High prevalence of erectile dysfunction in male patients with acute stroke was associated with age but not to modifiable cardiovascular risk factors.

Background: Erectile dysfunction (ED) and stroke share common risk factors, and symptoms of ED often precede the development of clinical cardiovascular disease (CVD). However, little is known about how ED is associated with cardiovascular (CV) risk factors in patients who had a stroke and if concomitant ED is a marker of more severe CVD. Aims: We aimed to identify the prevalence of ED and CV risk factors in patients admitted with a stroke or transient ischaemic attack (TIA). Further, we wanted to test if self-reported ED associated with presence of CV risk factors, and if patients with ED had increased stroke severity compared with patients without ED. Methods: This was a post hoc analysis of data retrieved in a cross-sectional survey from two non-comprehensive stroke units in Denmark. Multiple logistic regression adjusted for covariates was performed to investigate the association between CV risk factors and self-reported ED. Results: We included 287 male patients of which 116 (40.4%) had self-reported ED. Advanced age was significantly associated with self-reported ED (reference ≤60 years: OR 3.93, 95% CI 1.84 to 8.37 for men 71-80 years and OR 4.61, 95% CI 1.92 to 11.08 for men >80 years). Self-reported ED was not significantly associated with CV risk factors or stroke severity. Discussion: Four in 10 men with acute stroke or TIA reported to have ED prior to their stroke, and this was associated with age rather than CV risk factors. Hence, self-reported ED was not restricted to the CVD load, nor was ED a risk marker for increased stroke severity. However, our population was of high age with well-established CVD, and the presence of ED may be a stroke risk marker in younger patients who had a stroke. Based on the prevalence, potential treatment of ED should be addressed in stroke recovery.

Cardioembolic stroke in an HIV endemic region: underdiagnosed and severe.

Background and objectives: Cardioembolic stroke (CES) appears to be a rare cause of stroke (4%-9%) in people living with HIV (PLWH) in sub-Saharan Africa (SSA). However, due to limited access to diagnostic resources, this may be an underestimate. It is also unclear which cardiac pathologies are the major contributors to CES in this region. We sought to determine the prevalence and aetiology of CES in PLWH and to determine whether there are any differences compared with HIV negative stroke patients. Methods: This cross-sectional study recruited PLWH with new-onset stroke at a quaternary-level hospital in Johannesburg, South Africa, from 2014 to 2017, and compared them to age-matched and sex-matched HIV negative stroke patients. Comprehensive investigations were performed to determine the underlying stroke aetiology, including electrocardiography, echocardiography, CT angiography and cerebrospinal fluid examination. Results: 85 PLWH with ischaemic stroke were recruited and compared with 109 HIV negative controls. CES was identified in 17/85 (20.0%) of PLWH. These patients had more severe strokes than PLWH with non-CES (National Institutes of Health Stroke Scale score 14.9±6.7 vs 11.7±5.4, p=0.04). Cardiomyopathy was the predominant cardiac pathology in PLWH (76.4% vs 45.5% in HIV negative, p=0.04) while valvulopathy was more common in HIV negative patients (42.4% vs 11.8% in PLWH, p=0.03). Arrhythmia (n=1) and ischaemic heart disease (n=1) were uncommon in PLWH. Conclusion: CES is underdiagnosed in SSA and is more severe than non-CES. The identification of cardiomyopathy as the predominant underlying cardiac pathology may assist to target resources towards its detection using accessible cost-effective biomarkers.

The Burden of Inpatient Hospitalizations with Cardiac and Cerebrovascular Diseases in Patients with Type 1 Diabetes: Insights from the National Inpatient Sample in the US.

