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Accurate localization of premature ventricular contractions (PVC) focus is a prerequisite to successful catheter ablation.The objective was to evaluate the software View Into Ventricular Onset (VIVO) accuracy at locating the anatomical origins for premature ventricular contractions. The VIVO device noninvasively creates a model of the patient's heart and torso, with exact locations of 12‑lead ECG electrodes, and applies a mathematical algorithm from surface signals to determine the origin of the arrhythmia. We sought to compare the agreement between VIVO-predicted locations to invasive electroanatomical mapping results.51 consecutive patients who presented for PVC ablations at the study centers were recruited. VIVO images were collected at baseline preprocedure and all patients underwent invasive electroanatomical activation mapping of the clinical arrhythmia. Pacing was performed in pre-specified locations in the right and/or left ventricle. The successful sites of ablation and the pacing locations were compared to VIVO predicted locations. The results were adjudicated by physician experts in a blinded fashion.Seven patients were excluded from analyses. VIVO accurately identified the origin of the clinical premature ventricular contractions in 44/44 patients (100.00%). The accuracy in identifying the paced location for all patients (right and left sides of the heart) was 99.5% using the VIVO system. No adverse events were reported.VIVO is a novel noninvasive system that could be used to help guide ablation procedures with a high degree of accuracy. The VIVO algorithm is easy to use and may be useful in the workflow for ventricular arrhythmia ablation.

Atrial fibrillation induced stroke accounts for up to 15% of all strokes. These strokes are caused approximately 90% of the time by clot formation in the left atrial appendage (LAA). To prevent these clots, the most common approach is to administer blood thinners. However, contraindications prevent some people from being able to have blood thinners. Devices have been developed to seal the LAA to prevent clot formation in these patients. Current devices, such as the LARIAT® tie off the LAA theoretically preventing blood from entering the LAA. These have had limited clinical success mainly due to failure to completely close the LAA leaving holes and orifices for thrombi to form. To overcome this lack of complete closure, many surgeons use off-label approaches, classically filling the LAA filamentous coils, to cover these holes. Although this usually helps largely cover the holes, placement is challenging, the coils can migrate, the holes are not fully closed as there is space within and around the coils that don't fully mold to the LAA geometry. Furthermore, the coils can develop device related thrombi defeating their purpose. Therefore, these are not fully sufficient to complement the closure techniques in closing the LAA. To address limitation of the closure devices and coil sealing of remaining holes, we developed a thermally responsive hydrogel (Thermogel) that solidifies once injected into the LAA to uniformly and fully close off the LAA thus preventing clot formation and device related thrombi. This Thermogel consists of three portions: 1) a structural component composed of thiolated Pluronic F127 for gel to solid transition following injection, 2) Heparin for anticoagulation, and 3) Dopamine for adhesion to the surrounding endothelium in the turbulent flow encountered in cardiovascular applications. Here we have demonstrated that Thermogel, in conjunction with the LARIAT®, is capable of filling the defects in small and large animals through catheter injection. Thermogel was biocompatible and led to atrophy of the LAA at 5 weeks in a large animal model. Given the advantages of this Thermogel for sealing this defect and ability to be delivered through an endovascular approach, Thermogel presents a viable adjuvant to current occlusion-based treatments for sealing cardiovascular defects.

Aims Pre-clinical work suggests that upper thoracic spinal cord stimulation (SCS) may have therapeutic effects in the treatment of heart failure (HF). We therefore aim to assess the safety and feasibility of SCS in HF patients. Methods and results A prospective, randomized, double-blind, crossover pilot study was conducted in symptomatic HF patients receiving optimal medical therapy. Patients were implanted with an SCS system and randomized to an SCS-ACTIVE, delivered at 90% paraesthesia threshold, or an SCS-INACTIVE phase for 3 months, followed by a 1-month washout period and crossover to the alternative phase. The safety of SCS therapy was assessed by death and cardiac events. Implantable cardioverter defibrillator (ICD) function in the presence of SCS was tested by defibrillation testing during SCS system implant and review of real-time and stored electrograms during follow-up. The efficacy of SCS therapy was assessed by changes in patient symptoms, LV function, and BNP level. Nine patients were investigated. In all cases, ICD sensing, detection, and therapy delivery were unaffected by SCS. During follow-up, one patient died and one was hospitalized for HF while in the SCS-INACTIVE phase, and two patients had HF hospitalizations during the SCS-ACTIVE phase. Symptoms were improved in the majority of patients with SCS, while markers of cardiac structure and function were, in aggregate, unchanged. Conclusion This study shows that an SCS system can be safely implanted in patients with advanced HF and that the SCS system does not interfere with ICD function.

