Faculty Bibliography

OBJECTIVE:The optimal medical management strategy in the periprocedural period for patients undergoing carotid artery interventions is not well described. Renin-angiotensin-system blocking (RASB) agents are considered to be among the first line anti-hypertensive agents; however, their role in the perioperative period is unclear. The objective of this study was to examine the relationship between the use of RASB agents on periprocedural outcomes in patients undergoing carotid interventions-carotid endarterectomy (CEA), transfemoral carotid artery stenting (CAS), and transcervical carotid artery revascularization (TCAR). METHOD/METHODS:The Society for Vascular Surgery Quality Initiative database was queried for all patients undergoing CAS, CEA, and TCAR between 2003 and 2020. Patients were stratified into two groups based upon their use of RASB agents in the periprocedural period. The primary endpoint was periprocedural neurologic events (including both strokes and transient ischemic attacks (TIAs)). The secondary endpoints were peri-procedural mortality and significant cardiac events, including myocardial infarction, dysrhythmia, and congestive heart failure. RESULTS:= 0.461). CONCLUSION/CONCLUSIONS:The use of peri-procedural RASB agents was associated with a significantly decreased rate of neurologic events in patients undergoing both CEA and TCAR. This effect was not observed in patients undergoing CAS. As carotid interventions warrant absolute minimization of perioperative complications in order to provide maximum efficacy with regard to stroke protection, the potential neuro-protective effect associated with RASB agents use following CEA and TCAR warrants further examination.

Intracerebral hemorrhage (ICH) is classified as a subtype of stroke and Calcium (Ca²⁺) overload is a catalyst for ICH. This study explored the mechanisms of Stat1 (signal transducer and activator of transcription 1) in the neuronal Ca²⁺ overload after ICH. ICH mouse models and in vitro cell models were established. Stat1 and transient receptor potential melastatin 7 (Trpm7) were detected up-regulated in ICH models. Afterwards, the mice were infected with the lentivirus containing sh-Stat1, and HT22 cells were treated with si-Stat1 and the lentivirus containing pcDNA3.1-Trpm7. The neurologic functional impairment, histopathological damage, and Nissl body in mice were all measured. HT22 cell viability and apoptosis were identified. The levels of Ca²⁺, Trpm7 mRNA, H3K27 acetylation (H3K27ac), CaMKII-α, and p-Stat1 protein in the tissues and cells were determined. We found that silencing Stat1 alleviated ICH damage and repressed the neuronal Ca²⁺ overload after ICH. H3K27ac enrichment in the Trpm7 promoter region was examined and we found that p-Stat1 accelerated Trpm7 transcription via promoting H3K27ac in the Trpm7 promoter region. Besides, Trpm7 overexpression increased Ca²⁺ overload and aggravated ICH. Overall, p-Stat1 promoted Trpm7 transcription and further aggravated the Ca²⁺ overload after ICH.