BACKGROUND: This study aimed to evaluate the burden and impact of cardiac and cerebrovascular disease (CCD) on hospital inpatients with type 1 diabetes mellitus (T1DM). METHODS: This is a retrospective nationwide cohort study of people with T1DM with or without CCD in the US National Inpatient Sample between 2016 and 2019. The in-hospital mortality rates, length of stay (LoS), and healthcare costs were determined. RESULTS: A total of 59,860 T1DM patients had a primary diagnosis of CCD and 1,382,934 did not. The median LoS was longer for patients with CCD compared to no CCD (4.6 vs. 3 days). Patients with T1DM and CCD had greater in-hospital mortality compared to those without CCD (4.1% vs. 1.1%, p < 0.001). The estimated total care cost for all patients with T1DM with CCD was approximately USD 326 million. The adjusted odds of mortality compared to patients with non-CCD admission was greatest for intracranial hemorrhage (OR 17.37, 95%CI 12.68-23.79), pulmonary embolism (OR 4.39, 95%CI 2.70-7.13), endocarditis (OR 3.46, 95%CI 1.22-9.84), acute myocardial infarction (OR 2.31, 95%CI 1.92-2.77), and stroke (OR 1.47, 95%CI 1.04-2.09). CONCLUSIONS: The burden of CCD in patients with T1DM is substantial and significantly associated with increased hospital mortality and high healthcare expenditures.

White matter hyperintensity shape is related to long-term progression of cerebrovascular disease in community-dwelling older adults.

White matter hyperintensity (WMH) shape is associated with long-term dementia risk in community-dwelling older adults, however, the underlying structural correlates of this association are unknown. We therefore aimed to investigate the association between baseline WMH shape and cerebrovascular disease progression over time in community-dwelling older adults. The association of WMH shape and cerebrovascular disease markers was investigated using linear and logistic regression models in the Age, Gene/Environment Susceptibility-Reykjavik (AGES) study (n = 2297; average time to follow-up: 5.2 years). A more irregular shape of periventricular/confluent WMH at baseline was associated with a larger increase in WMH volume, and with occurrence of new subcortical infarcts, new microbleeds, new enlarged perivascular spaces, and new cerebellar infarcts at the 5.2-year follow-up (all p < 0.05). Furthermore, less elongated and more irregularly shaped deep WMHs were associated with a larger increase in WMH volume, and new cortical infarcts at follow-up (p < 0.05). A less elongated shape of deep WMH was associated with new microbleeds at follow-up (p < 0.05). Our findings show that WMH shape may be indicative of the type of cerebrovascular disease marker progression. This underlines the significance of WMH shape to aid in the assessment of cerebrovascular disease progression.

Tobacco cigarette smoking induces cerebrovascular dysfunction followed by oxidative neuronal injury with the onset of cognitive impairment.

While chronic smoking triggers cardiovascular disease, controversy remains regarding its effects on the brain and cognition. We investigated the effects of long-term cigarette smoke (CS) exposure (CSE) on cerebrovascular function, neuronal injury, and cognition in a novel mouse exposure model. Longitudinal studies were performed in CS or air-exposed mice, 2 hours/day, for up to 60 weeks. Hypertension and carotid vascular endothelial dysfunction (VED) occurred by 16 weeks of CSE, followed by reduced carotid artery blood flow, with oxidative stress detected in the carotid artery, and subsequently in the brain of CS-exposed mice with generation of reactive oxygen species (ROS) and secondary protein and DNA oxidation, microglial activation and astrocytosis. Brain small vessels exhibited decreased levels of endothelial NO synthase (eNOS), enlarged perivascular spaces with blood brain barrier (BBB) leak and decreased levels of tight-junction proteins. In the brain, amyloid-ß deposition and phosphorylated-tau were detected with increases out to 60 weeks, at which time mice exhibited impaired spatial learning and memory. Thus, long-term CSE initiates a cascade of ROS generation and oxidative damage, eNOS dysfunction with cerebral hypoperfusion, as well as cerebrovascular and BBB damage with intracerebral inflammation, and neuronal degeneration, followed by the onset of impaired cognition and memory.

Neuroimaging correlates of Alzheimer's disease biomarker concentrations in a racially diverse high-risk cohort of middle-aged adults.

