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Introduction: While steerable sheaths are widely used to improve catheter stability and contact force during radiofrequency (RF) catheter ablation in patients with atrial fibrillation (AF), steerable sheaths are less commonly used during transseptal puncture. This study evaluated whether left atrial catheterization efficiency can be improved using the VersaCross combined steerable sheath and transseptal system compared to previous standard workflow. Methods: This study retrospectively analyzed AF ablation performed using the Versacross Workflow consisting of VersaCross steerable sheath and RF wire for transseptal puncture and catheter ablation (VCW) to the standard workflow using a fixed curve sheath with RF needle followed by exchange for an Agilis steerable sheath for catheter ablation (STW). Results: Thirty patients underwent RF ablation for paroxysmal or persistent AF, 15 using the VCW and 15 using the STW. Transseptal puncture time was 10.8 mins faster with the VCW compared to the standard workflow (20.9 ± 5.9 min vs. 31.7 ± 15.1 min; p=0.024). Time to left atrial catheterization was 40% faster with the VCW compared to the STW (21.3 ± 5.8 min vs. 35.2 ± 14.4 min; p=0.003). Overall procedure time was 14.2 min faster in the VCW compared to the STW (86.3 ± 16.1 min vs. 100.5 ± 19.3 min; p=0.044). Conclusions: Use of the VersaCross steerable system significantly reduced time to transseptal puncture, time to left atrial catheterization, and overall RF ablation time.

Recent clinical trials using panoramic mapping techniques have shown success in targeting rotors and focal impulses in atrial fibrillation (AF). Ablations directed toward these organized sources improve outcomes in AF. The left atrial appendage (LAA) has been suspected as a possible extrapulmonary source of AF, and ablation within the LAA or electrical isolation of the LAA improves outcomes in certain cases. This case highlights a unique example of panoramic imaging created with a computational mapping algorithm integrated in 3-dimensional mapping, which identified rotors within the LAA. Furthermore, ablations performed near an identified rotor core within the LAA terminated AF.

The relationship between a fragmented QRS complex (fQRS) on 12-lead ECG and fatal arrhythmic events in hypertrophic cardiomyopathy (HCM) remains unclear.The purpose of this study was to investigate whether fQRS is associated with ventricular arrhythmic events (VAEs) in HCM patients.Of an initial cohort of 273 patients (57% male, mean age 55 years) diagnosed with HCM, 167 patients were included and divided into 2 groups: those with fQRS (n = 67) and those without fQRS (n = 100). fQRS was defined as notching of the R or S wave in 2 contiguous leads. VAEs were defined as nonsustained or sustained ventricular tachycardia (VT) or sudden cardiac death (SCD). Major arrhythmic events (MAEs) were sustained VT or SCD.During mean follow-up of 6.3 years, univariate analysis showed that fQRS was significantly associated with increased VAEs (unadjusted hazard ratio [HR] 6.17, 95% confidence interval [CI] 2.46-15.49, P.001) and MAEs (unadjusted HR 5.12, 95% CI 1.38-19.01, P = .014). Multivariate analysis revealed that fQRS was a strong independent predictor of VAEs (adjusted HR 6.28, 95% CI 2.49-15.84, P.001) and MAEs (adjusted HR 6.04, 95% CI 1.49-24.39, P = .011). fQRS in the inferior leads was most closely related to MAEs compared to fQRS in other myocardial territories, and its inclusion in a risk calculator for mortality in HCM patients increased the positive predictive value from 8% to 25% in low-risk patients.Presence of an fQRS may be a good candidate marker for prediction of VAE in patients with HCM.

Prolongation of the corrected QT (QTc) interval on 12-lead electrocardiogram is related to total mortality and sudden cardiac death. The value of the paced QTc interval in predicting mortality has not been investigated.To evaluate the relationship between the paced QTc interval and mortality.Of 1440 patients who underwent pacemaker implantation from January 1990 to March 2010, 766 had a recorded intrinsic and ventricular paced rhythm and were included in this study. The intrinsic and paced QTc intervals were measured on 12-lead electrocardiogram before and 1-month after implantation.During a mean follow-up period of 7 ± 5 years, 189 (24.4%) patients died, of which 63 (8.1%) were cardiac deaths. Compared with patients in the first tertile of the paced QTc interval (484 ms), patients in the third tertile (511 ms) were significantly more likely to die (19% vs 29%; P.05). A comparison of the third and first tertiles of the QTc interval showed that a prolonged paced QTc interval was a significant independent predictor of all-cause mortality (adjusted hazard ratio 2.08; 95% confidence interval 1.44-3.01; P.001) and cardiac mortality (adjusted hazard ratio 2.53; 95% confidence interval 1.29-4.95; P = .007) and a better predictor than was a prolonged intrinsic QTc interval. When treated as a continuous variable, a prolonged paced QTc interval predicted increased total mortality and cardiac mortality.The paced QTc interval appears to be a more useful marker in predicting bad prognosis than does the intrinsic QTc interval in patients with indications for a permanent pacemaker.

