Catheter ablation of parahisian premature ventricular complexes in patients with and without cardiac scar.

BACKGROUND: Ablation of premature ventricular complexes (PVCs) originating from the parahisian area is challenging. Late gadolinium-enhanced cardiac magnetic resonance (LGE-CMR) scar may influence procedural outcomes; the impact of cardiac scar on parahisian PVCs has not been described. OBJECTIVE: The objective of this study was to examine the incidence and significance of LGE-CMR scarring in patients undergoing ablation for parahisian PVCs. METHODS: Consecutive patients who underwent preprocedure LGE-CMR imaging and ablation of parahisian PVCs were included. Acute and long-term outcomes were examined. RESULTS: Forty-eight patients were included (male, n = 37; age, 66 ± 10 years; ejection fraction, 50% ± 12%; preprocedure PVC burden, 21% ± 12%). Intramural LGE-CMR scar was present in 33 of 48 (69%) patients. Cryoablation was used in 9 patients; ablation in multiple chambers was required in 28 (58%) patients. The PVC site of origin (SOO) was intramural (n = 25 patients), left ventricular (n = 5), and right ventricular (n = 18). Patients with LGE-CMR scar were more likely to have intramural PVCs (64% vs 27%; P < .04) and to require ablation in multiple cardiac chambers (58% vs 13%; P < .02). Patients with intramural scar required longer duration of ablation delivery (31 ± 20 minutes vs 17 ± 8 minutes; P < .02). Acute procedural success was 69%; PVC burden on follow-up was 6% ± 9% and similar for those with and without scar. CONCLUSION: Ablation of parahisian PVCs often requires mapping and ablation of multiple cardiac chambers, with an intramural SOO identified in most patients. An intramural scar was associated with an intramural SOO of the PVCs requiring more extensive ablation procedures, with similar long-term outcomes compared with those without scar.

Mitral Annular Substrate and Ventricular Arrhythmias in Arrhythmogenic Mitral Valve Prolapse With Mitral Annular Disjunction.

BACKGROUND: In patients with bileaflet mitral valve prolapse (MVP), mitral annular disjunction (MAD) is associated with increased risk of sudden cardiac death via incompletely understood mechanisms. OBJECTIVES: This study assessed the substrate for ventricular arrhythmias in patients with bileaflet MVP and MAD as well as outcomes of catheter ablation with an emphasis on sustained, monomorphic ventricular tachycardia (VT). METHODS: A total of 18 consecutive patients (11 women, mean age 54 ± 15 years) with bileaflet MVP and MAD underwent catheter ablation for VT, and/or premature ventricular complexes (PVCs). Eight patients had a prior cardiac arrest. RESULTS: PVCs were targeted for ablation in all 18 patients (symptomatic PVCs n = 15, PVC-induced ventricular fibrillation n = 3). Sustained monomorphic VT was targeted in 7 of 18 patients. Electroanatomic mapping showed low voltage in the area of the mitral annulus corresponding to VT target sites in 6 of 7 patients with sustained VT. Four of 7 patients had low voltage in the areas of MAD. Six of 7 patients with VT were rendered noninducible post-ablation. The PVC burden was reduced from 11.0% ± 10.4% to 4.0% ± 5.5% (P = 0.004). Over a mean follow-up of 33.9 ± 43.4 months, no VTs recurred. There were no major complications. No repeat ablations for VT occurred. Five of 18 patients required repeat ablation for PVCs. CONCLUSIONS: In patients with bileaflet MVP and MAD undergoing catheter ablation, the mitral valve annulus often contains low-voltage areas harboring the substrate for monomorphic VT and PVCs. Ablation in these patients was safe and improved arrhythmia control.

Comparison of warfarin with direct oral anticoagulants for thromboembolic prophylaxis after catheter ablation of ventricular tachycardia.

