Creating a safe workplace by universal testing of SARS-CoV-2 infection in asymptomatic patients and healthcare workers in the electrophysiology units: a multi-center experience.

BACKGROUND: As the coronavirus cases continue to surge, the urgent need for universal testing to identify positive cases for effective containment of this highly contagious pandemic has become the center of attention worldwide. However, in spite of extensive discussions, very few places have even attempted to implement it. We evaluated the efficacy of widespread testing in creating a safe workplace in our electrophysiology (EP) community. Furthermore, we assessed the new infection rate in patients undergoing EP procedure, to see if identification and exclusion of positive cases facilitated establishment of a risk-free operating environment. METHODS: Viral-RNA and serology tests were conducted in 1670 asymptomatic subjects including patients and their caregivers and staff in our EP units along with the Emergency Medical Service (EMS) staff. RESULTS: Of 1670, 758 (45.4%) were patients and the remaining 912 were caregivers, EMS staff, and staff from EP clinic and lab. Viral-RNA test revealed 64 (3.8%) positives in the population. A significant increase in positivity rate was observed from April to June 2020 (p = 0.02). Procedures of positive cases (n = 31) were postponed until they tested negative at retesting. Staff testing positive (n = 33) were retested before going back to work after 2 weeks. Because of suspected exposure, 67 staff were retested and source was traced. No new infections were reported in patients during or within 2 weeks after the hospital-stay. CONCLUSIONS: Universal testing to identify positive cases was helpful in creating and maintaining a safe working environment without exposing patients and staff to new infections in the EP units. TRIAL REGISTRATION: Trial Registration Number: clinicaltrials.gov : NCT04352764.

SR compartment calcium and cell apoptosis in SERCA overexpression.

The relationship between SR Ca2+ ATPase (SERCA) activities, cell calcium level, SR calcium store and cell cycle events is not clearly understood. We studied SERCA overexpression in Cos cells using an adenovirus vector. Twofold increases in SERCA mRNA and in protein were correlated with a 2.3-fold and a 1.6-fold paralleled increase in SR calcium pump activity (R = 0.97 and R = 0.99 respectively). Dose-related apoptotic cell death was associated with SERCA overexpression (R = 0.92). When serum was reduced to 4%, cell apoptosis further increased from 20.7 +/- 4.8% to 47.5 +/- 12.9% (M+/-SD; P<0.05; n=3). Flow cytometry identified cell cycle arrest at the G2/M phase. The interleukin-1 converting enzyme (ICE) inhibitor z-VAD-fmk reduced apoptosis for low-, medium- and high-expressing constructs, whereas the CPP-32 inhibitor z-DEVD-fmk had no effect. Flow cytometry using Fluo-3 and Fura-Red revealed a 1.5-fold higher basal calcium and a 10-fold SR calcium overload. ICE inhibitor z-VAD-fmk did not alter calcium loading. An epitope-tagged SERCA mutant, which has no intrinsic Ca2+-pump activities, had a much smaller effect on the SR calcium. These findings suggest that SERCA2A overexpression has an intrinsic role in altering cell-cycle progression, augmenting cellular and SR calcium loading, and precipitating ICE protease-mediated apoptosis; this represents as a novel model for primary SR calcium overload and associated cell apoptosis.

Development of a model of complete heart block in rats.

Atrioventricular (AV) block is a useful substrate for the study of cardiac physiology. The objective of this investigation was to develop a straightforward and reproducible model of permanent AV block in rats. Working through a sternotomy, we used an epicardial fat pad between the aortic root and the right atrial wall of the rat as a landmark for the site for injection of 70% ethanol (5-10 microl) into the myocardium 3 mm below the epicardial surface. Stable, complete heart block was produced in 23 of 28 rats (82%) with a success rate of 100% in the last 16 rats of the series. Saline injection produced no heart block in 15 rats. A separate group of 14 animals was allowed to recover. Chronic heart block was achieved in all ethanol-injected animals for up to 7 days before death. The survival rate in the recovered rats was 90% in the ethanol-injected group and 100% in the saline-injected control group. Acute hemodynamic changes following the production of heart block consisted of an increase in central venous pressure, a decrease in systolic blood pressure, a decrease in left ventricular pressure, and a decrease in change in pressure over time. Chronic hemodynamic changes demonstrated a return to baseline of the central venous pressure, a persistent decrease in systolic blood pressure, and a decrease in left ventricular pressure. After the rats were killed and the hearts were dissected, discrete areas of myocardial damage were identified histologically in the atrial septum near the AV conduction axis tissue in the ethanol-injected hearts. Complete heart block was associated only with lesions extending into the specialized muscle of the AV node or His bundle. Focal mild hemorrhage, inflammation, and damaged myocardial fibers were observed in the acute stage, whereas healing lesions were characterized by granulation tissue and fibrosis replacing conduction tissue. The simple technique described provides a reproducible model for permanent, complete heart block and the study of cardiac function.