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BACKGROUND: As the COVID-19 pandemic shifts to an endemic phase, an increasing proportion of patients with cancer and a preoperative history of COVID-19 will require surgery. This study aimed to assess the influence of preoperative COVID-19 on postoperative risk for major adverse cardiovascular and cerebrovascular events (MACEs) among those undergoing surgical cancer resection. Secondary objectives included determining optimal time-to-surgery guidelines based on COVID-19 severity and discerning the influence of vaccination status on MACE risk. STUDY DESIGN: National COVID Cohort Collaborative Data Enclave, a large multi-institutional dataset, was used to identify patients that underwent surgical cancer resection between January 2020 and February 2023. Multivariate regression analysis adjusting for demographics, comorbidities, and risk of surgery was performed to evaluate risk for 30-day postoperative MACE. RESULTS: Of 204,371 included patients, 21,313 (10.4%) patients had a history of preoperative COVID-19. History of COVID-19 was associated with an increased risk for postoperative composite MACE as well as 30-day mortality. Among patients with mild disease who did not require hospitalization, MACE risk was elevated for up to 4 weeks after infection. Postoperative MACE risk remained elevated more than 8 weeks after infection in those with moderate disease. Vaccination did not reduce risk for postoperative MACE. CONCLUSIONS: Together, these data highlight that assessment of the severity of preoperative COVID-19 infection should be a routine component of both preoperative patient screening as well as surgical risk stratification. In addition, strategies beyond vaccination that increase patients' cardiovascular fitness and prevent COVID-19 infection are needed. [ABSTRACT FROM AUTHOR]

Cerebrovascular events are linked to ankylosing spondylitis. Accelerated atherosclerosis and endothelial dysfunction against a backdrop of inflammation have been widely blamed for the increased cerebrovascular risk in ankylosing spondylitis. The absence of a comprehensive review encouraged us to consider the link between ankylosing spondylitis and cerebrovascular diseases. Web of Science, PubMed, Medline, Scopus, and EMBASE were searched to identify studies published from 2000 to June 10, 2023. All observational and cohort studies reporting myocardial infarction or stroke and considering classic cerebrovascular risk in ankylosing spondylitis patients and healthy controls were included. Most of the included studies reported that the risk of cerebrovascular disorders was greater in ankylosing spondylitis than in the general population. Also, most studies showed that for both sexes, the prevalence of cardiovascular illnesses rose with age, and this trend was consistent across all subgroups of cardiovascular disorders. Also, most studies reported that the rate of cerebrovascular accidents in ankylosing spondylitis patients was higher than in control groups. Some studies reported that the risk of developing an ischemic stroke was higher in young patients with ankylosing spondylitis, while others did not. Our systematic analysis found that most studies agreed that ankylosing spondylitis patients had a higher risk of cerebrovascular diseases than the general population. Still, this increased risk was influenced by several factors that need further research exploration. [ABSTRACT FROM AUTHOR]

This retrospective study investigated the long-term incidence and risk of postoperative complications following spinal fusion. This study included 640,366 participants from a National Health Examination cohort in the Republic of Korea. Among them, 11,699 individuals underwent spinal fusion, and 56,667 individuals who underwent non-fusion spinal procedures served as controls. Propensity score matching was used to account for patient characteristics including demographic factors, comorbidities, and other relevant variables. The participants were followed for 8 years to assess the occurrence of cerebrovascular disease (CVD), hemorrhagic infarction (HA), ischemic infarction (II), occlusion and stenosis, and ischemic heart disease (IHD). The incidence rates of CVD and IHD were found to be 27.58 and 31.45 per 1,000 person-years in the spinal fusion group compared to 18.68 and 25.73 per 1,000 person-years in the control group (p <.001), respectively. Patients who underwent spinal fusion had a higher risk of CVD, HA, and IHD than those in the control group (all p <.001). In the subgroup analysis, thoracolumbar and noncervical spinal fusion were associated with a higher risk of CVD, II, and IHD (all p <.005). Patients undergoing thoracolumbar fusion may have an increased association with CVD, II in cerebral arteries, and IHD. This suggests a need for careful consideration of vascular risks in such patient populations. [ABSTRACT FROM AUTHOR]