INTRODUCTION: Thromboembolic events after catheter ablation of ventricular tachycardia (VT) can result in significant morbidity. Thromboembolic prophylaxis after catheter ablation can be achieved by the use of antiplatelet agents, vitamin K antagonists, or direct oral anticoagulants (DOACs). The relative safety and efficacy of these modes of prophylaxis are uncertain. We sought to compare the outcomes of patients who received warfarin or DOACs for thromboembolic prophylaxis after catheter ablation of VT. METHODS AND RESULTS: Anticoagulation with DOACS was started after left ventricular VT ablation in a series of 42 consecutive patients with structural heart disease (67 ± 11 years, 3 women, ejection fraction 32 ± 14%). Duration of hospital stay, bleeding episodes, and thromboembolic events were compared to a historic consecutive group of patients (n = 38, 65 ± 13 years, 14 women, ejection fraction 36 ± 13%) in whom anticoagulation with a formerly described protocol of heparin and vitamin K antagonist was used after VT ablation procedures. Hospital stay was significantly shorter in the group where DOACs were used as compared to vitamin K antagonists (3.3 ± 1.8 vs. 5.0 ± 2.5 days postablation; p = 0.001) without an increase of bleeding or thromboembolic events. CONCLUSION: Anticoagulation with DOACs is safe and shortens hospital stay in patients with structural heart disease undergoing left ventricular VT ablation procedures.

Complications of catheter ablation for ventricular tachycardia.

With the increasing literature demonstrating benefits of catheter ablation for ventricular tachycardia (VT), the number of patients undergoing VT ablation has increased dramatically. As VT ablation is being performed more routinely, operators must be aware of potential complications of VT ablation. This review delves deeper into the practice of VT ablation with a focus on periprocedural complications.

Cardiac Involvement and Arrhythmias Associated with Myotonic Dystrophy.

Myotonic dystrophy is an autosomal dominant genetic disease of nucleotide expansion resulting in neuromuscular disease with two distinct subtypes. There are significant systemic manifestations of this condition including progressive muscular decline, neurologic abnormalities, and cardiac disease. Given the higher prevalence of cardiac dysfunction compared to the general population, there is significant interest in early diagnosis and prevention of cardiac morbidity and mortality. Cardiac dysfunction has an origin in abnormal and unstable nucleotide repeats in the DMPK and CNBP genes which have downstream effects leading to an increased propensity for arrhythmias and left ventricular systolic dysfunction. Current screening paradigms involve the use of routine screening electrocardiograms, ambulatory electrocardiographic monitors, and cardiac imaging to stratify risk and suggest further invasive evaluation. The most common cardiac abnormality is atrial arrhythmia, however there is significant mortality in this population from high-degree atrioventricular block and ventricular arrhythmia. In this review, we describe the cardiac manifestations of myotonic dystrophy with an emphasis on arrhythmia which is the second most common cause of death in this population after respiratory failure.

Pharmacologic Management for Ventricular Arrhythmias: Overview of Anti-Arrhythmic Drugs.

Ventricular arrhythmias (Vas) are a life-threatening condition and preventable cause of sudden cardiac death (SCD). With the increased utilization of implantable cardiac defibrillators (ICD), the focus of VA management has shifted toward reduction of morbidity from VAs and ICD therapies. Anti-arrhythmic drugs (AADs) can be an important adjunct therapy in the treatment of recurrent VAs. In the treatment of VAs secondary to structural heart disease, amiodarone remains the most well studied and current guideline-directed pharmacologic therapy. Beta blockers also serve as an important adjunct and are a largely underutilized medication with strong evidentiary support. In patients with defined syndromes in structurally normal hearts, AADs can offer tailored therapies in prevention of SCD and improvement in quality of life. Further clinical trials are warranted to investigate the role of newer therapeutic options and for the direct comparison of established AADs.

Association between biventricular pacing and incidence of ventricular arrhythmias in the early post-operative period after left ventricular assist device implantation.

INTRODUCTION: Cardiac resynchronization therapy (CRT) and left ventricular assist devices (LVAD) improve outcomes in heart failure patients. Early ventricular arrhythmias (VA) are common after LVAD and are associated with increased mortality. The association between left ventricular pacing (LVP) with CRT and VAs in the early post-LVAD period remains unclear. METHODS: This was a retrospective study of all patients undergoing LVAD implantation from 1/2016 to 12/2019. Patients were divided into those with CRT and active LVP (CRT-LVP) immediately post-LVAD implant versus those without CRT-LVP. Implantable cardiac defibrillator electrograms were reviewed and early VAs were defined as sustained ventricular tachycardia (VT)/ventricular fibrillation occurring within 30 days of LVAD implantation. RESULTS: Of 186 included patients (mean age 53 years, 75% male, mean body mass index 28), 72 had CRT devices, 63 of whom had LV pacing enabled after LVAD implant (CRT-LVP group). Patients with CRT-LVP were more likely to have VA in the early postoperative period (21% vs. 4%; p = .0001). All 9 patients with CRT in whom LVP was disabled had no early VA. Among those with early VA, patients with CRT-LVP were more likely to have monomorphic VT (77% vs. 40%; p = .07). In multiple logistic regression, CRT-LVP pacing remained an independent predictor of early VA after adjustment for history of VA and AF. CONCLUSIONS: Patients with CRT-LVP after LVAD implant had a higher incidence of early VA (specifically monomorphic VT). Epicardial LV pacing may be proarrhythmic in the early postoperative period after LVAD.

