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Background: Recent data suggest that luminal esophageal temperature (LET) monitoring during high-power short-duration (HPSD) ablation may be inadequate to prevent esophageal thermal injury during radiofrequency (RF) ablation. This is due in part to delayed responses to thermal latency and the continued temperature rise that occurs in tissues even after the cessation of RF energy with HPSD settings. Proactive esophageal cooling has been shown to reduce severe esophageal thermal injury during medium-power medium-duration RF ablation, but less is known about the effects in HPSD ablation. Objective: We aimed to quantify the time course of esophageal damage in scenarios with and without proactive esophageal cooling, hypothesizing a reduction in the resulting tissue damage with proactive esophageal cooling. Methods: Using a computer model of RF ablation in the left atrium adjacent to the esophagus, we calculated temperature over time using ablation power of 50 W for 10 s and 90 W for 4 s. We then determined the fraction of resulting damage to esophageal tissue via the Arrhenius equation and by the percentage of tissue above lethal isotherm temperature of 50°C. Transmurality of injury was then plotted over time, and results were compared between ablation with and without proactive esophageal cooling. Results: Esophageal damage increased even after the cessation of RF energy, suggesting significant thermal latency effects under HPSD ablation. Lesion growth continued for >10 s after cessation of 50 W ablation energy, and for >12 s after cessation of 90 W ablation energy without cooling. With proactive cooling, lesion growth after cessation of ablation energy was essentially halted. Without esophageal cooling, maximum injury transmurality reached 79% with 50 W, and 58% with 90 W. With esophageal cooling, injury transmurality remained below 20% with 50 W, and 10% with 90 W, representing reductions of 75% and 83%, respectively. Conclusions: RF ablation using HPSD settings demonstrates significant latency of effect, with tissue damage and lesion growth continuing beyond the cessation of application of RF energy. Proactive esophageal cooling significantly dampens this effect, reducing esophageal injury by up to 83%.

Transvenous neurostimulation of the phrenic nerve (PNS) is a potentially improved and unique approach to the treatment of central sleep apnea (CSA). There have been multiple studies with limited individuals evaluating the efficacy of PNS. Our aim was to review and pool those studies to better understand whether phrenic nerve stimulation is efficacious in the treatment of CSA. The initial search on Pubmed retrieved a total of 97 articles and after screening all articles, only 5 could be included in our quantitative analysis. Pooling of data from 5 studies with a total of 204 patients demonstrated a reduction of mean apnea hypopnea index with PNS compared to controls by -26.7 events/hour with 95% confidence interval and P value of [CI (-31.99, -21.46), I2 85, p 0.00]. The mean difference in central apnea index was -22.47 [CI (-25.19, -19.76), I2 0, p 0.00]. The mean reduction in the oxygen desaturation index of 4% or more demonstrated a decrease in PNS group by -24.16 events/hour [(CI -26.20, -22.12), I2 0, p 0.00] compared with controls. PNS resulted in mean reduction in arousal index of -13.77 [CI (-16.15, -11.40), I2 0, p 0.00]. The mean change in percent of time spent in rapid eye movement sleep demonstrated a nonsignificant increase in PNS group by 1.01 % [CI (-5.67, 7.86), I293, p 0.75]. In conclusion, PNS therapy for treating CSA demonstrated positive outcomes but larger randomized studies are needed to evaluate the safety and clinical outcomes.

