Citations

Background: Atypical Atrial Flutter (AAFL) prevalence is increasing due to the escalating Atrial Fibrillation (AF) ablations and cardiac surgeries. We wanted to explore the outcome of the AAFL ablation, considering the recent changes in mapping and ablation. Methods: This study was approved by the Institutional Review Board (IRB) of Mayo Clinic hospital. We retrospectively studied 419 patients who had undergone AAFL ablation at Mayo Clinic from January 2017 to June 2022. Thirteen patients declined research authorization, and 19 patients were lost to follow-up during the 90-day blanking period, resulting in a sample size of 387. The median follow-up time for patients was 25.7 months (95% CI 23.7, 32.3). Results: Recurrent symptoms with documentation of atrial arrhythmia Occurred in 226/387 (58.4%) patients, of which 151/226 (66.8%) occurred within the first year. The median time to recurrence was 8.5 months (max 57.8 months). Eleven patients died during the study period, 9 of whom experienced recurrence prior to death. Overall, the median recurrence-free survival (RFS) time was 16.6 months (95% CI 13.2, 20.0) with a 1-year RFS rate of 57.2% (95% CI 52.2, 62.7%). Acute termination occurred 324/387 (83.7%) during the ablation. The 1-year RFS rate was 58.9% (95% CI 53.5%, 64.9%) for patients with acute termination and 49.0% (95% CI 37.9%, 63.4%) for those without acute termination. The rate was not significantly different based on acute termination status (p = 0.11). Conclusions: The one-year RFS rate of 57.2% following AAFL ablation, even though 83.7% achieved acute termination during the procedure, signifies the extent of the underlying substrate abnormalities.

Abstract Atrial fibrillation is a common clinical manifestation in hospitalized patients with coronavirus disease 2019 (COVID‐19). Medications used to treat atrial fibrillation, such as antiarrhythmic drugs and anticoagulants, may have significant drug interactions with emerging COVID‐19 treatments. Common unintended nontherapeutic target effects of COVID‐19 treatment include potassium channel blockade, cytochrome P 450 isoenzyme inhibition or activation, and P‐glycoprotein inhibition. Drug‐drug interactions with antiarrhythmic drugs and anticoagulants in these patients may lead to significant bradycardia, ventricular arrhythmias, or severe bleeding. It is important for clinicians to be aware of these interactions, drug metabolism changes, and clinical consequences when choosing antiarrhythmic drugs and anticoagulants for COVID‐19 patients with atrial fibrillation. The objective of this review is to provide a practical guide for clinicians who are managing COVID‐19 patients with concomitant atrial fibrillation.

Modulation of mitochondrial respiratory chain, dehydrogenase, and nucleotide-metabolizing enzyme activities is fundamental to cellular protection. Here, we demonstrate that the potassium channel opener diazoxide, within its cardioprotective concentration range, modulated the activity of flavin adenine dinucleotide-dependent succinate dehydrogenase with an IC50of 32 μM and reduced the rate of succinate-supported generation of reactive oxygen species (ROS) in heart mitochondria. 5-Hydroxydecanoic fatty acid circumvented diazoxide-inhibited succinate dehydrogenase-driven electron flow, indicating a metabolism-dependent supply of redox equivalents to the respiratory chain. In perfused rat hearts, diazoxide diminished the generation of malondialdehyde, a marker of oxidative stress, which, however, increased on diazoxide washout. This effect of diazoxide mimicked ischemic preconditioning and was associated with reduced oxidative damage on ischemia-reperfusion. Diazoxide reduced cellular and mitochondrial ATPase activities, along with nucleotide degradation, contributing to preservation of myocardial ATP levels during ischemia. Thus, by targeting nucleotide-requiring enzymes, particularly mitochondrial succinate dehydrogenase and cellular ATPases, diazoxide reduces ROS generation and nucleotide degradation, resulting in preservation of myocardial energetics under stress.

Mitral Valve Injury with Catheter AblationIntroductionAn increasing number of catheter ablations involve the mitral annular region and valve apparatus, increasing the risk of catheter interaction with the mitral valve (MV) complex. We review our experience with catheter ablation‐related MV injury resulting in severe mitral regurgitation (MR) to delineate mechanisms of injury and outcomes.MethodsWe searched the Mayo Clinic MV surgical database over a 19‐year period (1993–2012) and the electrophysiologic procedures database over a 23‐year period (1990–2013) and identified 9 patients with catheter ablation related MV injury requiring clinical intervention.ResultsIndications for ablation included atrial fibrillation (AF) [n = 4], ventricular tachycardia (VT) [n = 3], and left‐sided accessory pathways [n = 2]. In all 4 AF patients, a circular mapping catheter entrapped in the MV apparatus was responsible for severe MR. In all 3 VT patients, radiofrequency energy delivery led to direct injury to the MV apparatus. In the 2 patients with accessory pathways, both mechanisms were involved (1 per patient). Six patients required surgical intervention (5 MV repair, 1 catheter removal). One patient developed severe functional MR upon successful endovascular catheter disentanglement that improved spontaneously. Two VT patients with persistent severe postablation MR were managed nonsurgically, 1 of whom died 3 months postprocedure.ConclusionCircular mapping catheter entrapment and ablation at the mitral annulus are the most common etiologies of MV injury during catheter ablation. Close surveillance of the MV is needed during such procedures and early surgical repair is important for successful salvage if significant injury occurs.