Heart failure remains a major public health concern with a 5-year mortality rate higher than that of most cancers. Myocardial disease in heart failure is frequently accompanied by impairment of the specialized electrical conduction system and myocardium. We introduce an epicardial mesh made of electrically conductive and mechanically elastic material, to resemble the innate cardiac tissue and confer cardiac conduction system function, to enable electromechanical cardioplasty. Our epicardium-like substrate mechanically integrated with the heart and acted as a structural element of cardiac chambers. The epicardial device was designed with elastic properties nearly identical to the epicardial tissue itself and was able to detect electrical signals reliably on the moving rat heart without impeding diastolic function 8 weeks after induced myocardial infarction. Synchronized electrical stimulation over the ventricles by the epicardial mesh with the high conductivity of 11,210 S/cm shortened total ventricular activation time, reduced inherent wall stress, and improved several measures of systolic function including increases of 51% in fractional shortening, ~90% in radial strain, and 42% in contractility. The epicardial mesh was also capable of delivering an electrical shock to terminate a ventricular tachyarrhythmia in rodents. Electromechanical cardioplasty using an epicardial mesh is a new pathway toward reconstruction of the cardiac tissue and its specialized functions.

Background— Implantable device therapy of atrial fibrillation (AF) is limited by pain from high-energy shocks. We developed a low-energy multistage defibrillation therapy and tested it in a canine model of AF. Methods and Results— AF was induced by burst pacing during vagus nerve stimulation. Our novel defibrillation therapy consisted of 3 stages: stage (ST) 1 (1–4 low-energy biphasic [BP] shocks), ST2 (6–10 ultralow-energy monophasic [MP] shocks), and ST3 (antitachycardia pacing). First, ST1 testing compared single or multiple MP and BP shocks. Second, several multistage therapies were tested: ST1 versus ST1+ST3 versus ST1+ST2+ST3. Third, 3 shock vectors were compared: superior vena cava to distal coronary sinus, proximal coronary sinus to left atrial appendage, and right atrial appendage to left atrial appendage. The atrial defibrillation threshold (DFT) of 1 BP shock was P =0.003). Two to 3 BP shocks terminated AF with lower peak voltage than 1 BP or 1 MP shock and with lower atrial DFT than 4 BP shocks. Compared with ST1 therapy alone, ST1+ST3 lowered the atrial DFT moderately (0.51±0.46 versus 0.95±0.32 J, P =0.036), whereas 3-stage therapy (ST1+ST2+ST3) dramatically lowered the atrial DFT (0.19±0.12 versus 0.95±0.32 J for ST1 alone, P =0.0012). Finally, the 3-stage therapy was equally effective for all studied vectors. Conclusions— Three-stage electrotherapy significantly reduces the AF DFT and opens the door to low-energy atrial defibrillation at or below the pain threshold.

Background Tissue refractoriness to conduction is a crucial electrophysiological factor in determining susceptibility to fibrillation. The relationship between atrial refractoriness and future onset of atrial fibrillation (AF) has not been well studied. Objectives We investigated whether atrial effective refractory period (AERP) was associated with AF occurrence in a relatively healthy population. Methods A total of 1308 patients with no overt structural heart diseases and no evidence of congestive heart failure who underwent electrophysiology studies for paroxysmal supraventricular tachycardia from January 1986 to January 2011 were included in the study (626 male, mean age 44 ± 16 years). Results AERP increased with increasing age. Over a mean follow-up of 12 years, 51 of 1308 subjects (3.9%) developed AF. In univariate analysis, baseline AERP ≥280 ms (hazard ratio [HR] 2.54, 95% confidence interval [CI] 1.27–5.07, P = .008) was strongly associated with new-onset AF. In multivariate Cox regression analysis, age (adjusted HR 1.40 per 10 years, 95% CI 1.15–1.70, P = .001) and AERP ≥280 ms (adjusted HR 2.08, 95% CI 1.03–4.21, P = .041) were associated with new-onset AF. Kaplan-Meier AF-free survival curves demonstrated that subjects with an AERP of ≥280 ms had significantly lower AF-free survival compared those with AERP of Conclusions AERP increases with age and AERP of ≥280 ms was predictive of patients at significantly increased future risk of developing AF.

