Brain-heart comorbidity diseases refer to the coexistence of pathological damage affecting the brain and the heart, characterized by high incidence, disability, and mortality rates. There is a significant comorbidity between cerebral and cardiovascular diseases, with approximately 37% of stroke patients concurrently suffering from ischemic heart disease, while cardiovascular diseases similarly increase the risk of cerebrovascular events. Patients with brain-heart comorbidity often experience motor dysfunction and autonomic nervous system dysregulation, predisposing them to secondary cardiopulmonary decline and ​further complicating rehabilitation. Cardiac rehabilitation (CR) improves cardiopulmonary fitness, exercise tolerance, and quality of life through comprehensive interventions including exercise training combined with psychological support. However, its application in brain-heart comorbidity diseases still face several challenges, including assessment methods, insufficient personalization of protocols, and poor patient adherence. This article reviews the epidemiology and pathological mechanisms of brain-heart comorbidity diseases, as well as advances in rehabilitation effectiveness based on multidimensional assessments and personalized interventions. Future research priorities include exploring innovative models such as telerehabilitation platforms and stratified management to optimize rehabilitation efficacy and enhance patient engagement.

To explore the impact of the total atherosclerosis burden of baroreceptor-resident arteries (TAB-BRA) on atrial fibrillation newly detected after stroke (AFDAS).

In this prospective cohort study, consecutive acute ischemic stroke (AIS) patients within 7 days of symptom onset who had no prior history of heart disease were recruited. We calculated TAB-BRA by scoring and summing the atherosclerosis severity across 10 segments of the carotid sinuses and aortic arch using one-step computed tomography angiography. Asymptomatic coronary artery stenosis (ACAS) ≥50% was also assessed. All participants underwent electrocardiogram and mobile electrocardiogram monitoring during the first week of hospitalization to detect AFDAS. Twenty-four-hour Holter monitoring was performed to obtain heart rate variability (HRV) parameters reflecting cardiac autonomic nervous system activity. Patients were divided into low-TAB-BRA (<5 points) and high-TAB-BRA (≥5 points) groups based on the median TAB-BRA score. Group differences in AFDAS incidence were analyzed. Multivariate logistic regression was used to determine independent associations of TAB-BRA and ACAS ≥50% with AFDAS. HRV parameters were compared between AFDAS and non-AFDAS groups, and multivariate linear regression assessed the relationship between AFDAS and the low-frequency/high-frequency (LF/HF) ratio.

Among 228 eligible AIS patients [mean age (59±12) years, median TAB-BRA score 5], 21 (9.2%) developed AFDAS. The high-TAB-BRA group had a significantly higher incidence of AFDAS than those in the low-TAB-BRA group (13.8% vs 4.5%, P<0.001). After adjusting for stroke severity, infarct volume, insular involvement, and ACAS ≥50%, TAB-BRA remained independently associated with AFDAS (OR=4.35, 95%CI: 1.58-10.47, P=0.008), whereas ACAS ≥50% showed no significant correlation (OR=0.24, 95%CI: 0.17-21.13, P=0.09). The AFDAS group exhibited a higher LF/HF ratio (median 2.4 vs 1.8, P=0.024), indicating sympathetic dominance. Multivariate analysis confirmed that AFDAS was associated with an elevated LF/HF ratio (β=1.41, 95%CI: 1.04-3.53, P=0.037), which correlated with TAB-BRA (r=0.197, P=0.012).

In AIS patients without pre-existing heart disease, AFDAS is independently linked to TAB-BRA, but not to ACAS ≥50%. Both AFDAS and TAB-BRA are associated with autonomic imbalance, potentially mediated by sympathetic-parasympathetic dysregulation in high-TAB-BRA patients.

To investigate the prevalence and distribution characteristics of extracranial and intracranial atherosclerotic disease in high- risk patients with coronary heart disease (CHD).

