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The rMVr procedure was associated with less atrial fibrillation, less frequent transfusion requirement, and shorter intensive care unit and hospital stay, without a significant difference in 3-year mortality, heart failure readmission, or mitral valve reintervention. In older patients, rMVr confers short-term advantages without a detriment to midterm outcomes.

Background and Purpose: Studies suggest an increased risk of adverse outcomes among patients with acute ischemic stroke (AIS) and coronavirus disease 2019 (COVID-19). Methods: Using Get With The Guidelines–Stroke, we identified 41 971 patients (AIS/COVID-19: 1143; AIS/no COVID-19: 40 828) with AIS hospitalized between February 4, 2020 and June 29, 2020, from 458 Get With The Guidelines–Stroke hospitals with at least one COVID-19 case and evaluated clinical characteristics, treatment patterns, and outcomes. Results: Compared with patients with AIS/no COVID-19, those with AIS/COVID-19 were younger, more likely to be non-Hispanic Black, Hispanic, or Asian, more likely to present with higher National Institutes of Health Stroke Scale scores, and had greater proportions of large vessel occlusions. Rates of thrombolysis and thrombectomy were similar between the groups. Door to computed tomography (median 55 [18–207] versus 35 [14–99] minutes, P <0.001), door to needle (59 [40–82] versus 46 [33–64] minutes, P <0.001), and door to endovascular therapy (114 [74–169] versus 90 [54–133] minutes, P =0.002) times were longer in the AIS/COVID-19 cohort. In adjusted models, patients with AIS/COVID-19 had decreased odds of discharge with modified Rankin Scale score of ≤2 (odds ratio, 0.65 [95% CI, 0.52–0.81], P <0.001) and increased odds of in-hospital mortality (odds ratio, 4.34 [95% CI, 3.48–5.40], P <0.001). ConclusionS: This analysis demonstrates younger age, greater stroke severity, longer times to evaluation and treatment, and worse morbidity and mortality in patients with AIS/COVID-19 compared with those with AIS/no COVID-19.

SummaryChromatin assembly factor 1 (CAF-1) was initially characterized as a histone deliverer in the process of DNA-replication-coupled chromatin assembly in eukaryotic cells. Here, we report that CAF-1 p180, the largest subunit of Drosophila CAF-1, participates in the process of heterochromatin formation and functions to maintain pericentric heterochromatin stability. We provide evidence that Drosophila CAF-1 p180 plays a role in both classes of position effect variegation (PEV) and in the expression of heterochromatic genes. A decrease in the expression of Drosophila CAF-1 p180 leads to a decrease in both H3K9 methylation at pericentric heterochromatin regions and the recruitment of heterochromatin protein 1 (HP1) to the chromocenter of the polytene chromosomes. The artificial targeting of HP1 to a euchromatin location leads to the enrichment of Drosophila CAF-1 p180 at this ectopic heterochromatin, suggesting the mutual recruitment of HP1 and CAF-1 p180. We also show that the spreading of heterochromatin is compromised in flies that have reduced CAF-1 p180. Furthermore, reduced CAF-1 p180 causes a defect in the dynamics of heterochromatic markers in early Drosophila embryos. Together, these findings suggest that Drosophila CAF-1 p180 is an essential factor in the epigenetic control of heterochromatin formation and/or maintenance.