .049), and age (RE‐0.249 and 95% CI −0.442, −0.056, p = .018) were associated with decrease in LVEF. This inverse relationship between the PVC burden and LVEF become more prominent when PVC burden was above 5%. A nomogram developed to estimate the individual risk for decrease in LVEF.ConclusionOur study showed that increase in PVC burden %, age, and PVC QRS duration were independently associated with decrease in LVEF in patients with idiopathic PVC. Also, inverse relationship between PVC burden and LVEF was observed in lower PVC burden than previously known.

Catheter ablation of premature ventricular complexes with low intraprocedural burden guided exclusively by pace-mapping.

Catheter ablation (CA) of idiopathic premature ventricular complexes (PVCs) is typically guided by both activation and pace-mapping, with ablation ideally delivered at the site of the earliest local activation. However, activation mapping requires sufficient intraprocedural quantity of PVCs. This study aimed to investigate the outcome of CA of infrequent PVCs guided exclusively by pace-mapping. We retrospectively analyzed all patients undergoing CA of idiopathic PVCs between 2014 and 2017. Among 327 patients, 24 (7.3%) had low intraprocedural PVC burden despite isoproterenol, including two patients with zero PVCs, rendering activation mapping impractical/impossible. All 24 had a history of symptomatic PVCs. During ablation, a median of 27 (17-55) pace-maps were performed, with best median PASO score of 97 (96-98)%. A median of 12 (8.75-18.75) radiofrequency (RF) lesions were delivered with 11.4 (8.5-17.6) minutes of total RF time. Clinical success, defined as more than 80% reduction in the burden of previously frequent PVCs and/or absence of symptoms as well as any documented clinical PVCs among those with infrequent or exercise-induced PVCs, was achieved in 19 (79%) patients over 9.2 (2.0-15.0) months of follow-up. When activation mapping cannot be performed due to inadequate intraprocedural PVC burden, detailed pace-mapping can frequently identify the precise arrhythmia site of origin, thereby guiding successful CA.

Bipolar radiofrequency ablation delivered from coronary veins and adjacent endocardium for treatment of refractory left ventricular summit arrhythmias.

Radiofrequency catheter ablation (RFCA) of premature ventricular complexes (PVC) and ventricular tachycardia (VT) can be an effective method of treatment. However, when arrhythmia originates from the left ventricular summit (LVS), an ablation performed with conventional unipolar energy sources can be challenging and may require alternative approaches. Bipolar RFCA from coronary veins and an adjacent endocardium in cases of refractory PVC/VT has not yet been studied. We retrospectively analysed cases of consecutive patients who underwent bipolar ablation in whom conventional unipolar ablation of LVS PVC/VT and antiarrhythmic drugs failed to abolish arrhythmia. Bipolar RFCA was delivered from the earliest PVC/VT activation located in the coronary venous circulation and opposite LV endocardial sites. A total number of 4 patients (1 female, age 55 ± 10years) underwent bipolar ablation of LVS from coronary veins and an adjacent endocardium. Bipolar RFCA led to acute elimination of PVC/VT in all patients. A mean bipolar RFCA time was 244 ± 15s. There were no complications during procedures and all antiarrhythmic drugs were discontinued. A follow-up lasted 15 ± 4months; there was no VT recurrence and the mean 83 ± 27% PVC burden reduction (24250 ± 1372 vs. 3000 ± 3600 PVC/d; p = 0.0228) was achieved. All patients remained symptom-free. Bipolar RFCA from coronary veins and an opposite endocardium can be used for safe and successful treatment of PVC/VT originating from a deep LV summit.

Heart Failure with Preserved Ejection Fraction is a Highly Arrhythmogenic Disease

Background Sudden cardiac death (SCD) is a relatively common mode of death in patients with heart failure preserved ejection fraction (HFpEF). However, the spectrum and burden of cardiac arrhythmias, particularly those of ventricular arrhythmias, has not well established in these patients. Methods We performed routine arrhythmia surveillance using a 14-day adhesive patch ambulatory ECG recorder (ZioPatch) in patients with HFpEF, enrolled in a subspecialty heart failure clinic. Cardiac electrophysiologists interpreted the ECG recordings. We extracted the clinical data from electronic medical records. Results A total of 40 patients (mean age 71.1±9.9 years, 53% women) with HFpEF underwent routine Ziopatch monitoring. Mean ejection fraction was 59.4±4.4% and 44% had history of coronary artery disease. Of the 40 patients, 32.5% had episodes of non-sustained ventricular tachycardia (VT) (mean 5±5.2 episodes), 15.0% had paroxysmal atrial fibrillation and 80.0% had episodes of supraventricular tachycardia during the monitored period. All patients had premature ventricular complexes (PVC) with 7.5% having a PVC burden that exceeded 5%. Patients with non-sustained VT had a relatively lower EF, higher NT-proBNP level and were more likely to be obese (Table). Conclusion Patients with HFpEF have a high, and possibly underappreciated, burden of cardiac arrhythmias. The frequent episodes of non-sustained VT in these patients may provide insight into the mechanism of SCD in HFpEF.

Premature Ventricular Complex-Induced Cardiomyopathy.

Frequent premature ventricular complexes (PVCs) can cause an often reversible form of cardiomyopathy. The mechanism for the development of premature ventricular complex-induced cardiomyopathy (PIC) continues to be investigated, and animal models as well as human clinical trials suggest ventricular dyssynchrony to be an important component. In addition to a high PVC burden, this review will detail other risk factors associated with the development of PIC. PVCs can be a marker for the presence of other underlying disease and a thorough work-up, including cardiac magnetic resonance imaging with delayed contrast enhancement, needs to be considered to rule out the presence of structural heart disease. Management of PIC can involve catheter ablation or pharmacotherapy. Multicenter studies have shown a high success rate paired with a low complication rate with catheter ablation, and hence catheter ablation has emerged as the preferred therapeutic option for most patients with PIC. Advances in ablation strategy and technology have enhanced our ability to address certain challenging PVC locations. Important challenges that remain include understanding the coexistence of PIC with other forms of cardiomyopathy, whether there is an associated risk of sudden cardiac death, and the long-term effects on cardiac substrate of exposure to frequent PVCs.