Background: Vascular dementia (VaD) is a prevalent neurodegenerative disease characterized by cognitive impairment due to cerebrovascular factors, affecting a significant portion of the aging population and highlighting the critical need to understand specific targets and mechanisms for effective prevention and treatment strategies. We aimed to identify pathways and crucial genes involved in the progression of VaD through bioinformatics analysis and subsequently validate these findings. Methods: We conducted differential expression analysis, Weighted Gene Co-expression Network Analysis (WGCNA), Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and Protein-Protein Interaction (PPI) analysis. We utilized pheochromocytoma 12 (PC12) cells to create an in vitro oxygen-glucose deprivation (OGD) model. We investigated the impact of overexpression and interference of adrenoceptor alpha 1D (ADRA1D) on OGD PC12 cells using TdT-mediated dUTP nick-end labeling (TUNEL), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot (WB), and Fluo-3-pentaacetoxymethyl ester (Fluo-3 AM) analysis. Results: We found 187 differentially expressed genes (DEGs) in the red module that were strongly associated with VaD and were primarily enriched in vasoconstric-tion, G protein-coupled amine receptor activity, and neuroactive ligand-receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, and cell adhesion. Among these pathways, we identified ADRA1D as a gene shared by vasoconstriction, G protein-coupled amine receptor activity, and neuroactive ligand-receptor interaction. The TUNEL assay revealed a significant decrease in PC12 cell apoptosis with ADRA1D overexpression (p<0.01) and a significant increase in apoptosis upon silencing ADRA1D (p < 0.01). RT-qPCR and WB analysis revealed elevated ADRA1D expression (p < 0.001) and decreased phospholipase C beta (PLCß) and inositol 1,4,5-trisphosphate receptor (IP3R) expression (p < 0.05) with ADRA1D overexpression. Moreover, the Fluo-3 AM assessment indicated significantly lower intracellular Ca2+ levels with ADRA1D overexpression (p < 0.001). Conversely, interference with ADRA1D yielded opposite results. Conclusion: Our study provides a new perspective on the pathogenic mechanisms of VaD and potential avenues for therapeutic intervention. The results highlight the role of ADRA1D in modulating cellular responses to OGD and VaD, suggesting its potential as a target for VaD treatment. [ABSTRACT FROM AUTHOR]

This Editorial comments on the article by Jauffret et al. in this issue. [ABSTRACT FROM AUTHOR]

Background: Few studies on the risk of incident major adverse cardiac and cerebrovascular events (MACCEs) in sarcopenia have been reported. The objective was to assess the association between presarcopenia and sarcopenia and a higher risk of MACCEs. Methods: This study on the UK Biobank prospective cohort, used data collected between 2006 and 2021. Community‐dwelling Caucasian participants aged 37 to 73 years were included if values for Handgrip Strength (HGS) and Skeletal Muscle Index (SMI) were available and if no history of MACCEs was reported. Exposure was assessed using the European Working Group on Sarcopenia in Older People 2 (EWGSOP2) criteria. Muscle strength was measured using HGS, and muscle mass using the SMI. Presarcopenia was defined through the two definitions available in the literature, as low HGS with normal SMI and as normal HGS with low SMI, whereas sarcopenia was defined as low HGS with low SMI. The main outcome was to determine whether presarcopenia and/or sarcopenia were predictors of MACCEs (composite events). Results: A total of 406,411 included participants (women: 55.7%) were included. At baseline, there were 18,257 (4.7%) presarcopenics—subgroup n°1 (low HGS only), 7940 (2.1%) presarcopenics—subgroup n°2 (low SMI only), and 1124 (0.3%) sarcopenics. Over a median follow‐up of 12.1 years (IQR: [11.4; 12.8]), 28,300 participants (7.0%) were diagnosed with at least one event. Compared to NonSarc, presarcopenic (subgroups n°1 and n°2) and sarcopenic status were significantly associated with a higher risk of MACCEs (respectively fully adjusted HRs: HR = 1.25 [95% CI: 1.19; 1.31], HR = 1.33 [95% CI: 1.23; 1.45] and HR = 1.62 [95% CI: 1.34; 1.95]). Conclusions: In a community‐dwelling population, the risk of MACCEs was higher in both presarcopenic and sarcopenic participants. See related editorial by Mirzai and Tang in this issue. [ABSTRACT FROM AUTHOR]