Background: New-onset atrial fibrillation (AF) in patients hospitalized with COVID-19 has been reported and associated with poor clinical outcomes. We aimed to understand the incidence of and outcomes associated with new-onset AF in a diverse and representative US cohort of patients hospitalized with COVID-19. Methods: We used data from the American Heart Association COVID-19 Cardiovascular Disease Registry. Patients were stratified by the presence versus absence of new-onset AF. The primary and secondary outcomes were in-hospital mortality and major adverse cardiovascular events (MACE; cardiovascular death, myocardial infarction, stroke, cardiogenic shock, and heart failure). The association of new-onset AF and the primary and secondary outcomes was evaluated using Cox proportional-hazards models for the primary time to event analyses. Results: Of the first 30 999 patients from 120 institutions across the United States hospitalized with COVID-19, 27 851 had no history of AF. One thousand five hundred seventeen (5.4%) developed new-onset AF during their index hospitalization. New-onset AF was associated with higher rates of death (45.2% versus 11.9%) and MACE (23.8% versus 6.5%). The unadjusted hazard ratio for mortality was 1.99 (95% CI, 1.81–2.18) and for MACE was 2.23 (95% CI, 1.98–2.53) for patients with versus without new-onset AF. After adjusting for demographics, clinical comorbidities, and severity of disease, the associations with death (hazard ratio, 1.10 [95% CI, 0.99–1.23]) fully attenuated and MACE (hazard ratio, 1.31 [95% CI, 1.14–1.50]) partially attenuated. Conclusions: New-onset AF was common (5.4%) among patients hospitalized with COVID-19. Almost half of patients with new-onset AF died during their index hospitalization. After multivariable adjustment for comorbidities and disease severity, new-onset AF was not statistically significantly associated with death, suggesting that new-onset AF in these patients may primarily be a marker of other adverse clinical factors rather than an independent driver of mortality. Causality between the MACE composites and AF needs to be further evaluated.

Introduction: Atrioesophageal fistula (AEF) is a severe complication of left atrial ablation for the treatment of atrial fibrillation. Thermal injury is the proposed mechanism, and a potential pathway occurs through exceeding the lethal isotherm of esophageal tissue in contact with the left atrial posterior wall. Active cooling with a novel cooling device has been shown to significantly reduce thermal injury, with no AEFs encountered after more than 4200 treatments worldwide. We aimed to evaluate the effects of active cooling when specifically using newer high-power short-duration (HPSD) ablation settings to further estimate the protective mechanisms of this novel approach to reduce serious injury. Hypothesis: Active cooling may preclude attainment of a lethal isotherm in esophageal tissue under HPSD ablation. Methods: We developed a model of the left atrium and esophagus, and simulated radiofrequency (RF) ablation of the left atrium under HPSD settings. Tissue thickness was set to typical posterior-wall parameters (Figure). Power settings were evaluated at 50 W for 10 seconds, and 90 W for 4 seconds. Active cooling was set to a typical 4 °C coolant temperature. Lethal isotherm temperature was taken as 50 °C. Results: In both scenarios of HPSD ablation, the peak esophageal mucosal temperature reached 39° C in control conditions, using no active cooling. With active cooling in place, peak temperatures remained below 11 °C (Figure). Peak temperatures at the epi-esophageal region of esophageal tissue exceeded the lethal isotherm of 50 °C in control conditions, but remained at or below the lethal isotherm with active cooling in place. Conclusions: Based on our mathematical modeling, esophageal cooling significantly reduced temperature rise and prevented the achievement of temperatures thought to be lethal to esophageal tissue. This finding may offer a mechanistic rationale for the absence of serious esophageal injury encountered to date using this approach.

Introduction Catheter ablation of ventricular tachycardia (VT) can be an effective therapy to reduce VT burden, but often it is limited by the potential for hemodynamic instability. Percutaneous left ventricular assist devices (pLVADs) have been used to maintain hemodynamic support during VT ablation but the evidence regarding its clinical impact has been inconclusive. Methods and results We sought to assess the clinical impact of pLVAD when used in VT ablation by conducting a meta-analysis of the current evidence. We searched Pubmed and found nine observational studies that compared clinical outcomes of VT ablation in patients with pLVAD support to controls with no pLVAD support. The pooled data did not show a significant difference in mortality between both groups, nor a difference in acute procedural success or in recurrence of VT. There was also no difference in the number of patients receiving a cardiac transplant or being enrolled in the transplant list. Although there was no difference in the ablation time between the groups, patients in the pLVAD group had a longer total procedural time and more procedure-related adverse effects. Conclusion This meta-analysis did not show clinical benefits from using pLVAD support during VT ablation, whereas it was associated with longer procedure times and more complications. This study was, however, limited by the observational nature of the data. In view of these data, the risk and benefit of pLVAD support during VT ablation should be considered on an individual basis.

The efficacy of implantable cardioverter defibrillators in reducing the risk of sudden cardiac death has been well established by several clinical trials. Several factors relating to device characteristics, patient attributes, and comorbidities should be considered when selecting the appropriate implantable cardioverter defibrillators for each patient. This review examines some of these issues.