Patients diagnosed with CHD by coronary angiography from March 2019 to February 2024 were retrospectively enrolled. Concurrent carotid ultrasonography and transcranial Doppler/color-coded sonography were performed. CHD was defined as ≥50% luminal stenosis in at least one major epicardial artery. Extracranial atherosclerotic disease (ECAD) was defined as ≥50% stenosis in any cervical artery on ultrasound, and intracranial atherosclerotic disease (ICAD) was defined as moderate-to-severe stenosis or occlusion in any major cerebral artery. CHD patients were stratified into non-high-risk (<3 risk factors, n=342) and high-risk groups (≥3 risk factors, n=720) based on the number of atherosclerotic risk factors. The prevalence and topographic patterns of multi-territorial atherosclerotic lesions were compared between the groups.

Among 1,062 CHD patients, the high-risk group had significantly higher prevalence rates of concurrent ECAD (31.9% vs 18.1%) and ICAD (26.3% vs 16.4%) (all P<0.001). High-risk patients showed a greater propensity for multi-vessel involvement across intracranial and extracranial territories, with the vertebral artery identified as the most commonly affected site.

High-risk CHD patients exhibit higher prevalence of coexisting ECAD and ICAD and more extensive multi-territorial atherosclerosis, particularly in posterior circulation. Targeted control of modifiable risk factors is warranted to mitigate long-term cerebrocardiovascular risks.

To analyze and compare the risk factors and spatial distribution of white matter lesions (WMLs) in patients with cerebral small vessel disease (CSVD) from Beijing and Xizang.

CSVD patients hospitalized at Peking University Third Hospital and Xizang Autonomous Region People's Hospital between January 2020 and December 2022 were prospectively recruited. Clinical and cranial magnetic resonance imaging (MRI) data were collected for all patients. The Fazekas scale and the age-related white matter changes (ARWMC) scale were used to evaluate the severity and spatial distribution of WMLs, respectively. Independent samples t-tests and χ² tests were used to compare baseline clinical characteristics between patients from Beijing and Xizang. Within each region, ANOVA and χ² tests compared characteristics across WML severity subgroups. For the Xizang cohort, multivariate logistic regression identified independent risk factors for WML severity (dependent variable), adjusting for female sex, age ≥70 years, hypertension, coronary heart disease, diabetes, hyperlipidemia, smoking, and alcohol consumption.

The study included 351 CSVD patients: Beijing (n=195; mean age 66.5±11.4 years; WML severity: mild=65, moderate=78, severe=52) and Xizang (n=156; mean age 63.9±11.8 years; WML severity: no/mild=53, moderate=65, severe=38). Compared to Beijing, Xizang had a significantly higher prevalence of WMLs (87.1% [136/156] vs 79.0% [154/195]; χ²=4.064, P=0.044). While WML severity grade distribution did not differ regionally regionally (P>0.05)，WML burden measured by ARWMC score was significantly higher in Xizang than in Beijing (median [IQR]: 10 [1, 16] vs 6 [1, 11]; Z=-2.226, P=0.019). Logistic regression identified age (OR=2.910, P=0.004) and hypertension (OR=3.881, P<0.001) as independent risk factors for WML severity in Xizang. WMLs in Xizang were predominantly located in the frontal subcortical and basal ganglia regions (64.7%).

Risk factors, severity, and spatial distribution of WMLs differ between CSVD patients in Xizang and Beijing. Age and hypertension are independent risk factors for WML severity in Xizang, suggesting the critical role of strict hypertension control in CSVD prevention strategies for this population.

To investigate the correlations between gait impairment, cognitive impairment, and neuroimaging features in patients with cerebral small vessel disease (CSVD).