Background Growing evidence suggests that some coronavirus disease 2019 (COVID-19) survivors experience a wide range of long-term postacute sequelae. We examined the postacute risk and burden of new-incident cardiovascular, cerebrovascular, and other thrombotic complications after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in a highly vaccinated multiethnic Southeast Asian population, during Delta predominance. Methods This cohort study used national testing and healthcare claims databases in Singapore to build a cohort of individuals who had a positive SARS-CoV-2 test between 1 September and 30 November 2021 when Delta predominated community transmission. Concurrently, we constructed a test-negative control group by enrolling individuals between 13 April 2020 and 31 December 2022 with no evidence of SARS-CoV-2 infection. Participants in both groups were followed up for a median of 300 days. We estimated risks of new-incident cardiovascular, cerebrovascular, and other thrombotic complications using doubly robust competing-risks survival analysis. Risks were reported using 2 measures: hazard ratio (HR) and excess burden (EB) with 95% confidence intervals. Results We included 106 012 infected cases and 1 684 085 test-negative controls. Compared with the control group, individuals with COVID-19 exhibited increased risk (HR, 1.157 [1.069–1.252]) and excess burden (EB, 0.70 [.53–.88]) of new-incident cardiovascular and cerebrovascular complications. Risks decreased in a graded fashion for fully vaccinated (HR, 1.11 [1.02–1.22]) and boosted (HR, 1.10 [.92–1.32]) individuals. Conversely, risks and burdens of subsequent cardiovascular/cerebrovascular complications increased for hospitalized and severe COVID-19 cases (compared to nonhospitalized cases). Conclusions Increased risks and excess burdens of new-incident cardiovascular/cerebrovascular complications were reported among infected individuals; risks can be attenuated with vaccination and boosting. [ABSTRACT FROM AUTHOR]

Objectives: Black older adults have a higher vascular burden compared to non‐Hispanic White (NHW) older adults, which may put them at risk for a form of depression known as vascular depression (VaDep). The literature examining VaDep in Black older adults is sparse. The current study addressed this important gap by examining whether vascular burden was associated with depressive symptoms in Black older adults. Methods: Participants included 113 Black older adults from the Healthy Brain Project, a substudy of the Health, Aging, and Body Composition Study. In multiple regression analyses, clinical vascular burden (sum of vascular conditions) and white matter hyperintensity (WMH) volume predicted depressive symptoms as measured by the Center for Epidemiologic Studies Depression Scale, controlling for demographic variables. Follow‐up analyses compared the associations in the Black subsample and in 179 NHW older adults. Results: Higher total WMH volume, but not clinically‐defined vascular burden, predicted higher concurrent depressive symptoms and higher average depressive symptoms over 4 years. Similar associations were found between uncinate fasciculus (UF) WMHs and concurrent depressive symptoms and between superior longitudinal fasciculus WMHs and average depressive symptoms. The association between depressive symptoms and UF WMH was stronger in Black compared to NHW individuals. Conclusion: This research is consistent with the VaDep hypothesis and extends it to Black older adults, a group that has historically been underrepresented in the literature. Results highlight WMH in the UF as particularly relevant to depressive symptoms in Black older adults and suggest this group may be particularly vulnerable to the negative effects of WMH. Key points: Total, uncinate fasciculus (UF), and superior longitudinal fasciculus white matter hyperintensities were associated with higher depressive symptoms in Black older adults, but clinically‐defined vascular burden was not.The relationship between UF white matter hyperintensity burden and depressive symptoms was stronger in Black than in White individuals.Findings are consistent with the VaDep framework and extend it to an older Black sample. [ABSTRACT FROM AUTHOR]

Background: Cumulative burden from vascular risk factors (VRFs) has been associated with an increased risk of depressive symptoms in mid- and later life. It has been hypothesised that this association arises because VRFs disconnect fronto-subcortical white matter tracts involved in mood regulation, which puts older adults at higher risk of developing depressive symptoms. However, evidence for the hypothesis that disconnection of white matter tracts underlies the association between VRF burden and depressive symptoms from longitudinal studies is scarce. Methods: This preregistered study analysed longitudinal data from 6,964 middle-aged and older adults from the UK Biobank who participated in consecutive assessments of VRFs, brain imaging, and depressive symptoms. Using mediation modelling, we directly tested to what extend white matter microstructure mediates the longitudinal association between VRF burden and depressive symptoms. Results: VRF burden showed a small association with depressive symptoms at follow-up. However, there was no evidence that fractional anisotropy (FA) of white matter tracts mediated this association. Additional analyses also yielded no mediating effects using alternative operationalisations of VRF burden, mean diffusivity (MD) of single tracts, or overall average of tract-based white matter microstructure (global FA, global MD, white matter hyperintensity volume). Conclusions: Our results lend no support to the hypothesis that disconnection of white matter tracts underlies the association between VRF burden and depressive symptoms, while highlighting the relevance of using longitudinal data to directly test pathways linking vascular and mental health. [ABSTRACT FROM AUTHOR]