Recent clinical trials using panoramic mapping techniques have shown success in targeting rotors and focal impulses in atrial fibrillation (AF). Ablations directed toward these organized sources improve outcomes in AF. The left atrial appendage (LAA) has been suspected as a possible extrapulmonary source of AF, and ablation within the LAA or electrical isolation of the LAA improves outcomes in certain cases. This case highlights a unique example of panoramic imaging created with a computational mapping algorithm integrated in 3-dimensional mapping, which identified rotors within the LAA. Furthermore, ablations performed near an identified rotor core within the LAA terminated AF.

ObjectivesThe goal of this study was to develop a low-energy, implantable device–based multistage electrotherapy (MSE) to terminate atrial fibrillation (AF).BackgroundPrevious attempts to perform cardioversion of AF by using an implantable device were limited by the pain caused by use of a high-energy single biphasic shock (BPS).MethodsTransvenous leads were implanted into the right atrium (RA), coronary sinus, and left pulmonary artery of 14 dogs. Self-sustaining AF was induced by 6 ± 2 weeks of high-rate RA pacing. Atrial defibrillation thresholds of standard versus experimental electrotherapies were measured in vivo and studied by using optical imaging in vitro.ResultsThe mean AF cycle length (CL) in vivo was 112 ± 21 ms (534 beats/min). The impedances of the RA–left pulmonary artery and RA–coronary sinus shock vectors were similar (121 ± 11 Ω vs. 126 ± 9 Ω; p = 0.27). BPS required 1.48 ± 0.91 J (165 ± 34 V) to terminate AF. In contrast, MSE terminated AF with significantly less energy (0.16 ± 0.16 J; p < 0.001) and significantly lower peak voltage (31.1 ± 19.3 V; p < 0.001). In vitro optical imaging studies found that AF was maintained by localized foci originating from pulmonary vein–left atrium interfaces. MSE Stage 1 shocks temporarily disrupted localized foci; MSE Stage 2 entrainment shocks continued to silence the localized foci driving AF; and MSE Stage 3 pacing stimuli enabled consistent RA–left atrium activation until sinus rhythm was restored.ConclusionsLow-energy MSE significantly reduced the atrial defibrillation thresholds compared with BPS in a canine model of AF. MSE may enable painless, device-based AF therapy.

Heart failure (HF) is an increasing public health problem accelerated by a rapidly aging global population. Despite considerable progress in managing the disease, the development of new therapies for effective treatment of HF remains a challenge. To identify targets for early diagnosis and therapeutic intervention, it is essential to understand the molecular and cellular basis of calcium handling and the signaling pathways governing the functional remodeling associated with HF in humans. Calcium (Ca(2+)) cycling is an essential mediator of cardiac contractile function, and remodeling of calcium handling is thought to be one of the major factors contributing to the mechanical and electrical dysfunction observed in HF. Active research in this field aims to bridge the gap between basic research and effective clinical treatments of HF. This chapter reviews the most relevant studies of calcium remodeling in failing human hearts and discusses their connections to current and emerging clinical therapies for HF patients.

Background A source-sink mechanism plays a crucial role in transmission of electrical impulse to tissue. We hypothesized that partial uncoupling of impulse source to tissue by ablation might generate ectopic beats. Methods Canine right atrial preparations (n = 5) were coronary perfused and optically mapped using ANBDQBS, a near-infrared voltage-sensitive dye, to assess the origin and spread of excitation in transmural layers. The sinus node (SN) and surrounding atrial tissue in the field of view were reconstructed after Masson-trichrome, H&E, and immunofluorescence. Masson-trichrome histology was merged with the optical mapping. Cryoablation at –70°C for >3 minutes was performed in the SN and the atrial tissue. Results At baseline, sinus impulse originated from a specific cluster of the histologically demarcated SN (n = 5, 124 ± 23 bpm). Random extensive cryoablation on the SN and atrial tissue caused de novo activation of the ectopic foci outside the field of view (n = 3/5). We also observed the ectopic focus outside the histologic SN independently producing only spontaneous electrical oscillatory waves at baseline before ablation (n = 1), which was composed of HCN4 + cells in immunohistochemistry. However, this isolated electrical activity failed to propagate to the large atrium, as evidenced by the inability of this cluster to generate P waves on the pseudo-ECG. We created partial uncoupling of the nonpropagated ectopic source to the large atrium by cryoablation. In contrast to preablation, the nonpropagated ectopic source acquired the ability to propagate to the surviving atrial myocardium and generated ectopic beats. Conclusions The current study suggests that incomplete ablation may induce ectopic beats through paradoxical improvement of impulse conduction to the cardiac tissue by reducing coupling of impulse source to atrial sink. The current study may provide a mechanistic insight and clinical implications on generation of ectopic beats.