A total of 140 patients diagnosed with CSVD by neuroimaging examinations at the Department of Neurology, the Third Hospital of Hebei Medical University from April to November 2023 were retrospectively and consecutively enrolled. CSVD burden was quantified using established imaging markers (white matter hyperintensity, lacunes, cerebral microbleeds, enlarged perivascular spaces) and summed into a total score (range: 0-4). Participants were stratified by burden severity: mild (0-1, n=61) and severe (2-4, n=79). Based on the montreal cognitive assessment (MoCA) score, patients were divided into the cognitive-impaired group (0-25 points, n=105) and the cognitive-impaired group (26-30 points, n=35). Univariate analysis (t-test and χ² test) was used to compare differences in clinical and imaging data between different groups. Multiple linear regression analysis was applied to investigate the associations between CSVD total burden and gait/cognitive impairment. Multivariate logistic regression was used to identify independent influencing factors for cognitive impairment. Receiver operating characteristic (ROC) curve analysis was employed to evaluate diagnostic performance of key predictors.

Compared to the mild-burden patients the severe-burden patients exhibited significantly slower gait speed [(0.34±0.12) m/s vs (0.47±0.11) m/s, t=6.166, P<0.001], reduced stride length [(0.39±0.13) m vs (0.45±0.10) m, t=3.054, P=0.003], lower Tinetti performance-oriented mobility assessment (POMA) score [(20.90±4.42) vs (23.95±2.44), t=4.849, P<0.001], and worse MoCA score [(20.46±5.07) vs (24.43±4.04), t=5.013, P<0.001]. Conversely, they had significantly wider stride width [(0.16±0.06) m vs (0.13±0.06) m, t=-2.950, P=0.004] longer and timed up and go (TUG) test time [(17.84±9.10) s vs (12.69±4.06) s, t=-4.115, P<0.001]. Multiple linear regression analysis showed that after adjusting for age, activities of daily living (ADL) score, and hypertension, CSVD total burden was negatively correlated with gait speed, stride length, Tinetti POMA score, and MoCA score, and positively correlated with stride width and TUG time (all P<0.05). Compared with the cognitively normal group, the cognitive impairment group had significantly higher age [(67.00±8.83) years vs (63.34±8.38) years, t=-2.149, P=0.033], homocysteine levels [(18.02±10.52) μmol/L vs (14.13±6.45) μmol/L, t=-2.017, P=0.046], proportions of moderate-to-severe white matter hyperintensity (67.6% vs 28.6%, χ²=16.415, P<0.001), proportions of cerebral microbleeds (44.8% vs 14.3%, χ²=10.443, P=0.001), and CSVD total burden score [(2.21±1.17) vs (1.23±1.09), t=4.382, P<0.001]. They also had significantly lower gait speed [(0.37±0.13) m/s vs (0.48±0.10) m/s, t=4.627, P<0.001]. Multivariate logistic regression analysis showed that after adjusting for confounding factors such as age and homocysteine levels, severe CSVD total burden (OR=1.714, 95%CI: 1.074-2.736, P<0.05) and decreased gait speed (OR=0.954, 95%CI: 0.914-0.995, P<0.05) remained significantly associated with cognitive impairment. ROC curve analysis showed that the combination of CSVD total burden and gait speed had the highest predictive efficacy for cognitive impairment in CSVD patients, with an area under the curve (AUC) of 0.779 (95%CI: 0.695-0.863).

Severe CSVD burden leads to gait and cognitive impairment in CSVD patients, increasing fall risk. Integrating neuroimaging burden quantification with gait speed assessment provides a clinically viable strategy for early identification of cognitive impairment in CSVD patients.

To investigate the incidence and clinical significance of pulmonary arteriovenous communications PACs undetectable by CT pulmonary angiography (CTPA).

This retrospective study included patients undergoing contrast transthoracic echocardiography (cTTE) at Xuanwu Hospital, Capital Medical University from August 2023 to February 2025. Patients with confirmed extracardiac right-to-left shunt (RLS) by contrast transesophageal echocardiography (cTEE) were selected and underwent CTPA to identify pulmonary arteriovenous malformations (PAVM). Participants were divided into PAVM and non-PAVM groups based on imaging findings. Baseline characteristics, cTTE/cTEE features, accompanying symptoms, and cerebrovascular events were compared between groups. 