Double ProGlide preclose technique for vascular access closure after leadless pacemaker implantation.

PURPOSE: The use of vascular closure devices in patients receiving the Micra leadless pacemaker may shorten time to ambulation, facilitate same-day discharge, and reduce risk of venous thrombosis associated with manual hemostasis. We sought evaluate the feasibility of double Perclose ProGlide (Abbott, CA) preclosure for access site hemostasis after leadless pacemaker implant. METHODS: Patients with leadless pacemaker implant and double preclosure for access hemostasis from 2020 to 2021 were reviewed for complications requiring increase of flat time or transfusion, incidence of venous thromboembolism, and hemoglobin decrement. Two ProGlide devices were deployed with a double preclose technique after ultrasound guided wire access. Patients were instructed to lay flat for 2-4 h and were allowed to ambulate after. RESULTS: A total of 36 patients (age 74.5 ± 15.1 years, BMI 27.9 ± 9.0 kg/m2, 30% female gender) were included with 6 having prior venous thromboembolism, 21 with AF, and 15 with chronic kidney disease. Anticoagulation was continued in 14 (8 direct oral anticoagulants, 2 warfarin, 4 intravenous heparin) and interrupted in 5. In one patient, minor rebleeding prompted 10 min of manual pressure and extension of flat time by 2 h. No patients had other complications, prolongation of flat time, transfusion, delayed re-initiation of anticoagulation, or venous thromboembolism within 30 days. CONCLUSIONS: The double preclose technique is a safe and feasible method of achieving access site hemostasis and facilitates early ambulation after leadless pacemaker implantation.

Atypical Antipsychotic Safety in the CICU.

Atypical antipsychotics are used in cardiac intensive care units (CICU) to treat delirium despite limited data on safety in patients with acute cardiovascular conditions. Patients treated with these agents may be at higher risk for adverse events such as QTc prolongation and arrhythmias. We performed a retrospective cohort study of 144 adult patients who were not receiving antipsychotics before admission and received olanzapine (n = 50) or quetiapine (n = 94) in the Michigan Medicine CICU. Data on baseline characteristics, antipsychotic dose and duration, length of stay, and adverse events were collected. Adverse events included ventricular tachycardia (sustained ventricular tachycardia attributed to the medication), hypotension (systolic blood pressure <90 mm Hg attributed to the medication), and QTc prolongation (QTc increase by ≥60 ms or to an interval ≥500 ms). Twenty-six patients (18%) experienced an adverse event. Of those adverse events, 20 patients (14%) experienced QTc prolongation, 3 patients (2%) had ventricular tachycardia, and 3 patients (2%) had hypotension. Patients who received quetiapine had a higher rate of adverse events (25% vs 6%, p = 0.01) including QTc prolongation (18% vs 6%, p = 0.046). Intensive care unit length of stay was shorter in patients who received olanzapine (6.5 vs 9.5 days, p = 0.047). Eighteen patients (13%) had their antipsychotic continued at discharge from the hospital. In conclusion, QTc prolongation was more common in patients treated with quetiapine versus olanzapine although the number of events was relatively low with both agents in a CICU cohort.

Confirmation and variability of the Allee effect inDictyostelium discoideumcell populations, possible role of chemical signaling within cell clusters.