INTRODUCTION: In this study, we investigated biomarkers in a midlife, racially diverse, at-risk cohort to facilitate early identification and intervention. We examined neuroimaging measures, including resting state functional magnetic resonance imaging (fMRI), white matter hyperintensity vo (WMH), and hippocampal volumes, alongside cerebrospinal fluid (CSF) markers. METHODS: Our data set included 76 cognitively unimpaired, middle-aged, Black Americans (N = 29, F/M = 17/12) and Non-Hispanic White (N = 47, F/M = 27/20) individuals. We compared cerebrospinal fluid phosphorylated tau141 and amyloid beta (Aß)42 to fMRI default mode network (DMN) subnetwork connectivity, WMH volumes, and hippocampal volumes. RESULTS: Results revealed a significant race × Aß42 interaction in Black Americans: lower Aß42 was associated with reduced DMN connectivity and increased WMH volumes regions but not in non-Hispanic White individuals. DISCUSSION: Our findings suggest that precuneus DMN connectivity and temporal WMHs may be linked to Alzheimer's disease risk pathology during middle age, particularly in Black Americans. HIGHLIGHTS: Cerebrospinal fluid (CSF) amyloid beta (Aß)42 relates to precuneus functional connectivity in Black, but not White, Americans. Higher white matter hyperintensity volume relates to lower CSF Aß42 in Black Americans. Precuneus may be a hub for early Alzheimer's disease pathology changes detected by functional connectivity.

Screening for carotid atherosclerosis: development and validation of a high-precision risk scoring tool.

Objective: This study aimed to investigate the prevalence of carotid atherosclerosis (CAS), especially among seniors, and develop a precise risk assessment tool to facilitate screening and early intervention for high-risk individuals. Methods: A comprehensive approach was employed, integrating traditional epidemiological methods with advanced machine learning techniques, including support vector machines, XGBoost, decision trees, random forests, and logistic regression. Results: Among 1,515 participants, CAS prevalence reached 57.4%, concentrated within older individuals. Positive correlations were identified with age, systolic blood pressure, a history of hypertension, male gender, and total cholesterol. High-density lipoprotein (HDL) emerged as a protective factor against CAS, with total cholesterol and HDL levels proving significant predictors. Conclusions: This research illuminates the risk factors linked to CAS and introduces a validated risk scoring tool, highlighted by the logistic classifier's consistent performance during training and testing. This tool shows potential for pinpointing high-risk individuals in community health programs, streamlining screening and intervention by clinical physicians. By stressing the significance of managing cholesterol levels, especially HDL, our findings provide actionable insights for CAS prevention. Nonetheless, rigorous validation is paramount to guarantee its practicality and efficacy in real-world scenarios.

Investigating the Added Value of Beck's Depression Inventory in Atherosclerosis Prediction: Lessons from Paracelsus 10,000.

Background: Depression is the most common mental illness worldwide and generates an enormous health and economic burden. Furthermore, it is known to be associated with an elevated risk of arteriosclerotic cardiovascular diseases (ASCVD), particularly stroke. However, it is not a factor reflected in many ASCVD risk models, including SCORE2. Thus, we analysed the relationship between depression, ASCVD and SCORE2 in our cohort. Methods: We analysed 9350 subjects from the Paracelsus 10,000 cohort, who underwent both a carotid artery ultrasound and completed a Beck Depression Inventory (BDI) screening. Patients were categorised binomially based on the BDI score. Atherosclerotic carotid plaque or absence was dichotomised for logistic regression modelling. Odds ratios and adjusted relative risks were calculated using Stata. Results: Subjects with an elevated BDI (≥14) had higher odds for carotid plaques compared to subjects with normal BDI, especially after adjusting for classical risk factors included in SCORE2 (1.21; 95%CI 1.03-1.43, p = 0.023). The adjusted relative risk for plaques was also increased (1.09; 95%CI 1.01-1.18, p = 0.021). Subgroup analysis showed an increased odds of plaques with increases in depressive symptoms, particularly in women and patients ≤55 yrs. Conclusions: In our cohort, the BDI score is associated with subclinical atherosclerosis beyond classical risk factors. Thus, depression might be an independent risk factor which may improve risk stratification if considered in ASCVD risk prediction models, such as SCORE2. Furthermore, reminding clinicians to take mental health into consideration to identify individuals at increased atherosclerosis risk may provide added opportunities to address measures which can reduce the risk of ASCVD.

The Impact of Neurological Disorders on Clinical and Functional Outcomes after Shoulder Arthroplasty: A Systematic Review.