Conduction abnormalities are known to occur after heart transplantation. In some cases, a permanent pacemaker is required. Conventional transvenous pacemakers can result in several complications, mainly related to the leads and device pocket. Leadless pacemaker technology was developed to overcome these issues. We report what we believe is the first US case of a leadless pacemaker implant (specifically in a heart transplant recipient) with the longest reported duration of follow-up.

Background: The prevalence of atrial fibrillation (AF) in active astronauts is ≈5%, similar to the general population but at a younger age. Risk factors for AF include left atrial enlargement, increased number of premature atrial complexes, and certain parameters on signal-averaged electrocardiography, such as P-wave duration, root mean square voltage for the terminal 20 ms of the signal-averaged P wave, and P-wave amplitude. We aimed to evaluate changes in atrial structure, supraventricular beats, and atrial electrophysiology to determine whether spaceflight could increase the risk of AF. Methods: Thirteen astronauts underwent cardiac magnetic resonance imaging to assess atrial structure and function before and after 6 months in space and high-resolution Holter monitoring for multiple 48-hour time periods before flight, during flight, and on landing day. RESULTS: Left atrial volume transiently increased after 6 months in space (12±18 mL; P =0.03) without changing atrial function. Right atrial size remained unchanged. No changes in supraventricular beats were noted. One astronaut had a large increase in supraventricular ectopic beats but none developed AF. Filtered P-wave duration did not change over time, but root mean square voltage for the terminal 20 ms decreased on all fight days except landing day. No changes in P-wave amplitude were seen in leads II or V 1 except landing day for lead V 1 . Conclusions: Six months of spaceflight may be sufficient to cause transient changes in left atrial structure and atrial electrophysiology that increase the risk of AF. However, there was no definite evidence of increased supraventricular arrhythmias and no identified episodes of AF.

Background Mountain activities characterized by strenuous exercise in a hypoxic setting place unique demands on the body. The mortality rate associated with mountain activities is high, with sudden cardiac death (SCD) representing the most frequent of all nontraumatic deaths. We evaluated the possible effect of acclimatization in reduction of SCD during high-altitude sojourns. Methods This was a retrospective cohort study involving all deaths (N = 559) that occurred during mountain activities in Austria from 1985 through 1993. Baseline patient demographics, cardiovascular comorbidities, smoking history, family history of SCD, sleeping altitude, annual mountaineering frequency, and physical activity on the day of SCD were included in a questionnaire previously used in a pilot study. Results Data from 301 of 599 individuals without prespecified exclusions were available for analysis (79% of eligible cohort). Sudden cardiac deaths happened mostly around noon (29%), and mean altitude at which SCDs occurred was 1,710 ± 501 m. When sleeping altitude was divided into quartiles ( 1,299 m), the odds ratio for SCD on the first day at altitude when sleeping below 700 m was 5.7 (95% CI 2.8-11.6) as compared with sleeping above 1,299 m. Conclusion For males >34 years, those with history of coronary artery disease and/or prior infarction, and those unaccustomed to physical activity at altitude, sleeping at moderate altitude before exercising at altitude may reduce the risk of SCD.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, contributing significantly to cardiac morbidity and mortality. Currently available agents for pharmacologic management of AF are limited by suboptimal efficacy and proarrhythmic risk. Therapeutic strategies are broadly categorized as rhythm control, where therapy is directed at minimizing AF burden, and rate control, in which the ventricular response is targeted. Medical and interventional treatments focusing on rhythm control for patients with paroxysmal and persistent AF have improved significantly over the past two decades with the introduction of new antiarrhythmic agents and advances in ablation therapy. However, over the same time period, little progress has emerged in available options to control ventricular rate in patients with AF. Most medications used for rate control slow conduction through the AV node by increasing refractoriness. Beta-blockers remain the most commonly prescribed agents for rate control, followed by calcium channel blockers and digoxin.1 Each of these agents slows AV nodal conduction. A second mechanism by which the ventricular rate is reduced in AF may be by altering the dominant frequency within the fibrillating atria. Some have postulated that decreasing the dominant AF frequency, with fewer impulses engaging the AV node, will reduce ventricular rate.2 In a report in this issue of the Journal, new rate control strategies are tested that combine these two mechanisms using drugs that were developed to treat angina: ivabradine and ranolazine.2

