抗血栓治疗是心血管疾病治疗的重要手段，临床研究显示抗血栓治疗增加脑微出血灶数量，并可能导致脑出血，临床医生可能会因此削弱原有的抗血栓治疗强度。然而，目前的专家共识或指南未明确在脑微出血情况下抗血栓方案的调整策略。该文回顾近年文献资料，认为以脑淀粉样血管病为病因的脑微出血导致的脑出血风险更高，但总体出血事件发生率仍低于缺血性卒中发生率。目前的证据尚不支持因脑微出血的存在而改变抗血栓策略，但在合并脑淀粉样血管病的高龄患者或合并高危表型的患者中，应调整抗凝方案，并动态监测脑微出血灶的变化。.

UNASSIGNED: To explore the associations between dietary zinc intake and cardiovascular diseases (CVDs), including congestive heart failure (CHF), coronary heart disease (CHD), angina, heart attack, and cerebrovascular accident (CVA), this study was performed.
UNASSIGNED: Data from the National Health and Nutrition Examination Survey (2005-2018) were used in this study. Dietary zinc intake was stratified into quartiles. Restricted cubic splines were constructed to assess nonlinear associations and identify cut-off values based on the type of nonlinearity. Binary logistic regressions were performed using the cut-offs.
UNASSIGNED: Positive associations were detected between the second, third, and fourth quantiles of dietary zinc intake and decreased risks of overall CVDs (Q2: OR = 0.83, 95 % CI = 0.72-0.96; Q3: OR = 0.83, 95 % CI = 0.71-0.96; Q4: OR = 0.79, 95 % CI = 0.67-0.93). The second, third, and fourth quantiles were significantly associated with decreased risks of various CVDs (all P < 0.05), except for CHD and angina (all P > 0.05). Restricted cubic spline regression revealed significant nonlinear trends for associations of dietary zinc intake with the risk of developing CVDs and CHF (both P for nonlinear <0.05), whereas those for heart attack and CVA were marginally significant (P for nonlinear = 0.072, and 0.075, respectively).
UNASSIGNED: This study revealed that high dietary zinc intake is associated with reduced risks of developing CVDs, CHF, heart attack, and CVA, but not CHD or angina.

BACKGROUND: Alzheimer\'s disease (AD) is characterised biologically by beta-amyloid (Aβ) plaques and tau tangles, but autopsy studies reveal that most older adults also present with cerebrovascular disease (CVD) markers. Effects of biological AD on cognition in the context of concurrent CVD remain unclear. In older adults with CVD pathology, this study sought to determine ante-mortem cognitive trajectories associated with Aβ/tau positivity or negativity (+/-) at autopsy.
METHODS: Participants aged 65-95 classified as cognitively unimpaired at baseline from the National Alzheimer\'s Coordinating Center database, with ≥1 follow-up between 2005-2015, and available autopsy/APOE data were included (N = 924). Autopsy indicated that all participants had at least one of six CVD pathology markers. Participants were classified into four groups (A-T-, A+T-, A-T+, A+T+) based on semiquantitative Consortium to Establish a Registry for Alzheimer\'s Disease neuritic plaque staging and Braak staging. Linear mixed models including group × time interactions assessed rate of change in Preclinical Alzheimer\'s Cognitive Composite scores, episodic memory, and executive function. Interactions between age, sex, APOE ε4 × time and the interval between death/the final study visit were included as covariates.
RESULTS: A+T+ adults demonstrated significantly faster cognitive decline on all outcomes in the ∼10 years preceding death compared to A-T-, A+T-, and A-T+ adults (Table 1, Figure 1, d = 0.15 - 0.39). At final visit prior to death, a greater proportion of A+T+ adults (36%) received a dementia diagnosis compared to A-T+ (14%) or A+T- (15%) (p <.001). When analyses were restricted to exclude dementia diagnoses, significantly faster decline on all outcomes (p\'s <.001, d = 0.06 - 0.36) was similarly observed in A+T+ adults compared to A-T-, A+T- and A-T+ adults (Figure 2). Cognitive trajectories were equivalent between A-T- and A+T- for all outcomes (p\'s >.55).
CONCLUSIONS: ln older adults with CVD pathology, A+T+ at autopsy was associated with greater cognitive decline over 10 years preceding death compared to A+T-, A-T+, and A-T- older adults. Faster cognitive decline in this group in the context of low final visit dementia diagnoses may suggest that post-mortem A+T+ is associated with a steep trajectory of cognitive decline ante-mortem, but that dementia progression is not inevitable.