BACKGROUND: Patients with pre-existing neurologic disorders present a unique set of challenges for shoulder arthroplasty (SA) surgeons due to the presence of concomitant contractures, muscle weakness, and spasticity, which may affect outcomes and complication rates after shoulder arthroplasty. The goal of this systematic review was to evaluate the clinical and functional outcomes after SA in patients pre-existing with neurologic disorders, focusing on complication and reoperation rates. METHODS: This systematic review was performed in adherence to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines outlined by Cochrane Collaboration. A search of PubMed, the Medline Library, and EMBASE from inception until September 2023 was conducted to obtain studies reporting on outcomes after SA in patients with neurological disorders. Study demographics and information on outcomes including patient-reported outcomes and complication rates were collected. The methodological quality of included primary studies was appraised using the MINORS scoring system. RESULTS: Twenty articles published between 1997 and 2023 met inclusion criteria. In total, 13,126 patients with neurological conditions with 7 different neurological disorders (Parkinson's disease (PD), epilepsy and seizures, cerebral palsy (CP), poliomyelitis, Charcot neuropathy (CN), cerebrovascular disease (CVD) and multiple sclerosis (MS)) were included. The mean patient age was 64.3 years (range, 33.0 - 75.8 years), 51.4% of patients were male, and the mean postoperative follow-up time was 5.1 years (range, 1.4 - 9.9 years). PD was the most reported neurological disorder (9 studies, 8,033 patients), followed by epilepsy (4 studies, 3,783 patients), and MS (1 study, 1,077 patients). While these patients did experience improvements in outcomes following SA, high complication and revision rates were noted. CONCLUSIONS: Patients with neurologic disorders demonstrate improvements in pain and function after SA but have higher reported complication and revision rates when compared with patients without neurologic conditions. This systematic review offers valuable data for both the surgeon and patient regarding anticipated clinical results and possible complications from SA in patients with neurologic disorders that may aid in shared decision-making when considering SA.

Cardiovascular risk factors are associated with cognitive trajectory in the first year after stroke.

Introduction: Stroke often leads to cognitive impairment, but its progression and influencing factors over time remain poorly understood. This study evaluates immediate post-stroke cognitive impacts and investigates the influence of concurrent factors on cognitive evolution over the first year. Patients and methods: In the STRATEGIC study, 179 patients with first symptomatic ischemic stroke underwent neuropsychological assessments within three months post-stroke, and 141 were re-evaluated at 12 months. Risk factors tested for associations with cognitive outcome included demographic variables, cardiovascular and other medical factors, and lesion characteristics. Cognitive performance was primarily measured via the Montreal Cognitive Assessment (MoCA), with domain-specific assessments for episodic memory (Free and Cued Selective Reminding Task), short-term memory (Digit Span forward), and working memory (Digit Span backward). Results: At the time of stroke, participants ranged in age from 46 to 89 years (M = 70, SD = 9.5) and 36.9% were female. Ischemic heart disease predicted cognitive non-improvement between 3 and 12 months. Atrial fibrillation and carotid stenosis were linked to changes in episodic and working memory, respectively. Moreover, female sex and lower education correlated with stagnant global cognition and episodic memory. Discussion and conclusion: Our findings underscore the important influence of cardiovascular risk factors on cognitive functional recovery after stroke. Interventions targeting these risk factors may improve cognitive prognosis and affect traditional outcome measures such as recurrent vascular events. Future trials should include cognitive measures to fully capture the potential benefits of intensive risk factor intervention.

Expanding the Neurological Phenotype of Anderson-Fabry Disease: Proof of Concept for an Extrapyramidal Neurodegenerative Pattern and Comparison with Monogenic Vascular Parkinsonism.

Anderson-Fabry disease (AFD) is a genetic sphingolipidosis involving virtually the entire body. Among its manifestation, the involvement of the central and peripheral nervous system is frequent. In recent decades, it has become evident that, besides cerebrovascular damage, a pure neuronal phenotype of AFD exists in the central nervous system, which is supported by clinical, pathological, and neuroimaging data. This neurodegenerative phenotype is often clinically characterized by an extrapyramidal component similar to the one seen in prodromal Parkinson's disease (PD). We analyzed the biological, clinical pathological, and neuroimaging data supporting this phenotype recently proposed in the literature. Moreover, we compared the neurodegenerative PD phenotype of AFD with a classical monogenic vascular disease responsible for vascular parkinsonism and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). A substantial difference in the clinical and neuroimaging features of neurodegenerative and vascular parkinsonism phenotypes emerged, with AFD being potentially responsible for both forms of the extrapyramidal involvement, and CADASIL mainly associated with the vascular subtype. The available studies share some limitations regarding both patients' information and neurological and genetic investigations. Further studies are needed to clarify the potential association between AFD and extrapyramidal manifestations.

