Physical Activity in Cardiac Implantable Electronic Device Recipients During the COVID-19 Pandemic.

OBJECTIVE: To characterize the physical activity (PA) level in patients with a cardiac implantable electronic device (CIED) during the coronavirus disease 2019 (COVID-19) pandemic and compare PA level during the pandemic in 2020 with the year 2019. METHODS: We performed a retrospective analysis of PA activity in individuals implanted with a CIED enrolled in the BIOTRONIK CERTITUDE Registry. Mean daily and weekly PA from January to August 2020 was compared with 2019. RESULTS: A total of 21,660 individuals met eligibility criteria, with mean age of 72.6±11.6 years, and 12,411 (57.3)% were males. A significant decline in daily PA was noted following the pandemic declaration in 2020, with a maximum mean reduction of -24.5±36.3 minutes (P<.0001) observed in April 2020 compared with 2019. PA in 2020 increased from April to May (120.6±67.4 to 129.2±70.9 min/d). PA was lower for all months in 2020 compared with 2019. The decrease in PA was observed in all prespecified groups based on age, sex, type of device, and region of the country. CONCLUSION: After the declaration of the coronavirus disease 2019 pandemic, a significant decline in daily PA was observed in individuals with a CIED. Future investigation to establish the impact of this reduction on short and long-term cardiovascular outcomes is required.

Amyloid-beta peptide induces temporal membrane biphasic changes in astrocytes through cytosolic phospholipase A2.

Oligomeric amyloid-beta peptide (Abeta) is known to induce cytotoxic effects and to damage cell functions in Alzheimer's disease. However, mechanisms underlying the effects of Abeta on cell membranes have yet to be fully elucidated. In this study, Abeta 1-42 (Abeta(42)) was shown to cause a temporal biphasic change in membranes of astrocytic DITNC cells using fluorescence microscopy of Laurdan. Abeta(42) made astrocyte membranes became more molecularly-disordered within the first 30 min to 1 h, but gradually changed to more molecularly-ordered after 3 h. However, Abeta(42) caused artificial membranes of vesicles made of rat whole brain lipid extract to become more disordered only. The trend for more molecularly-ordered membranes in astrocytes induced by Abeta(42) was abrogated by either an NADPH oxidase inhibitor, apocynin, or an inhibitor of cytosolic phospholipase A(2) (cPLA(2)), but not by an inhibitor of calcium-independent PLA(2) (iPLA(2)). Apocynin also suppressed the increased production of superoxide anions (O(2)(-)) and phosphorylation of cPLA(2) induced by Abeta(42). In addition, hydrolyzed products of cPLA(2), arachidonic acid (AA), but not lysophosphatidylcholine (LPC) caused astrocyte membranes to become more molecularly-ordered. These results suggest (1) a direct interaction of Abeta(42) with cell membranes making them more molecularly-disordered, and (2) Abeta(42) also indirectly makes membranes become more molecularly-ordered by triggering the signaling pathway involving NADPH oxidase and cPLA(2) in astrocytes.