Hodge, David O.

BackgroundAlthough sudden death (SD) is a rare complication after atrioventricular junction (AVJ) ablation and permanent pacemaker implantation, the risk factors leading to this SD remain unknown. The purpose of this study was to investigate SD and its risk factors after ablate‐and‐pace strategy for rate control in atrial fibrillation (AF) patients during long‐term follow‐up.HypothesisMethodsFrom January 2005 to December 2009, we enrolled into this study 517 AF patients with AVJ ablation and right ventricular pacemaker implantation. Patients were divided into 2 groups, SD and non‐SD. Cox proportional hazards models were used to assess potential risk factors for overall mortality and SD.ResultsDuring a mean follow‐up of 25.8 ± 18.6 months (range, 3 days to 63.8 months), 53 patients died (15 with SD). Cox proportional hazards models showed that the presence of congestive heart failure, New York Heart Association functional class, chronic renal failure, and nonsustained ventricular tachycardia were risk factors that predicted overall mortality. For SD, the presence of dilated cardiomyopathy and mitral stenosis were associated risk factors. SD was exclusively seen in patients who had narrow QRS complex or right bundle branch block prior to AVJ ablation and pacemaker implantation; SD was not seen in any patient with preexisting complete left bundle branch block.ConclusionsDilated cardiomyopathy, mitral stenosis, and baseline QRS morphology should be examined as potential risk factors for SD after AVJ ablation and pacemaker implantation.

Catheter Ablation for Atrial Arrhythmias in Patients With CABackgroundCardiac amyloidosis (CA) is associated with increased atrial arrhythmias risk. The efficacy/safety of catheter‐based ablation therapy in patients with CA has not been adequately assessed.Methods and ResultsAll diagnosed CA patients who underwent atrial arrhythmia ablation therapy from 1995 to 2015 were reviewed. Arrhythmia recurrence, NYHA symptoms, and mortality were recorded. A total of 26 patients with CA and atrial arrhythmias were included; there were 7 light‐chain (AL), 17 wild‐type transthyretin (ATTRwt), and 2 mutated transthyretin (ATTRm) amyloidosis patients in total. Of which 13 underwent atrial arrhythmia ablation (CA‐A) and 13 underwent AV nodal ablation (CA‐AVN). In the CA‐A group, there were: 3 with atrial fibrillation (AF); 6 with atrial flutter (AFL); 2 with AF/AFL; and 2 with atrial tachycardia (AT). One‐year and 3‐year recurrence‐free survival were 75% and 60%, respectively. NYHA symptom improvement 6 months postablation was observed in both CA‐A and CA‐AVN groups: 7/10 (70%) and 4/8 (50%), respectively. Eleven patients with CA died (8 in CA‐AVN group vs. 3 in CA‐A group).ConclusionsCatheter‐based ablation for patients with CA appears to provide important symptomatic relief. However, mortality from the underlying disease remains a significant issue for the amyloid light‐chain subtype.

Abstract Aims We have previously reported that asymptomatic systolic heart failure (HF) is characterized by an impaired renal response to volume expansion due to lack of activation of urinary cGMP which is corrected by subcutaneous (SQ) BNP. In the current study, we sought to define the cardiorenal response to intravascular volume expansion after 12 weeks of SQ BNP therapy. Methods and results We utilized a double-blinded, placebo-controlled study to compare 12 weeks of twice-daily SQ BNP 10 µg/kg (n = 22) or placebo (n = 12) in asymptomatic systolic HF. Subjects underwent two study visits: baseline and after 12 weeks of therapy. At each study visit, echocardiography, renal, and neurohumoral assessments were performed before and after intravascular volume expansion. The primary endpoint was change in urinary sodium excretion in response to volume expansion at 12 weeks, and we observed a greater increase in urinary sodium excretion [166 (77, 290) vs. 15 (−39, 72) mEq/min; P = 0.02] with SQ BNP treatment vs. placebo. Secondary endpoints included change in urine flow and glomerular filtration rate (GFR) in response to volume expansion at 12 weeks. We observed a significant increase in urine flow (P < 0.01) and trend for differential response in GFR (P = 0.08) with SQ BNP treatment vs. placebo. Conclusion Among patients with asymptomatic systolic HF, twice-daily SQ BNP therapy improved the cardiorenal response to volume expansion at 12-week follow-up. Further studies are warranted to determine if these beneficial physiological observations with chronic natriuretic peptide administration translate into a delay in the progression to symptomatic HF.

Direct Pulmonary Vein Ablation With Stenosis Prevention TherapyIntroductionThe dominant location of electrical triggers for initiating atrial fibrillation (AF) originates from the muscle sleeves inside pulmonary veins (PVs). Currently, radiofrequency ablation (RFA) is performed outside of the PVs to isolate, rather than directly ablate these tissues, due to the risk of intraluminal PV stenosis.MethodsIn 4 chronic canine experiments, we performed direct PV muscle sleeve RFA ± postablation drug‐coated balloon (DCB) treatment with paclitaxel/everolimus. Of the 4 PVs, 2 PVs were ablated and treated with DCB, 1 PV was ablated without DCB treatment (positive control), and 1 PV was left as a negative control. Local electrograms were assessed in PVs for near‐field signals and were targeted for ablation. After 12–14 weeks survival, PVs were interrogated for absence of near‐field PV potentials, and each PV was assessed for stenosis.ResultsAll canines survived the study period without cardiorespiratory complications, and remained ambulatory. In all canines, PVs that were ablated and treated with DCB remained without any significant intraluminal stenosis. In contrast, PVs that were ablated and not treated with DCB showed near or complete intraluminal stenosis. At terminal study, PV potentials remained undetectable. A blinded, histologic analysis demonstrated that ablated PVs without DCB treatment had extensive thrombus, fibrin, mineralization, and elastin disruption.ConclusionOur chronic canine data suggest that direct PV tissue ablation without subsequent stenosis is feasible with the use of postablation DCBs.

ObjectivesTo determine the frequency and predictors of pericardial effusion following epicardial sheath removal.BackgroundPericardial effusion can occur following cardiac surgical or interventional procedures including percutaneous epicardial access (EpiAcc), which is increasingly used as part of electrophysiology ablation procedures.MethodsA retrospective analysis of the Mayo Clinic comprehensive electronic medical record was performed from all patients who underwent planned EpiAcc as part of an electrophysiology ablation procedure between January 1, 2004 and June 30, 2013.ResultsOf 144 patients (mean age 51.3 ± 15.5 years, 68% male) who underwent planned EpiAcc as part of an electrophysiology ablation (95.8% pericardial access success rate), seven (4.9%) developed a postoperative pericardial effusion requiring repeat EpiAcc. Inferior access was utilized in 74 (51.4%) patients. Patients with pericardial effusion tended to be younger (41.1 years vs 51.8 years, P = 0.08) and were more likely to have undergone inferior approach access (85.7% vs 49.6%, P = 0.06) than those who did not develop postoperative pericardial effusion. Seventy‐one percent of patients with postoperative pericardial effusion versus 32.1% of patients without postoperative pericardial effusion had a preprocedure ejection fraction ≥55% (P = 0.03). There were no procedural‐related deaths, and no difference in mortality between groups.ConclusionsPostoperative pericardial effusion requiring repeat access/drainage was relatively infrequent, occurring in 4.9% of patients shortly after epicardial procedures. While the majority occur early and therefore require close observation, some patients may present in a delayed manner.