Lipoprotein (a) and cerebrovascular disease.

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.

Modified Rankin Scale Disability Status at Day 4 Poststroke is an Informative Predictor of Long-Term Day 90 Outcome.

BACKGROUND: Long-term disability after stroke is standardly assessed 3 months post-onset, using the modified Rankin Scale (mRS). The value of an early, day 4 mRS assessment for projecting the 3-month disability outcome has not been formally investigated. METHODS: In this cohort of patients with acute cerebral ischemia and intracranial hemorrhage, we analyzed day 4 and day 90 mRS assessments in the NIH Field Administration of Stroke Therapy- Magnesium (FAST-MAG) Phase 3 trial. The performance of day 4 mRS, alone and as part of multivariate models, in predicting day 90 mRS was assessed using correlation coefficients, percent agreement, and the kappa statistics. RESULTS: Among the 1573 acute cerebrovascular disease (ACVD) patients, 1206 (76.7%) had acute cerebral ischemia (ACI), while 367 (23.3%) had intracranial hemorrhage. Among all 1573 ACVD patients, day 4 mRS and day 90 mRS correlated strongly, Spearman's rho=0.79, in unadjusted analysis with weighted kappa of 0.59. For dichotomized outcomes, simple carry-forward of the day 4 mRS performed fairly well in agreeing with day 90 mRS: mRS 0-1 (kappa=0.67), 85.4%; mRS 0-2 (k=0.59), 79.5%; fatal outcome, 88% (k=0.33). Correlations of 4d and 90d mRS were stronger for ACI than ICH patients, 0.76 vs 0.71. CONCLUSIONS: In this acute cerebrovascular disease patient cohort, assessment of global disability performed on day 4 is highly informative regarding long-term, 3-month mRS disability outcome, alone, and even more strongly in combination with baseline prognostic variables. The day 4 mRS is a useful measure for imputing the final patient disability outcome in clinical trials and quality improvement programs.

Cerebrovascular Disease Detected on Preprocedural Computed Tomography in Patients With Severe Aortic Stenosis Undergoing Aortic Valve Replacement.

BACKGROUND: There is a scarcity of data on the prevalence and clinical impact of cerebrovascular disease detected on preprocedural computed tomography (CT) before aortic valve replacement (AVR) in patients with severe aortic stenosis. METHODS AND RESULTS: Among patients with severe aortic stenosis undergoing AVR, the authors compared clinical outcomes between patients with and without cerebrovascular disease detected on preprocedural CT, which was defined as chronic brain infarction or hemorrhage. The primary outcome measure in this study was a composite of all-cause death or stroke. Among 567 study patients, 200 patients (35.3%) had cerebrovascular disease on preprocedural CT. Among 200 patients with cerebrovascular disease on preprocedural CT, only 28.5% of patients had a clinical history of symptomatic stroke. The cumulative 3-year incidence of death or stroke was higher in patients with cerebrovascular disease on preprocedural CT than in those without cerebrovascular disease on preprocedural CT (40.7% versus 24.1%, log-rank P<0.001). After adjusting for confounders, the higher risk of patients with cerebrovascular disease on preprocedural CT relative to those without remained significant for death or stroke (hazard ratio [HR], 1.42 [95% CI, 1.02-1.98]; P=0.04). Among 200 patients with cerebrovascular disease on preprocedural CT, patients with prior symptomatic stroke compared with those without were not associated with higher adjusted risk for death or stroke (HR, 1.18 [95% CI, 0.72-1.94]; P=0.52). CONCLUSIONS: Among patients with severe aortic stenosis undergoing AVR, a substantial proportion had cerebrovascular disease on preprocedural CT, with a clinical history of symptomatic stroke in one-fourth of patients. Regardless of history of symptomatic stroke, patients with cerebrovascular disease on preprocedural CT had worse clinical outcomes compared with those without cerebrovascular disease on preprocedural CT.

Neuro-molecular perspectives on long COVID-19 impacted cerebrovascular diseases - a role for dipeptidyl peptidase IV.

