Long-Term Psychological Distress Among Surrogate Decision Makers for Mexican American and Non-Hispanic White Patients With Severe Stroke.

BACKGROUND AND OBJECTIVES: During acute hospitalizations, physicians often focus on the stroke patient and not family who may be traumatized by this sudden change to their loved one. We investigated long-term psychological distress among family surrogate decision makers for Mexican American (MA) and non-Hispanic White (NHW) severe stroke patients. Previous work in other diseases suggested worse psychological outcomes in MA than NHW caregivers. METHODS: This was a population-based, prospective cohort study in Nueces County, TX. Stroke patient participants and their surrogate decision makers were enrolled soon after any stroke between April, 2016, and October, 2020, if surrogates had made decisions about life-sustaining treatments. Surrogates completed validated measures of posttraumatic stress, National Stressful Events Survey for Posttraumatic Stress Disorder Short Scale; anxiety, Generalized Anxiety Disorder-7; and depression, Patient Health Questionnaire-8 at discharge, 3, 6, and 12 months. Ethnic differences were assessed with multilevel linear mixed models, sequentially adjusted for prespecified patient and surrogate demographic, socioeconomic, and clinical covariates. RESULTS: There were 301 family surrogates for 241 severe stroke patients. The mean follow-up was 315 days. High scores on measures of psychological distress ranged between 17% and 28% of surrogates. One or more high levels of the psychological outcomes were found in 17%-43% of surrogates; 2 or more were found in 12%-27%; and all 3 were found in 5%-16% of surrogates. All psychological outcomes were worse among MAs on unadjusted analyses. In fully adjusted models, posttraumatic stress remained worse among MAs (0.36, 95% CI 0.17-0.56); ethnic differences were attenuated and no longer significant in the final model for anxiety (0.59, 95% CI -0.55 to 1.74) and depression (0.97, 95% CI -0.25 to 2.19). The trajectory for depression did differ by ethnicity (interaction p = 0.03), with depression score improving more rapidly over time among NHWs than MAs. Advance care plans did not seem to confound any ethnic differences. DISCUSSION: Psychological distress is common among family surrogate decision makers in the year after stroke and may be worse among MAs. Efforts are needed to support family members of all ethnic groups after severe stroke.

Stroke Outcomes Among English- and Spanish-Speaking Mexican American Patients.

OBJECTIVES: We examined whether language preference was associated with 90-day poststroke outcomes among Mexican American (MA) patients. METHODS: Patients with ischemic stroke and intracerebral hemorrhage from the population-based Brain Attack Surveillance in Corpus Christi project (2009-2018) were compared by language preference in 90-day neurologic, functional, and cognitive outcomes using weighted Tobit regression. Models were adjusted for demographics, initial NIH Stroke Scale (NIHSS), medical history, stroke characteristics, and insurance status. RESULTS: Of 1,096 stroke patients, 926 were English-speaking and 170 were Spanish-only-speaking. Spanish speakers were older (p < 0.01), received less education (p < 0.01), had higher initial NIHSS values (p = 0.02), had higher prevalence of atrial fibrillation (p < 0.01), and had lower prevalence of smoking (p = 0.01) than English speakers. In fully adjusted models, Spanish-only speakers had worse neurologic outcome (NIHSS, range 0-44 [higher worse], mean difference: 1.93, p < 0.01) but no difference in functional outcome measured by activities of daily living/instrumental activities of daily living or cognitive outcome compared with English speakers. DISCUSSION: This population-based study found worse neurologic but similar functional and cognitive stroke outcomes among Spanish-only-speaking MA patients compared with English-speaking MA patients.

miR-26a-5p protects against myocardial ischemia/reperfusion injury by regulating the PTEN/PI3K/AKT signaling pathway.

Reperfusion strategies in acute myocardial infarction (AMI) can cause a series of additional clinical damage, defined as myocardial ischemia/reperfusion (I/R) injury, and thus there is a need for effective therapeutic methods to attenuate I/R injury. miR-26a-5p has been proven to be an essential regulator for biological processes in different cell types. Nevertheless, the role of miR-26a-5p in myocardial I/R injury has not yet been reported. We established an I/R injury model in vitro and in vivo. In vitro, we used cardiomyocytes to simulate I/R injury using hypoxia/reoxygenation (H/R) assay. In vivo, we used C57BL/6 mice to construct I/R injury model. The infarct area was examined by TTC staining. The level of miR-26a-5p and PTEN was determined by bioinformatics methods, qRT-PCR, and western blot. In addition, the viability and apoptosis of cardiomyocytes were separately detected by MTT and flow cytometry. The targeting relationship between miR-26a-5p and PTEN was analyzed by the TargetScan website and luciferase reporter assay. I/R and H/R treatment induced myocardial tissue injury and cardiomyocyte apoptosis, respectively. The results showed that miR-26a-5p was down-regulated in myocardial I/R injury. PTEN was found to be a direct target of miR-26a-5p. Furthermore, miR-26a-5p effectively improved viability and inhibited apoptosis in cardiomyocytes upon I/R injury by inhibiting PTEN expression to activate the PI3K/AKT signaling pathway. miR-26a-5p could protect cardiomyocytes against I/R injury by regulating the PTEN/PI3K/AKT pathway, which offers a potential approach for myocardial I/R injury treatment.

miR-26a-5p protects against myocardial ischemia/reperfusion injury by regulating the PTEN/PI3K/AKT signaling pathway

Reperfusion strategies in acute myocardial infarction (AMI) can cause a series of additional clinical damage, defined as myocardial ischemia/reperfusion (I/R) injury, and thus there is a need for effective therapeutic methods to attenuate I/R injury. miR-26a-5p has been proven to be an essential regulator for biological processes in different cell types. Nevertheless, the role of miR-26a-5p in myocardial I/R injury has not yet been reported. We established an I/R injury model in vitro and in vivo. In vitro, we used cardiomyocytes to simulate I/R injury using hypoxia/reoxygenation (H/R) assay. In vivo, we used C57BL/6 mice to construct I/R injury model. The infarct area was examined by TTC staining. The level of miR-26a-5p and PTEN was determined by bioinformatics methods, qRT-PCR, and western blot. In addition, the viability and apoptosis of cardiomyocytes were separately detected by MTT and flow cytometry. The targeting relationship between miR-26a-5p and PTEN was analyzed by the TargetScan website and luciferase reporter assay. I/R and H/R treatment induced myocardial tissue injury and cardiomyocyte apoptosis, respectively. The results showed that miR-26a-5p was down-regulated in myocardial I/R injury. PTEN was found to be a direct target of miR-26a-5p. Furthermore, miR-26a-5p effectively improved viability and inhibited apoptosis in cardiomyocytes upon I/R injury by inhibiting PTEN expression to activate the PI3K/AKT signaling pathway. miR-26a-5p could protect cardiomyocytes against I/R injury by regulating the PTEN/PI3K/AKT pathway, which offers a potential approach for myocardial I/R injury treatment.