Among 362 patients with RLS detected by cTTE, 21 showed cTEE-confirmed extracardiac RLS. CTPA revealed visible PAVMs in 4 cases (19.0%) and microscopic pulmonary arteriovenous shunts in 17 cases (81.0%). All PAVM group patients exhibited grade 3 RLS on both cTTE/cTEE with complete left atrial filling on cTTE. In the non-PAVM group, 88.2% showed grade 3 RLS and 23.5% demonstrated complete left atrial filling. The PAVM group included 3 cases of ischemic stroke/transient ischemic attack (TIA) and 1 asymptomatic cerebral infarction. The non-PAVM group had 3 (17.6%) stroke/TIA cases and 12 (70.6%) asymptomatic cerebral infarctions.

Most extracardiac RLSs manifest as microscopic PACs rather than CTPA-visible PAVMs. Despite their subradiographic nature, these shunts are associated with substantial intracranial ischemic risk, necessitating heightened clinical vigilance and alternative diagnostic strategies.

 To investigate the associations between serum levels of macrophage migration inhibitory factor (MIF), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor-A (VEGF-A) and acute cerebral infarction (ACI) complicated by cardio-cerebral syndrome (CCS). 

A total of 124 ACI patients admitted to Handan Central Hospital from May 2022 to August 2023 were retrospectively included. Based on CCS occurrence within one week of admission, they were divided into the CCS group (n=49) and non-CCS group (n=75). Additionally, 50 healthy individuals from the same hospital were included as controls. Analysis of variance (ANOVA) was used to compare clinical data and serum biomarker levels across the three groups; independent samples t-tests compared clinical data between non-CCS and CCS groups. Logistic regression identified risk factors for CCS, while receiver operating characteristic (ROC) curves evaluated the predictive value of MIF, HIF-1α, and VEGF-A for CCS. 

Among 124 ACI patients, 49 (39.52%) developed CCS. Serum levels of MIF, HIF-1α, and VEGF-A progressively increased across healthy, non-CCS, and CCS groups: MIF: (12.60±2.15) μg/L vs (47.42±7.42) μg/L vs (69.53±11.27) μg/L; HIF-1α: (38.86±6.10) ng/mL vs (312.88±43.63) ng/mL vs (608.94±93.32) ng/mL; VEGF-A: (43.37±9.08) ng/mL vs (582.24±62.20) ng/mL vs (1087.41±116.65) ng/mL (all F=675.050, 1226.840, 2446.440; P<0.001). Compared to the non-CCS group, the CCS group had higher NIHSS scores [(9.48±2.25) vs (8.57±2.14); t=2.268, P=0.025] and lower LVEF [(45.52±6.17)% vs (53.60±5.88)%; t= 7.336, P<0.001]. Elevated MIF (OR=1.637, P=0.001), HIF-1α (OR=2.112, P<0.001), and VEGF-A (OR=2.756, P<0.001) were independent risk factors for CCS, while higher LVEF was protective (OR=0.830, P<0.001). ROC analysis showed that combined detection of the three biomarkers achieved sensitivity, specificity, and AUC of 89.80%, 86.67%, and 0.901, respectively, outperforming individual markers (P<0.05). 

Serum MIF, HIF-1α, and VEGF-A are significantly elevated in ACI patients with CCS and serve as independent risk factors. Their combined detection demonstrates powerful predictive validity for identifying ACI patients at high risk of CCS.

To investigate the neuroprotective effect of vccarin on ischemic brain injury in mice.