Traumatic brain injury (TBI) survivors face debilitating long-term psychosocial consequences, including social isolation and depression. TBI modifies neurovascular physiology and behavior but the chronic physiological implications of altered brain perfusion on social interactions are unknown. Adult C57/BL6 male mice received a moderate cortical TBI, and social behaviors were assessed at baseline, 3-, 7-, 14-, 30-, and 60-days post injury (dpi). Magnetic resonance imaging (MRI, 9.4T) using dynamic susceptibility contrast perfusion weighted MRI were acquired. At 60dpi mice underwent histological angioarchitectural mapping. Analysis utilized standardized protocols followed by cross-correlation metrics. Social behavior deficits at 60dpi emerged as reduced interactions with a familiar cage-mate (partner) that mirrored significant reductions in cerebral blood flow (CBF) at 60dpi. CBF perturbations were dynamic temporally and across brain regions including regions known to regulate social behavior such as hippocampus, hypothalamus, and rhinal cortex. Social isolation in TBI-mice emerged with a significant decline in preference to spend time with a cage mate. Cortical vascular density was also reduced corroborating the decline in brain perfusion and social interactions. Thus, the late emergence of social interaction deficits mirrored the reduced vascular density and CBF in regions known to be involved in social behaviors. Vascular morphology and function improved prior to the late decrements in social function and our correlations strongly implicate a linkage between vascular density, cerebral perfusion, and social interactions. Our study provides a clinically relevant timeline of alterations in social deficits alongside functional vascular recovery that can guide future therapeutics.

Cardiovascular and cerebrovascular disease (CCVD) is a complex disease with a long latency period, and the most effective diagnosis and treatment methods are risk assessment and preventive interventions before onset. According to traditional Chinese medicine (TCM), Zhu-Ye-Qing wine (ZYQW) has the effect of invigorating blood and removing blood stasis. However, whether ZYQW can improve the progression of CCVD has not been reported. This study aims to explore the possible mechanism of ZYQW on CCVD through network pharmacology, and finally 249 potential targets of ZYQW and 2080 potential targets of CCVD are obtained. The key targets mainly include MAPK3, TP53, RELA, MAPK1 and AKT1. The main KEGG pathways include TNF signaling pathway, lipid and atherosclerosis pathway signaling pathway. The components in ZYQW are identified by ultra-performance liquid chromatography-mass spectrometry (UHPLC-CQE-CQE-MS/MS). Through network pharmacology, molecular docking and molecular dynamics simulation, the potential key components and prevention mechanisms of ZYQW in the prevention of CCVD are determined. ZYQW may be an effective and safe health food for the prevention of CCVD, providing guidance and basis for the further development of medicinal foods.

The role of lipoprotein (a) [Lp(a)] in cerebrovascular disease is a topic of importance. In this narrative review, pertinent studies have been leveraged to comprehensively examine this relationship from diverse perspectives.Lp(a) shares structural traits with low-density lipoprotein cholesterol. Lp(a) is synthesized by hepatocytes, and its plasma levels are genetically determined by the LPA gene, which produces apolipoprotein (a).Numerous epidemiological studies have confirmed the positive correlation between elevated serum Lp(a) levels and the occurrence or recurrence of cerebrovascular events, especially ischemic strokes, in adults. It should be noted that the correlation strength varies among studies and is marginal in Mendelian randomization studies.Regarding pediatric patients, screening is currently limited to those with a relevant medical history. Lp(a) seems to play a significant role in the pathogenesis of arterial ischemic stroke in children because environmental thrombotic and atherogenic factors are generally not present.Phase 3 trials of novel Lp(a) targeting agents, such as pelacarsen and olpasiran, are anticipated to demonstrate their efficacy in reducing the incidence of stroke. Given the richness of the literature, new guidelines regarding Lp(a) screening and management in targeted populations are warranted to provide more effective primary and secondary prevention.

Renin-angiotensin system (RAS) modulators, including Angiotensin receptor blockers (ARB) and angiotensin-converting enzyme inhibitors (ACEI), are effective medications for controlling blood pressure. Cognitive deficits, including lack of concentration, memory loss, and confusion, were reported after COVID-19 infection. ARBs or ACEI increase the expression of angiotensin-converting enzyme-2 (ACE-2), a functional receptor that allows binding of SARS-CoV-2 spike protein for cellular invasion. To date, the association between the use of RAS modulators and the severity of COVID-19 cognitive dysfunction is still controversial.
OBJECTIVE: This study addressed the following questions: 1) Does prior treatment with RAS modulator worsen COVID-19-induced cerebrovascular and cognitive dysfunction? 2) Can post-treatment with RAS modulator improve cognitive performance and cerebrovascular function following COVID-19? We hypothesize that pre-treatment exacerbates COVID-19-induced detrimental effects while post-treatment displays protective effects.
METHODS: Clinical study: Patients diagnosed with COVID-19 between May 2020 and December 2022 were identified through the electronic medical record system. Inclusion criteria comprised a documented medical history of hypertension treated with at least one antihypertensive medication. Subsequently, patients were categorized into two groups: those who had been prescribed ACEIs or ARBs before admission and those who had not received such treatment before admission. Each patient was evaluated on admission for signs of neurologic dysfunction. Pre-clinical study: Humanized ACE-2 transgenic knock-in mice received the SARS-CoV-2 spike protein via jugular vein injection for 2 weeks. One group had received Losartan (10 mg/kg), an ARB, in their drinking water for two weeks before the injection, while the other group began Losartan treatment after the spike protein injection. Cognitive functions, cerebral blood flow, and cerebrovascular density were determined in all experimental groups. Moreover, vascular inflammation and cell death were assessed.
RESULTS: Signs of neurological dysfunction were observed in 97 out of 177 patients (51%) taking ACEIs/ARBs prior to admission, compared to 32 out of 118 patients (27%) not receiving ACEI or ARBs. In animal studies, spike protein injection increased vascular inflammation, increased endothelial cell apoptosis, and reduced cerebrovascular density. In parallel, spike protein decreased cerebral blood flow and cognitive function. Our results showed that pretreatment with Losartan exacerbated these effects. However, post-treatment with Losartan prevented spike protein-induced vascular and neurological dysfunctions.
CONCLUSIONS: Our clinical data showed that the use of RAS modulators before encountering COVID-19 can initially exacerbate vascular and neurological dysfunctions. Similar findings were demonstrated in the in-vivo experiments; however, the protective effects of targeting the RAS become apparent in the animal model when the treatment is initiated after spike protein injection.

