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Competing Interests: Funding Support and Author Disclosures Dr Tedrow has received consulting fees from Biosense Webster and Thermedical Inc; serves on an Advisory Board for Biosense Webster; and has received honoraria for educational courses from Biosense Webster, Baylis Medical, Boston Scientific, Medtronic, and Abbot Medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

The authors describe 3 patients presenting with cardiac sarcoidosis (CS) flare and ventricular tachycardia (VT) storm following infection with severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), the causative agent of COVID-19. COVID-19-related cardiac manifestations can vary and include arrythmias, myocarditis, and exacerbation of underlying cardiovascular disease. The exact mechanism of myocardial involvement is not clear but may include abnormal host immune response and direct myocardial injury, thereby predisposing to enhanced arrhythmic risk. Arrhythmias account for 20% of COVID-19-related complications with ventricular arrythmias occurring in 5.9% of cases. Further studies are needed to better understand mechanisms underlying the intersection between COVID-19 infection and inflammatory cardiomyopathies., Competing Interests: Funding Support and Author Disclosures Dr John was supported by the Pierce Family Fellowship. Dr Winterfield has received institutional research support from Abbott Medical and Biosense Webster; and has received consulting fees from Abbott Medical, Biosense Webster, Thermedical, and Biotronik. Dr Houston has received institutional research support from Medtronic Inc and CVRx; and has received consulting fees from Edwards Lifesciences and Medtronic. Dr Tedrow has received consulting fees from Biosense Webster and Thermedical Inch; has served on an advisory board for Biosense Webster; and has received honoraria for educational courses from Biosense Webster, Boston Scientific, Medtronic, and Abbott medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: This study sought to describe the burden of atrial fibrillation (AF)/atrial flutter (AFL) in patients with left ventricular assist devices (LVAD) and to evaluate the impact of rhythm control strategies., Background: AF and AFL among patients with LVADs are poorly characterized., Methods: Retrospective multivariable survival analysis of all LVAD recipients at the Cleveland Clinic from January 1, 2004 to June 30, 2016 examining the association of death, thromboembolism, and major bleeding with AF/AFL and exposure to rhythm control measures., Results: Among 418 patients (median age: 58 [interquartile range: 50 to 67] years, 80% male) with median follow-up of 445 (interquartile range: 165 to 936) days, AF (n = 287 of 418, 69%) and AFL (n = 61 of 418, 15%) were highly prevalent. Patients with AF/AFL (n = 302 of 418, 72%) and without AF/AFL (n = 116 of 418, 28%) had similar mortality (39% vs. 38%; p = 0.88) and major bleeding (46% vs. 49%; p = 0.53); AF/AFL patients had fewer thromboembolic events (13% vs. 23%; p < 0.01). Paroxysmal or persistent AF/AFL was present in 238 patients (57%), and rhythm control exposure (n = 166, 70%) was not associated with decreased mortality (39% vs. 43%; p = 0.57), thromboembolism (13% vs. 17%; p = 0.41), or bleeding (49% vs. 39%; p = 0.16). In the multivariable survival analysis only prior valve surgery (hazard ratio: 2.0; 95% confidence interval: 1.3 to 3.0; p = 0.002) was associated with increased hazard; AF/AFL had no association with risk of death, thromboembolism, or bleeding., Conclusions: Though highly prevalent among LVAD patients, AF/AFL was not associated with increased mortality, thromboembolism, or bleeding, and among paroxysmal/persistent AF patients, rhythm control measures were not associated with improved outcomes., (Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Acute pancreatitis is a painful, life-threatening disorder of the pancreas whose etiology is often multi-factorial. It is of great importance to understand the interplay between factors that predispose patients to develop the disease. One such factor is an excessive elevation in pancreatic acinar cell Ca(2+). These aberrant Ca(2+) elevations are triggered by release of Ca(2+) from apical Ca(2+) pools that are gated by the inositol 1,4,5-trisphosphate receptor (IP3R) types 2 and 3. In this study, we examined the role of IP3R type 2 (IP3R2) using mice deficient in this Ca(2+) release channel (IP3R2(-/-)). Using live acinar cell Ca(2+) imaging we found that loss of IP3R2 reduced the amplitude of the apical Ca(2+) signal and caused a delay in its initiation. This was associated with a reduction in carbachol-stimulated amylase release and an accumulation of zymogen granules (ZGs). Specifically, there was a 2-fold increase in the number of ZGs (P<0.05) and an expansion of the ZG pool area within the cell. There was also a 1.6- and 2.6-fold increase in cellular amylase and trypsinogen, respectively. However, the mice did not have evidence of pancreatic injury at baseline, other than an elevated serum amylase level. Further, pancreatitis outcomes using a mild caerulein hyperstimulation model were similar between IP3R2(-/-) and wild type mice. In summary, IP3R2 modulates apical acinar cell Ca(2+) signals and pancreatic enzyme secretion. IP3R-deficient acinar cells accumulate ZGs, but the mice do not succumb to pancreatic damage or worse pancreatitis outcomes.