Introduction: Shoulder pain and disability ipsilateral to the implant site is a common complication of cardiac rhythm device implantation, yet very little has been published about this morbidity. We designed a study to assess the potential benefit of a simple exercise protocol in preventing shoulder pain postoperatively. Methods and Results: Patients undergoing subcutaneous device implantation were randomized to one of two groups. The control group received standard instructions, whereas the exercise group was instructed on specific exercises aimed at strengthening or stretching the shoulder girdle, to be completed 3 days per week. Groups were postoperatively monitored for the development of shoulder discomfort and shoulder impingement by using physical examination and disability questionnaires. At 1 month, seven of 21 control patients reported developing shoulder pain or discomfort compared to one of 23 in the exercise group (P = 0.02). At 6 months, four of 23 control patients still reported worsening shoulder symptoms, compared to none in the exercise group (P = 0.11). In the control group, five of 19 patients developed a positive impingement test at 1 month, versus none in the exercise group (P = 0.01). Scores for the questionnaires designed to assess shoulder pain and dysfunction were worse in the control group. There were no activity-related complications in either group. Conclusion: Shoulder pain and disability occurs often following cardiac rhythm management device implantation. A simple exercise program aimed at strengthening the shoulder girdle is effective at preventing this complication. (PACE 2011; 672–678)

Introduction: Multiple pharmacological therapies currently in prevalent clinical use for cardiac diseases have antifibrotic properties. Spironolactone, a potent antifibrotic agent, is currently used for advanced heart failure. Therapies such as HMG-CoA reductase inhibitors (statins) and angiotensin-converting enzyme inhibitors (ACEi) also have antifibrotic properties. However, the effect of these medications on the ventricular arrhythmia phenotype is currently unknown. Therefore, we set out to define the ventricular arrhythmia rates in patients actively treated with such therapies. Methods and Results: We retrospectively evaluated the ventricular tachycardia (VT) rates in patients with structural heart disease actively treated with therapies with antifibrotic properties. VT rates were significantly diminished in patients treated with spironolactone (158 ± 26 beats per minute [bpm], n = 21) compared to patients on no medications (205 ± 22 bpm, n = 13) or those who were on similar heart-failure therapies but not on spironolactone (186 ± 32 bpm, n = 82). In addition, we observed that VT rates showed a significant trend toward lower rates in patients receiving either statins or ACEi, compared to patients on no medical therapy. In multivariate analysis, spironolactone therapy was identified as the single most significant variable for reduced VT rate. Conclusion: Use of spironolactone in patients with heart failure is associated with reduced VT rate. Similar but less-significant reductions in VT rates were observed with use of other pharmacological agents with antifibrotic properties, such as statins and ACEi. Our findings, at least in part, could account for reduction in sudden cardiac death rates documented with use of these therapies. (PACE 2011; 34:309–314))

Implantable Defibrillators in Octogenarians. Background: The use of implantable cardioverter-defibrillators (ICDs) in octogenarians is poorly defined. Objective: To assess baseline electrocardiographic (ECG) findings, arrhythmia episodes, and development of severe nonarrhythmic illness or death in patients aged ≥80 years at ICD implantation, and to compare them with younger patients. Methods: Medical records and device interrogations for 199 patients ≥70 years old who underwent ICD implantation were reviewed. Patients were divided into 3 groups based on age at the time of implant: age 70–74 (group 1; 88 patients), age 75–79 (group 2; 67 patients), and age ≥80 (group 3; 44 patients). Results: ECGs: Octogenarians were more likely to have sinus bradycardia (SB) (P = 0.047) and left bundle branch block (LBBB) (P = 0.043) compared to younger patients. There was no difference among groups in the proportion of patients with atrial fibrillation or any degree of AV block. Therapies: There was no difference between age groups in any therapy (P = 0.78), appropriate therapy (P = 0.54), or inappropriate therapy (P = 0.21) per patient-year. There was no difference between groups in time-to-first therapy of any type (P = 0.71). Nonarrhythmic death/morbidity: There was no difference between groups in time to death or serious illness. Conclusion: Our study is the first to evaluate in detail the therapies received by octogenarians after ICD placement. The higher incidence of SB and LBBB might influence the number of pacing sites in octogenarian patients. Very elderly patients have similar rates of arrhythmic episodes and development of severe comorbidities as septuagenarians, and they should not be denied ICD implantation based solely on age. (J Cardiovasc Electrophysiol, Vol. 21, pp. 236–241, March 2010)