Sneddon's syndrome is a rare condition characterized by the presence of neurocutaneous lesions, including reticular livedo and an increase in thrombotic risk, and it is associated with a greater risk of cerebrovascular disease. It is diagnosed through a skin biopsy and neurological manifestations. In this study, we present a clinical report of a 39-year-old nurse exposed to shift and night work in an intensive care unit. She was diagnosed with Sneddon's syndrome, whose workplace had to be readapted, considering the complications and restrictions of her condition and aiming her protection and healthcare promotion. Night work can exacerbate cerebral and cardiovascular events due to its impact on metabolism, blood pressure profile, and hormone concentrations. Therefore, given a syndrome characterized by an increased thrombotic risk associated with cerebrovascular events, the restriction of night work is imperative. The occupational physician is responsible for intervening in the workplace and preventing long-term consequences for employees. [ABSTRACT FROM AUTHOR]

Although studies have indicated that physical activity (PA) is related to cardiovascular disease, the specific association between PA and incident cerebrovascular disease (CBVD) remains uncertain. The current study aimed to investigate the associations between PA levels and the CBVD incidence or all-cause mortality. Prospective cohort study. Older participants (aged >60 years) from the UK Biobank. The baseline PA was classified as total, light, moderate, and vigorous PA based on the metabolic equivalent–minutes per week (MET-min/wk) and considered as exposures, whereas CBVD incidence and all-cause mortality were considered as the outcomes. Cox proportional hazards were used to calculate the hazard ratios (HRs) and 95% CIs for the influence of the association between PA and CBVD incidence and all-cause mortality. A total of 146,742 participants aged 60 years and older were included. During a median follow-up period of 13.5 years (interquartile range of 12.8-14.2), 9338 older individuals developed CBVD and 3033 death were recorded (including 767 CBVD-related deaths). High volumes of PA were consistently associated with lower risks of CBVD and all-cause mortality. The lowest risk of CBVD incidence was observed at 2001-2500 MET-min/wk of total PA (HR 0.61, 95% CI 0.53-0.70), and the lowest risk of all-cause mortality was observed at 2501-5000 MET-min/wk (HR 0.52, 95% CI 0.43-0.63) in older adults. Total PA at 2001-2500 MET-min/wk significantly reduced the CBVD incidence in older women (HR 0.57, 95% CI 0.46-0.71), which was more pronounced than that in older men (HR for 2001-2500 MET-min/wk: 0.64, 95% CI 0.50-0.77). Total PA at 2001-2500 MET-min/wk significantly reduced the risk of incident CBVD and all-cause mortality in adults aged >60 years, although the extents of risk reduction vary in men and women. [ABSTRACT FROM AUTHOR]

