Background And Purpose: The coronavirus disease 2019 (COVID-19) outbreak has added challenges to providing quality acute stroke care due to the reallocation of stroke resources to COVID-19. Case series suggest that patients with COVID-19 have more severe strokes; however, no large series have compared stroke outcomes with contemporary non-COVID-19 patients. Purpose was to analyze the impact of COVID-19 pandemic in stroke care and to evaluate stroke outcomes according to the diagnosis of COVID-19.
Methods: Retrospective multicenter cohort study including consecutive acute stroke patients admitted to 7 stroke centers from February 25 to April 25, 2020 (first 2 months of the COVID-19 outbreak in Madrid). The quality of stroke care was measured by the number of admissions, recanalization treatments, and time metrics. The primary outcome was death or dependence at discharge.
Results: A total of 550 acute stroke patients were admitted. A significant reduction in the number of admissions and secondary interhospital transfers was found. COVID-19 was confirmed in 105 (19.1%) patients, and a further 19 patients were managed as suspected COVID-19 (3.5%). No differences were found in the rates of reperfusion therapies in ischemic strokes (45.5% non-COVID-19, 35.7% confirmed COVID-19, and 40% suspected COVID-19; =0.265). However, the COVID-19 group had longer median door-to-puncture time (110 versus 80 minutes), which was associated with the performance of chest computed tomography. Multivariate analysis confirmed poorer outcomes for confirmed or suspected COVID-19 (adjusted odds ratios, 2.05 [95% CI, 1.12-3.76] and 3.56 [95% CI, 1.15-11.05], respectively).
Conclusions: This study confirms that patients with COVID-19 have more severe strokes and poorer outcomes despite similar acute management. A well-established stroke care network helps to diminish the impact of such an outbreak in stroke care, reducing secondary transfers and allowing maintenance of reperfusion therapies, with a minor impact on door-to-puncture times, which were longer in patients who underwent chest computed tomography.
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http://dx.doi.org/10.1161/STROKEAHA.120.031769 | DOI Listing |
Ann Intern Med
January 2025
959 Medical Operations Squadron, U.S. Air Force, Department of Neurology, Brooke Army Medical Center, San Antonio, Texas (T.K.).
Description: In July 2024, the U.S. Department of Veterans Affairs (VA) and U.
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Department of Public Health and Hygiene, Faculty of Medicine, Pavol Jozef Safarik University in Kosice, Kosice, Slovak Republic.
Objective: Anxiety and depression in patients following cerebrovascular accidents are among frequently occurring complications of the medical condition. The consequences affect personal, family, professional, and social life. They cause severe functional and cognitive impairments, limit the ability to perform normal daily activities, which can result in complete disability.
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January 2025
Institute of Cerebrovascular Disease Research, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing, 100053, China.
High concentrations of neutrophil degranulation products in the plasma and thrombi are poor prognostic indicators in patients with acute ischemic stroke (AIS). This study aimed to identify candidate effectors capable of mediating neutrophil degranulation post-AIS, and to reveal their underlying epigenetic mechanisms. Microarrays and ChIP-seq were applied to analyze the neutrophils of patients with AIS.
View Article and Find Full Text PDFIntensive Care Med
January 2025
Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Hum Cell
January 2025
The First Branch, Hongqi Hospital Affiliated to Mudanjiang Medical University, No. 5 Tongxiang Street, Aimin District, Mudanjiang, 157000, China.
Subarachnoid hemorrhage (SAH) is a type of hemorrhagic stroke, and the neuroprotective effects of nimodipine following SAH have been well-documented. Sirtuin 3 (SIRT3), a mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, plays a significant role in mitigating oxidative stress in various neurodegenerative conditions. However, the role of SIRT3 in the neuroprotective mechanisms of nimodipine after SAH remains unclear.
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