Embolic Cerebrovascular Accident Secondary to Device-Related Thrombus Post WATCHMAN Device Implantation.

Atrial fibrillation (AF) is one of the most common cardiac arrhythmias encountered. Aggressive and appropriate management, along with identification and modification of risk factors, remains at the forefront of evidence-based practice. Thrombus formation (primarily in the left atrial appendage) and consequent thromboembolism are risks associated with AF. Anticoagulation is utilized to prevent and reduce AF-induced complications such as stroke, heart failure, and death. However, in instances when the risk of bleeding from anticoagulation outweighs the benefits of stroke prevention, other modalities such as left atrial appendage closure (LAAC) devices like the WATCHMAN device (Boston Scientific, MA) are utilized. LAAC devices, such as the WATCHMAN device, are also not without significant risks, one of them being device-related thrombus (DRT) formation. We present a case of device-related thrombus formation post WATCHMAN implantation and a subsequent embolic cerebrovascular accident (CVA).

SOD isoforms play no role in lifespan in ad lib or dietary restricted conditions, but mutational inactivation of SOD-1 reduces life extension by cold.

The free radical theory of aging is one of the most prominent theories of aging and senescence, but has yet to be definitively proven. If free radicals are the cause of senescence, then the cellular anti-oxidant system should play a large role in lifespan determination. Because superoxide dismutase (SOD) plays a central role in detoxifying superoxide radicals, we have examined the effects of mutational inactivation of each isoform of sod on normal lifespan and lifespan extension by dietary restriction (DR) or cold-/hypothermic-induced longevity (CHIL). We find no significant decrease in lifespan for control worms or worms undergoing DR when sod isoforms are knocked-out even though sod mutational inactivation produces hypersensitivity to paraquat. In contrast, sod-1 inactivation significantly reduces lifespan extension by CHIL, suggesting that CHIL requires a specific genetic program beyond simple reduction in metabolic rate. Furthermore, CHIL paradoxically increases lifespan while reducing resistance to oxidative stress, further disassociating oxidative stress resistance and lifespan.