Frailty is commonly observed in stroke patients and it is associated with adverse outcomes. However, there remains a gap in longitudinal studies investigating the causal relationship between baseline frailty and short-term prognosis in discharged adult stroke patients. To examine the causal impact of frailty on non-elective readmission and major adverse cardiac and cerebral events, and investigate its associations with cognitive impairment and post-stroke disability. A multicenter prospective cohort study. Two tertiary hospitals in Central and Northwest China. 667 adult stroke patients in stroke units were included from January 2022 to June 2022. Baseline frailty was assessed by the Frailty Scale. Custom-designed questions were utilized to assess non-elective readmission and major adverse cardiac and cerebral events as primary outcomes. Cognitive impairment, assessed using the Mini-Mental State Examination Scale (MMSE), and post-stroke disability, measured with the Modified Rankin Scale (mRS), were considered secondary outcomes at a 3-month follow-up. The impact of baseline frailty on non-elective readmission and major adverse cardiac and cerebral events was examined using bivariate and multiple Cox regression analyses. Furthermore, associations between baseline frailty and cognitive impairment, or post-stroke disability, were investigated through generalized linear models. A total of 5 participants died, 12 had major adverse cardiac and cerebral events, and 57 had non-selective readmission among 667 adult stroke patients. Frailty was an independent risk factor for non-selective readmission (hazard ratio [HR]: 2.71, 95 % confidence interval [CI]: 1.59, 4.62) and major adverse cardiac and cerebral events (HR: 3.77, 95 % CI: 1.07, 13.22) for stroke patients. Baseline frailty was correlated with cognitive impairment (regression coefficient [β]: − 2.68, 95 % CI: − 3.78, − 1.58) adjusting for socio-demographic and clinical factors and follow-up interval. However, the relationship between frailty and cognitive impairment did not reach statistical significance when further adjusting for baseline MMSE (β: − 0.39, 95 % CI: − 1.43, 0.64). Moreover, baseline frailty was associated with post-stroke disability (β: 0.36, 95 % CI: 0.08, 0.65) adjusting for socio-demographic and clinical variables, follow-up interval, and baseline mRS. The finding highlights the importance of assessing baseline frailty in discharged adult stroke patients, as it is significantly associated with non-elective readmission, major adverse cardiac and cerebral events, and post-stroke disability at 3 months. These results highlight the crucial role of screening and evaluating frailty status in improving short-term prognosis for adult stroke patients. Interventions should be developed to address baseline frailty and mitigate the short-term prognosis of stroke. Baseline frailty predicts non-elective readmission, major adverse cardiac and cerebral events, and post-stroke disability in adult stroke patients. @haiyanhexyyy [ABSTRACT FROM AUTHOR]

Triple-negative breast cancer (TNBC) is more aggressive as compared to other subtypes of breast cancer with characteristic metastatic patterns and a poor prognosis. The standard of care for early-stage TNBC is historically anthracycline and taxane-based chemotherapy (ATAX). Despite the effectiveness of this regimen, anthracyclines carry a small but important risk of cardiotoxicity, which is specifically a concern in the older population. This study evaluates major adverse cardiovascular events (MACE) in older women with TNBC treated with ATAX compared to taxane-based chemotherapy (TAX). Using the Surveillance, Epidemiology, and End Results (SEER)-Medicare database, we identified women aged 66 and older with TNBC diagnosed between 2010 and 2015 (N = 2215). We compared patient and clinical characteristics according to adjuvant chemotherapy regimen (chemotherapy versus no chemotherapy and ATAX versus TAX). Logistic regression was performed to estimate the odds ratios (OR) and 95% confidence intervals (CIs), Kaplan-Meier survival curves were generated to estimate three-year overall survival (OS) and cancer specific survival (CSS). Cox proportional hazards models were used to analyze OS and CSS while controlling for patient and tumor characteristics. MACE was defined as acute myocardial infarction, heart failure, potentially fatal arrhythmia, and cerebral vascular incidence. Few patients experienced a cardiac death and therefore this was excluded in the analysis. Of the 2215 patients in our cohort, most patients (n = 1334; 60.26%) received TAX compared to ATAX (n = 881; 39.78%). Patients who received ATAX were not statistically significantly more likely than those who received TAX to experience acute myocardial infarction, cerebral vascular accident (CVA), or potentially fatal arrhythmia when controlling for traditional risk factors. Among patients who experienced MACE, there was no difference in OS or CSS in patients who received TAX vs ATAX. Patients who received ATAX were less likely to develop heart failure than those who received TAX (OR 0.63, 95% CI [0.45–0.88], p < 0.01). Patients who developed MACE and who were > 76 years old had worse OS compared to those who experienced MACE and were age 66–75 years old (HR 1.67, 95% CI [1.07–2.62], p = 0.02). Among older women with TNBC, receipt of adjuvant chemotherapy with ATAX was not associated with increased risk of major adverse cardiac events. For those who experienced a cardiac event, there was no difference in survival amongst those who received TAX vs ATAX. Other factors including additional chemotherapy toxicities should be investigated as a potential etiology for the inferior OS previously observed with ATAX vs TAX in older women with node negative or 1–3 positive lymph nodes. • Older patients with TNBC are at higher risk for anthracycline-induced cardiotoxicity. • Receipt of ATAX did not increase risk of cardiac outcomes or affect survival. • Age may serve as a predictor for poorer survival once a cardiac event occurs. • Trials evaluating non-anthracycline regimens in TNBC should include age > 65. [ABSTRACT FROM AUTHOR]