In studies of the unicellular eukaryoteDictyostelium discoideum, many have anecdotally observed that cell dilution below a certain 'threshold density' causes cells to undergo a period of slow growth (lag). However, little is documented about the slow growth phase and the reason for different growth dynamics below and above this threshold density. In this paper, we extend and correct our earlier work to report an extensive set of experiments, including the use of new cell counting technology, that set this slow-to-fast growth transition on a much firmer biological basis. We show that dilution below a certain density (around 104cells ml-1) causes cells to grow slower on average and exhibit a large degree of variability: sometimes a sample does not lag at all, while sometimes it takes many moderate density cell cycle times to recover back to fast growth. We perform conditioned media experiments to demonstrate that a chemical signal mediates this endogenous phenomenon. Finally, we argue that while simple models involving fluid transport of signal molecules or cluster-based signaling explain typical behavior, they do not capture the high degree of variability between samples but nevertheless favor an intra-cluster mechanism.

Efficacy and tolerability of quinidine as salvage therapy for monomorphic ventricular tachycardia in patients with structural heart disease.

INTRODUCTION: Quinidine is an effective therapy for a subset of polymorphic ventricular tachycardia and ventricular fibrillation (VF) syndromes; however, the efficacy of quinidine in scar-related monomorphic ventricular tachycardia (MMVT) is unclear. METHODS AND RESULTS: Between 2009 and 2020 a single VT referral center, a total of 23 patients with MMVT and structural heart disease (age 66.7 ± 10.9, 20 males, 15 with ischemic cardiomyopathy, mean LVEF 22.2 ± 12.3%, 9 with left ventricular assist device [LVAD]) were treated with quinidine (14 quinidine gluconate; 996 ± 321 mg, 8 quinidine sulfate; 1062 ± 588 mg). Quinidine was used in combination with other antiarrhythmics (AAD) in 19 (13 also on amiodarone). All patients previously failed >1 AAD (amiodarone 100%, mexiletine 73%, sotalol 32%, other 32%) and eight had prior ablations (median of 1.5). Quinidine was initiated in the setting of VT storm despite AADs (6), inability to tolerate other AADs (4), or recurrent VT(12). Ventricular arrhythmias recurred despite quinidine in 13 (59%) patients at a median of 26 (4-240) days after quinidine initiation. In patients with recurrent MMVT, VT cycle length increased from 359 to 434 ms (p = .02). Six (27.3%) patients remained on quinidine at 1 year with recurrence of ventricular arrhythmias in all. The following adverse effects were seen: gastrointestinal side effects (6), QT prolongation (2), rash (1), thrombocytopenia (1), neurologic side effects (1). One patient discontinued due to cost. CONCLUSION: Quinidine therapy has limited tolerability and long-term efficacy when used in the management of amiodarone-refractory scar-related MMVT.

Effect of metformin on outcomes of catheter ablation for atrial fibrillation.

BACKGROUND: Diabetes mellitus (DM) is a risk factor for atrial fibrillation (AF). The effect of antidiabetic medications on AF or the outcomes of catheter ablation (CA) has not been well described. We sought to determine whether metformin treatment is associated with a lower risk of atrial arrhythmias after CA in patients with DM and AF. METHODS AND RESULTS: A first CA was performed in 271 consecutive patients with DM and AF (age: 65 ± 9 years, women: 34%; and paroxysmal AF: 51%). At a median of 13 months after CA (interquartile range: 6-30), 100/182 patients (55%) treated with metformin remained in sinus rhythm without antiarrhythmic drug therapy, compared with 36/89 patients (40%) not receiving metformin (p = .03). There was a significant association between metformin therapy and freedom from recurrent atrial arrhythmias after CA in multivariable Cox hazards models (hazard ratio [HR]: 0.66; ±95% confidence interval [CI]: 0.44-0.98; p = .04) that adjusted for age, sex, body mass index, AF type (paroxysmal vs. nonparoxysmal), antiarrhythmic medication, obstructive sleep apnea, chronic kidney disease, coronary artery disease, left ventricular ejection fraction, and left atrial diameter. A Cox model that also incorporated other antidiabetic agents and fasting blood glucose demonstrated a similar reduction in the risk of recurrent atrial arrhythmias with metformin treatment (HR: 0.63; ±95% CI: 0.42-0.96; p = .03). CONCLUSIONS: In patients with DM, treatment with metformin appears to be independently associated with a significant reduction in the risk of recurrent atrial arrhythmias after CA for AF. Whether this effect is due to glycemic control or pleiotropic effects on electroanatomical mechanisms of AF remains to be determined.