The risk-benefit ratio of left atrial appendage closure (LAAC) versus systemic therapy (warfarin) for prevention of stroke, systemic embolism, and cardiovascular death in nonvalvular atrial fibrillation (NVAF) requires continued evaluation.This study sought to assess composite data regarding left atrial appendage closure (LAAC) in 2 randomized trials compared to warfarin for prevention of stroke, systemic embolism, and cardiovascular death in patients with nonvalvular AF.Our meta-analysis included 2,406 patients with 5,931 patient-years (PY) of follow-up from the PROTECT AF (Watchman Left Atrial Appendage System for Embolic Protection in Patients with Atrial Fibrillation) and PREVAIL (Prospective Randomized Evaluation of the Watchman LAA Closure Device In Patients With Atrial Fibrillation Versus Long Term Warfarin Therapy) trials, and their respective registries (Continued Access to PROTECT AF registry and Continued Access to PREVAIL registry).With mean follow-up of 2.69 years, patients receiving LAAC with the Watchman device had significantly fewer hemorrhagic strokes (0.15 vs. 0.96 events/100 patient-years [PY]; hazard ratio [HR]: 0.22; p = 0.004), cardiovascular/unexplained death (1.1 vs. 2.3 events/100 PY; HR: 0.48; p = 0.006), and nonprocedural bleeding (6.0% vs. 11.3%; HR: 0.51; p = 0.006) compared with warfarin. All-cause stroke or systemic embolism was similar between both strategies (1.75 vs. 1.87 events/100 PY; HR: 1.02; 95% CI: 0.62 to 1.7; p = 0.94). There were more ischemic strokes in the device group (1.6 vs. 0.9 and 0.2 vs. 1.0 events/100 PY; HR: 1.95 and 0.22, respectively; p = 0.05 and 0.004, respectively). Both trials and registries identified similar event rates and consistent device effect in multiple subsets.In patients with NVAF at increased risk for stroke or bleeding who are candidates for chronic anticoagulation, LAAC resulted in improved rates of hemorrhagic stroke, cardiovascular/unexplained death, and nonprocedural bleeding compared to warfarin.

Background: In recent years there has been an increase in the use of class III antiarrhyth mic drugs such as sotalol, amiodarone, and the so-called pure class III compound for the control of cardiac arrhythmias. It appears there has been a corresponding increase in the frequency of torsades de pointes (TdP). Methods and Results: The case reported here, a patient on daily renal dialysis for end-stage renal disease, has important implications for class III agents, which are excreted largely by the kidneys. A relatively low dose of sotalol administered for the prevention of recurrences of atrial fibrillation, with a fast ventricular response producing angina, led to modest increases in the QT interval and moderate bradycardia. This culminated in the development of TdP, which deteriorated into ventricular fibrillation, from which the patient could be resuscitated with considerable difficulty. Dialysis after the occurrence of TdP led to further and striking prolongation of the QT interval associated with numerous episodes of TdP for several days before control was achieved. The atrial fibrillation and recurrences of TdP were eventually controlled with oral amiodarone. Conclusions: This case emphasizes that in the absence of significant renal function, use of sotalol may not be safe because drug accumulation may not be controlled adequately with renal dialysis. In view of this, in patients with end-stage renal disease, the use of sotalol for arrhythmia control appears contraindicated and alternative agents, the excretion of which does not occur by the renal route, should be used.

Cardiac resynchronization therapy implants entail significant radiation exposure for patients and physicians. A novel 3D electromagnetic cardiovascular navigation system (MediGuide™) was designed to superimpose the real-time location of sensors embedded in delivery tools on prerecorded coronary sinus (CS) venograms while adjusting for patient movement and variations in heart rate under different C-arm angulations. We studied the accuracy and efficacy of MediGuide™ in reducing radiation exposure during LV lead implants.Fluoroscopy durations and radiation exposures were measured in 6 canines undergoing both conventional and MediGuide™-guided LV lead implants. The in vivo accuracy of MediGuide™ was evaluated by obtaining CS venograms at 3 different C-arm angulations at 3 different heart rates and measuring the separation between the projected sensor icon of a MediGuide™ sensor-enabled guidewire and the encompassing branch on prerecorded venograms.Mediguide™-guided implants resulted in significant reductions in fluoroscopy time (52 ± 120 [median 6] vs 129 ± 118 [median 90] sec, P0.001) and radiation exposure (13.8 ± 32.4 [median 1.7] vs 49.2 ± 45.3 [median 27.2] μGym(2) , P = 0.03) compared to conventional implants. LV lead delivery time was not significantly different between the 2 implant techniques (P = 0.27). The mean separation between the projected guidewire sensor icon and its encompassing branch was 0.48 ± 0.94 (median 0.00) mm. System accuracy was not affected by variations in heart rate or C-arm angulations.The novel 3D cardiovascular navigation system enabled accurate and reliable tracking of sensor-enabled tools at varying heart rates and C-arm angulations with minimal need for fluoroscopy guidance, significantly reducing fluoroscopy time and radiation exposure.

Some individuals with mutations in the cardiac ryanodine receptor gene (RyR2) develop stress-induced atrial fibrillation (AF), but the underlying mechanisms are unknown. This study explored the molecular basis of AF susceptibility in mice heterozygous for the human arrhythmia-linked RyR2 mutation R176Q (RQ mice). AF inducibility was assessed with atrial burst pacing in WT (n=34), RQ mice (n=43) and RQ mice crossed with transgenic mice expressing the CaMKII-inhibitory peptide AC3I (RQxAC3I, n=6) or the inactive analog AC3C (RQxAC3C, n=9). Dual voltage (RH237) and calcium (Rhod-2 AM) optical mapping was applied to monitor simultaneous Ca2+ and membrane-voltage changes. Ca2+ fluorescence (Fluo-4 AM) was used to study SR Ca2+ release. Expression/phosphorylation of CaMKII and RyR2 were determined by immunostaining in mice and human atrial biopsies from sinus rhythm (SR) (n=7) and chronic AF (n=7) patients. Atrial burst pacing-induced AF was more common in RQ (55%) than in WT mice (11%*; *P This research has received full or partial funding support from the American Heart Association, AHA South Central Affiliate (Arkansas, New Mexico, Oklahoma & Texas).