The coronavirus disease 2019 (COVID-19) has caused immense devastation globally with many outcomes that are now extending to its long-term sequel called long COVID. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects not only lungs, but also the brain and heart in association with endothelial cell dysfunction, coagulation abnormalities, and thrombosis leading to cardio-cerebrovascular health issues. Fatigue, cognitive decline, and brain fog are common neurological symptoms in persisting long COVID. Neurodegenerative processes and SARS-CoV-2 infection manifest overlapping molecular mechanisms, such as cytokine dysregulation, inflammation, protein aggregation, mitochondrial dysfunction, and oxidative stress. Identifying the key molecules in these processes is of importance for prevention and treatment of this disease. In particular, Dipeptidyl peptidase IV (DPPIV), a multifunctional peptidase has recently drawn attention as a potential co-receptor for SARS-CoV-2 infection and cellular entry. DPPIV is a known co-receptor for some other COVID viruses including MERS-Co-V. DPPIV regulates the immune responses, obesity, glucose metabolism, diabetes, and hypertension that are associated with cerebrovascular manifestations including stroke. DPPIV likely worsens persisting COVID-19 by disrupting inflammatory signaling pathways and the neurovascular system. This review highlights the neurological, cellular and molecular processes concerning long COVID, and DPPIV as a potential key factor contributing to cerebrovascular dysfunctions following SARS-CoV-2 infection.

The joint impact of PM2.5 constituents on the risk of cerebrovascular diseases hospitalization: A large community-based cohort study.

Air pollution poses significant health risks to urban areas, with limited focus on the chronic association of PM2.5 and its constituents on cerebrovascular diseases (CERs), especially regarding the joint associations. This study explores the individual and joint associations between PM2.5 constituents and CER hospitalization risks through a cohort analysis of 36,271 adults in the Pearl River Delta, South China, from 2015 to 2020. Cox proportional hazards regression and quantile-based g-computation models were used to quantify the individual and joint associations of annual mean concentrations of PM2.5 constituents with hospitalization for CERs. 1151 participants were hospitalized due to CERs during the five-year follow-up period. Joint associations analyses identified that one quartile increase in co-exposure may result in hazard ratios of 1.530 (1.441-1.623), 1.840 (1.710-1.980), and 1.609 (1.491-1.737) for CERs, total, and ischemic stroke hospitalization, respectively. The adverse effect was primarily driven by organic matter and chlorine. Men, those with a history of tobacco or alcohol use or with low residential greenness, were more susceptible to CERs hospitalization following PM2.5 constituents co-exposure. Upcoming strategies should focus on monitoring and regulating PM2.5 constituents, encouraging healthy lifestyles, and enhancing urban greenery.

Risk of stroke development following retinal vein occlusion: A systematic review and meta-analysis.

Retinal vein occlusion (RVO) and cerebrovascular disease share common risk factors and may be independently associated; however, the strength and nature of this association remain unclear. We conducted a systematic review and meta-analysis, informed by studies from PubMed, Scopus, EMBASE, Web of Science, and Google Scholar until January 6, 2024, aimed to clarify this relationship. Eligible studies included cohorts observing stroke incidence in RVO patients for over a year. Pooled effect estimates were calculated using random-effects models, with subgroup analyses evaluating associations between RVO types (central and branch) and stroke subtypes (ischemic and hemorrhagic). Ten cohort studies with a total of 428,650 participants (86,299 RVO patients) were included. Compared to controls, RVO patients exhibited a significantly increased risk of stroke (pooled risk ratio [RR]=1.38, 95 % confidence interval (95 %CI)=1.34-1.41). Subgroup analyses indicated elevated risk for both ischemic (RR=1.37, 95 %CI=1.32-1.42) and hemorrhagic (RR=1.55, 95 %CI=1.08-2.22) strokes in RVO patients. Additionally, both central (RR=1.50, 95 %CI=1.27-1.78) and branch (RR=1.41, 95 %CI=1.32-1.50) RVO were associated with stroke risk. Sensitivity analyses confirmed consistent results across various criteria, and funnel plots indicated no publication bias. RVO significantly increases the risk of both ischemic and hemorrhagic stroke, regardless of RVO type, suggesting a strong independent association between these conditions.