Potential targets of vaccarin and ischemic brain injury were predicted using databases such as GeneCard, Swiss Target Prediction, Targetnet, Pharmmapper, and TTD (search date: October 30, 2024). Intersecting targets were identified and analyzed via protein-protein interaction (PPI) network construction (STRING database; visualization with Cytoscape). Functional enrichment analysis (GO and KEGG pathways) was performed using DAVID and MicrobeDB. Molecular docking (AutoDock Vina) assessed binding affinities between vaccarin and core targets (degree ≥40). In animal experiments, focal cerebral ischemia was induced in mice via distal middle cerebral artery occlusion (dMCAO). Vaccarin (10, 20, 40 mg/kg) or vehicle was administered intraperitoneally for 5 days post-surgery. Neurological function scores and rotarod tests were performed on days 1, 3, and 5 post-surgery. After drug administration on day 5, triphenyltetrazolium chloride (TTC) staining and histopathological section staining were performed to verify the effects of vaccarin on ischemic brain injury in mice.

After removing duplicates and obtaining the intersection of the targets, a total of 63 overlapping targets of vaccarin and ischemic stroke (IS) were identified. The PPI network of the intersecting targets was constructed using the Sting platform. GO and KEGG enrichment analysis indicated that vaccarin primarily regulated biological processes such as hypoxia response, inflammation, and apoptosis, and Highlighted VEGF and IL-17 signaling pathways. Molecular docking results showed that the binding energies of vaccarin with core targets (degree≥40) were strong, with binding energies all less than -7 kcal/mol. In animal experiments, vaccarin significantly reduced the mNSS neurological scores and prolonged the time spent on the rotarod in ischemic mice, with statistically significant differences (P<0.05 or P<0.01). Compared to the sham group, vaccarin intervention significantly reduced the infarct volume in mice, with statistical significance (P<0.05 or P<0.01). Pathological staining showed that vaccarin significantly alleviated the loss of neurons and improved neuronal morphology. The loss of Nissl bodies was also notably reduced.

Vaccarin confers neuroprotection in ischemic brain injury by modulating hypoxia-inflammatory-apoptosis pathways via multi-target interactions, with VEGF and IL-17 signaling as key mechanistic components.

To characterize clinical and neuroimaging manifestations in acute carbon monoxide (CO) poisoning by analyzing etiology, symptomatology, laboratory profiles, and neuroimaging features.

Clinical characteristics analysis: each patient's exposure history, neurological symptoms, and laboratory tests were carefully analyzed and compared. Imaging analysis: each patient underwent cranial MRI to evaluate the intracranial imaging features and dynamics following acute CO poisoning.

Among the 5 patients with acute CO poisoning (1 severe case, 4 mild cases), COHb levels were significantly elevated. Patients with mild poisoning manifested clinical symptoms such as dizziness, transient consciousness disturbances, and limb convulsions, while the severe case exhibited persistent consciousness disturbances. Some patients showed elevated levels of laboratory indicators, including white blood cells, alanine aminotransferase, creatine kinase, troponin, and brain natriuretic peptide. Notably the severe patient demonstraed significantly lower mini-mental state examination (MMSE) and Montreal cognitive assessment (MoCA) scores compared to the normal range, indicative of notable cognitive impairment. In terms of imaging, MRI of the severe case revealed abnormal signals (long T1 and long T2) in the bilateral cerebral peduncle and globus pallidus, and CT of the head showed low-density lesions in the bilateral globus pallidus. For the mild cases, cranial MRI displayed widespread high signals in the diffusion weighted imaging (DWI) sequence along the cortex, which gradually disappeared after treatment, likely reflecting ischemic and hypoxic changes.

Early diagnosis and prompt treatment are imperative for patients with acute CO poisoning. In severe acute cases, imaging typically shows abnormal symmetrical signals in the globus pallidus and cerebral peduncles, whereas mild cases primarily exhibit hypoxic-ischemic changes in the cerebral cortex. Timely initiation of hyperbaric oxygen therapy during the acute phase is crucial for preventing delayed encephalopathy caused by CO poisoning and improving prognosis.