The disparity between the sexes in stroke mortality has been demonstrated in people from different locations. The objective of this study was to analyze the disparity between sexes in stroke mortality in adults in the metropolitan area of Greater Vitoria between 2000 and 2021. Ecological time series design was conducted with a database of the Brazilian Health System Informatics Department. The annual percentage change and average annual percentage change were calculated through joinpoint regression. Pairwise comparisons using parallelism and coincidence tests were applied to compare temporal trends between men and women. Men had higher mortality rates in most years between 2000 and 2021. In contrast, women had higher proportional mortality values in all years evaluated from 2000 to 2021. The paired comparison revealed a disparity between the sexes in the proportional mortality time series (parallelism test: p = 0.003; coincidence test: p < 0.001). However, the time series of the mortality rates showed no disparity between the sexes (parallelism test: p = 0.114; coincidence test: p = 0.093). From 2000 to 2021, there was a disparity in proportional mortality from stroke between the sexes of the population in the metropolitan area of Greater Vitoria, Brazil. However, the time series of mortality rates between the sexes did not reveal any disparity in the study period.

UNASSIGNED: Previous studies have suggested that triglyceride glucose-body mass index (TyG-BMI) is associated with cardiovascular mortality in patients undergoing peritoneal dialysis. However, the predictive value of TyG-BMI in the prognosis of acute myocardial infarction (AMI) remains unclear.
UNASSIGNED: In total, 408 AMI patients who underwent PCI were consecutively included in this study. All included patients were then divided into three groups according to tertiles of TyG-BMI. The association between TyG-BMI and major adverse cardiovascular and cerebrovascular events (MACCEs) were investigated.
UNASSIGNED: Participants were divided into three groups: tertile 1(≤199.4, n=136), tertile 2 (199.4-231.8, n=136), and tertile 3 (≥231.8, n=136). Eighty (19.6%) patients had MACCEs: 18 (13.2%) in tertile 1, 26 (19.1%) in tertile 2, and 36 (25.7%) in tertile 3. The incidence of MACCEs increased as the tertiles of TyG-BMI increased (p<0.05). Multivariate Cox regression analysis revealed that diabetes mellitus and TyG-BMI were independent predictors of MACCEs in AMI patients after PCI (p<0.05). The receiver operating characteristic (ROC) curve showed that when TyG-BMI was ≥192.4, the sensitivity and specificity were 60.1% and 65.4%, respectively, and the area under the ROC curve (AUC) was 0.632 (95% confidence interval [CI]: 0.562-0.703; p < 0.001).
UNASSIGNED: Elevated TyG-BMI level was an independent predictor of the composite MACCEs in patients with AMI after PCI.

Chemokine like factor 1 (CKLF1) is a novel atypical chemokine, playing a crucial role in cardiovascular and cerebrovascular diseases (CCVDs) demonstrated by a growing body of works. In cardiovascular diseases including atherosclerosis and myocardial infarction, meanwhile in cerebrovascular diseases such as ischemic stroke and hemorrhagic stroke, the expression levels of CKLF1 change markedly, which triggers downstream signaling pathways by binding with its functional receptors, and then exerts multiple effects to participate in the occurrence and development of these CCVDs. The functional roles of CKLF1 are dynamic and CKLF1 may act as a double-edged sword. The CCVDs-promoting role is related to recruiting inflammatory cells, enhancing the proliferation of vascular smooth muscle cells and endothelial cells, while the CCVDs-suppressing role may correlate with migration of nerve cells and promotion of hematopoietic stem cell proliferation which contributes to disease recovery. Based on this, the paper intends to review expression shifts, potential roles, and molecular mechanisms of CKLF1 in CCVDs, and the current status of CKLF1 targeted therapeutic strategies is also included. We hope this review may provide a valuable reference for using CKLF1 as a diagnostic and prognostic biomarker for CCVDs or developing novel treatments.