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Importance: Although an emergency coronary angiogram (CAG) is recommended for patients who experience an out-of-hospital cardiac arrest (OHCA) with ST-segment elevation on the postresuscitation electrocardiogram (ECG), this strategy is still debated in patients without ST-segment elevation.
Objective: To assess the 180-day survival rate with Cerebral Performance Category (CPC) 1 or 2 of patients who experience an OHCA without ST-segment elevation on ECG and undergo emergency CAG vs delayed CAG.
Design, Setting, And Participants: The Emergency vs Delayed Coronary Angiogram in Survivors of Out-of-Hospital Cardiac Arrest (EMERGE) trial randomly assigned survivors of an OHCA without ST-segment elevation on ECG to either emergency or delayed (48 to 96 hours) CAG in 22 French centers. The trial took place from January 19, 2017, to November 23, 2020. Data were analyzed from November 24, 2020, to July 30, 2021.
Main Outcomes And Measures: The primary outcome was the 180-day survival rate with CPC of 2 or less. The secondary end points were occurrence of shock, ventricular tachycardia, and/or fibrillation within 48 hours, change in left ventricular ejection fraction between baseline and 180 days, CPC scale at intensive care unit discharge and day 90, survival rate, and hospital length of stay.
Results: A total of 279 patients (mean [SD] age, 64.7 [14.6] years; 195 men [69.9%]) were enrolled, with 141 (50.5%) in the emergency CAG group and 138 (49.5%) in the delayed CAG group. The study was underpowered. The mean (SD) time delay between randomization and CAG was 0.6 (3.7) hours in the emergency CAG group and 55.1 (37.2) hours in the delayed CAG group. The 180-day survival rates among patients with a CPC of 2 or less were 34.1% (47 of 141) in the emergency CAG group and 30.7% (42 of 138) in the delayed CAG group (hazard ratio [HR], 0.87; 95% CI, 0.65-1.15; P = .32). There was no difference in the overall survival rate at 180 days (emergency CAG, 36.2% [51 of 141] vs delayed CAG, 33.3% [46 of 138]; HR, 0.86; 95% CI, 0.64-1.15; P = .31) and in secondary outcomes between the 2 groups.
Conclusions And Relevance: In this randomized clinical trial, for patients who experience an OHCA without ST-segment elevation on ECG, a strategy of emergency CAG was not better than a strategy of delayed CAG with respect to 180-day survival rate and minimal neurologic sequelae.
Trial Registration: ClinicalTrials.gov Identifier: NCT02876458.
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http://dx.doi.org/10.1001/jamacardio.2022.1416 | DOI Listing |
RSC Med Chem
September 2025
NodThera Ltd. Suite 8, The Mansion, Chesterford Research Park, Little Chesterford, Saffron Walden Essex CB10 1XL UK
Inhibition of the NLRP3 inflammasome has emerged as a high potential treatment paradigm for the treatment of neuroinflammation, with demonstrated anti-neuroinflammatory effects in Parkinson's disease patients and a strong rationale in Alzheimer's disease and amyotrophic lateral sclerosis. To facilitate further progress in this field, brain penetrant NLRP3 inflammasome inhibitors as leads and tool compounds are required. We discovered a small molecule NLRP3 inflammasome inhibitor, NT-0527 (11), and extensively profiled this to reveal a highly potent, selective and brain penetrant compound.
View Article and Find Full Text PDFNeurogenetics
September 2025
Nur International University, 54600, Lahore, Punjab, Pakistan.
Huntington's disease (HD) is a progressive, autosomal dominant neurodegenerative disorder characterized by motor dysfunction, cognitive decline, and psychiatric disturbances. It is caused by CAG repeat expansions in the HTT gene, resulting in the formation of mutant huntingtin protein that aggregates and disrupts neuronal function. This review outlines the pathogenesis of HD, including genetic, molecular, and environmental factors.
View Article and Find Full Text PDFIn Silico Pharmacol
September 2025
School of Pharmacy, Swami Ramanand Teerth Marathwada University, Nanded, Maharashtra India.
Unlabelled: Huntington's disease (HD) is a progressive neurodegenerative disorder characterized by CAG repeat expansion in the HTT gene, leading to oxidative stress, mitochondrial dysfunction, and neuroinflammation. Conventional therapies offer only symptomatic relief with limited efficacy. This study aimed to explore the neuroprotective potential of (MP) and (BS) through an integrative bioinformatics approach, targeting multiple pathological mechanisms implicated in HD.
View Article and Find Full Text PDFBiomolecules
July 2025
Department of Ophthalmology, Emory University, Atlanta, GA 30322, USA.
The retinal pigment epithelium (RPE), a monolayer of pigmented cells, is critical for visual function through its interaction with the neural retina. In healthy eyes, RPE cells exhibit a uniform hexagonal arrangement, but under stress or disease, such as age-related macular degeneration (AMD), dysmorphic traits like cell enlargement and apparent multinucleation emerge. Multinucleation has been hypothesized to result from cellular fusion, a compensatory mechanism to maintain cell-to-cell contact and barrier function, as well as conserve resources in unhealthy tissue.
View Article and Find Full Text PDFBrain Sci
July 2025
Neurodegenerative Disorders Research Pty Ltd., Perth, WA 6005, Australia; Tel.: +61-8-6317-9472.
Background: The mechanisms by which sporadic young-onset neurodegenerative processes develop are uncertain.
Methods: We have previously proposed that stochastic processes involving sequence changes at a DNA, RNA, or protein level in critical genes and proteins might be important to this process. Further investigation points to the contribution of probabilistic states in other factors involved in neurodegenerative conditions, such as-in the case of young onset Alzheimer's disease-head injury, apolipoprotein ε4 alleles and other elements that, by the interaction of conditional probabilities in these variables, influence the evolution of neurodegenerative conditions.