Highlights d Mechanotransduction regulates actin at the tips of mammalian cochlear stereocilia d With transduction onset, ADF/cofilin localize to mechanotransducing stereocilia tips d Actin-severing proteins increase available F-actin barbed ends at stereocilia tips d Normal stereocilia length and width depend on ADF and cofilin-1
Objectives
We sought to evaluate the safety, efficacy and feasibility of same‐day discharge after uncomplicated, minimalist TAVR.
Background
At the start of the COVID‐19 pandemic, we created a same‐day discharge (SDD) pathway after conscious sedation, transfemoral (minimalist) TAVR to help minimize risk of viral transmission and conserve hospital resources. Studies support that next‐day discharge (NDD) for carefully selected patients following minimalist TAVR is safe and feasible. There is a paucity of data regarding the safety of SDD after TAVR.
Methods
In‐hospital and 30 day outcomes of consecutive patients meeting pre‐specified criteria for SDD after minimalist TAVR at our institution between March and July of 2020 were reviewed. Outcomes were compared to a NDD cohort from July 2018 through July 2020 that would have met SDD criteria. Primary endpoints were mortality, delayed pacemaker placement, stroke and cardiovascular readmission at 30 days.
Results
Twenty nine patients were discharged via the SDD pathway after TAVR. 128 prior NDD patients were identified who met all criteria for SDD. The STS scores were similar between the two groups (SDD 2.6% ±1.5 vs. NDD 2.3% ± 1.2). There were no deaths at 30 days in either group. There was no significant difference in delayed pacemaker placement (SDD 0% vs. NDD 0.8%, p > .99) or cardiovascular readmission (SDD 0% vs. NDD 5.5%, p = .35) at 30 days.
Conclusions
Same day discharge following uncomplicated, minimalist TAVR in selected patients appears to be safe, achieving similar 30 day outcomes as a cohort of next day discharge patients.
SUMMARYThe assembly and maintenance of actin-based mechanosensitive stereocilia in the cochlea is critical for lifelong hearing. Myosin-15 (MYO15) is hypothesized to modulate stereocilia height by trafficking actin regulatory proteins to their tip compartments, where actin polymerization must be precisely controlled during development. We identified a mutation (p.D1647G) in the MYO15 motor-domain that initially maintained trafficking, but caused progressive hearing loss by stunting stereocilia growth, revealing an additional function for MYO15. Consistent with its maintenance of tip trafficking in vivo, purified p.D1647G MYO15 modestly reduced actin-stimulated ATPase activity in vitro. Using ensemble and single-filament fluorescence in vitro assays, we demonstrated that wild-type MYO15 directly accelerated actin filament polymerization by driving nucleation, whilst p.D1647G MYO15 blocked this activity. Collectively, our studies suggest direct actin nucleation by MYO15 at the stereocilia tip is necessary for elongation in vivo, and that this is a primary mechanism disrupted in DFNB3 hereditary human hearing loss.
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