To conduct an umbrella review of systematic reviews/Meta-analyses evaluating the impact of atrial fibrillation (AF) treatment strategies on cognitive function in AF patients, thereby providing evidence-based insights for clinical practice. 

PubMed, Web of Science, Ovid, SinoMed, CNKI, Wanfang, and VIP databases (from inception to March 22, 2025) were systematically searched to identify systematic reviews/Meta-analyses assessing the effects of AF treatment strategies on cognitive function. Two researchers independently screened studies, extracted data, and evaluated methodological quality, risk of bias, reporting compliance, and evidence certainty using AMSTAR 2, ROBIS, PRISMA, and GRADE tools.

A total of 24 studies were included. Methodological quality was rated as high in 7 studies (29.17%), moderate in 6 (25.00%), low in 7 (29.17%), and critically low in 4 (16.67%). Risk of bias was low in 4 studies (16.67%) and high in 20 (83.33%). Reporting quality was high in 4 studies (16.67%), moderate in 18 (75.00%), and low in 2 (8.33%). Evidence certainty was moderate for 11 outcomes (21.15%), low for 23 (44.23%), and very low for 18 (34.62%). Results indicated that anticoagulation therapy (particularly direct oral anticoagulants) and catheter ablation might reduce the risk of cognitive impairment in AF patients, but conclusions on dementia subtypes (e.g., Alzheimer's disease, vascular dementia) remained inconsistent. 

AF treatment may delay cognitive decline; however, the overall quality of existing systematic reviews is limited. High-quality studies are urgently needed to validate therapeutic efficacy and explore underlying mechanisms.

Intercellular adhesion molecule-1 (ICAM-1), a member of the immunoglobulin superfamily, is widely expressed on the surfaces of vascular endothelial cells and is recognized as one of the most sensitive biomarkers in vascular pathology. Extensive studies have demonstrate a close relationship between ICAM-1 and the occurrence, progression, treatment, and prognosis of stroke. This review synthesizes recent global research on the interactions between ICAM-1 and stroke, summarizes the regulatory roles and mechanisms of ICAM-1 in disease progression, and elaborates on its potential therapeutic targets and clinical applications. The findings aim to provide new insights for stroke prevention and treatment strategies.

Over recent decades, significant advancements have been achieved in endovascular treatment techniques for intracranial aneurysms, alongside the continuous emergence of novel endovascular devices. Among these, intrasaccular flow disruptors represent a relatively new class of devices developed in recent years. These devices bears a strong resemblance to flow-diverting stents and are primarily employed for treating vascular abnormalities such as cerebral aneurysms and arteriovenous malformations (AVMs). Currently, mainstream intrasaccular flow disruptors include the Woven EndoBridge (WEB) device, the Luna Aneurysm Embolization System, the Medina Embolic Device, the Contour Neurovascular System, and the Neqstent Coil-Assisted Flow Diverter. Research on intrasaccular flow disruptors has already been extensively conducted internationally, with their safety and efficacy preliminarily established. However, domestic research in this area remains limited. This significant research gap underscores the necessity and urgency of conducting studies on intrasaccular flow disruptors within China. Therefore, this review aims to provide a comprehensive retrospective analysis and summary of existing flow disruptors and related treatment experiences, with the goal of bridging the domestic research gap in this field.

With the widespread application of antiretroviral therapy, the life expectancy of individuals infected with the human immunodeficiency virus (HIV) has significantly increased. Against this backdrop, non-communicable diseases—particularly intracerebral hemorrhage (ICH)—have emerged as a key focus of research. Current studies indicate a strong association between HIV infection and ICH, highlighting the elevated mortality risk in HIV-infected patients who develop ICH. Therefore, this review synthesizes recent advances in epidemiological trends, pathological mechanisms, risk factors, clinical phenotypes, and therapeutic strategies related to HIV-associated ICH.