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Stroke is a rare and severe complication of giant cell arteritis (GCA). Although early diagnosis and treatment initiation are essential, the mechanism of stroke is often related to vasculitis complicated by arterial stenosis and occlusion. Its recurrence is often attributed to early steroid resistance or late GCA relapse, so immunosuppressive treatment is often reinforced. However, many questions concerning the mechanisms of stroke remain elusive, and no review to date has examined the whole data set concerning GCA-related stroke. We therefore undertook this scoping review. GCA-related stroke does not necessarily display general signs and inflammatory parameters are sometimes normal, so clinicians should observe caution. Ischemic lesions often show patterns predating watershed areas and are associated with stenosis or thrombosis of the respective arteries, which are often bilateral. Lesions predominate in the siphon in the internal carotid arteries, whereas all the vertebral arteries may be involved with a predominance in the V3-V4 segments. Ultrasonography of the cervical arteries may reveal edema of the intima (halo sign), which is highly sensitive and specific of GCA, and precedes stenosis. The brain arteries are spared although very proximal arteritis may rarely occur, if the patient has microstructural anatomical variants. Temporal artery biopsy reveals the combination of mechanisms leading to slit-like stenosis, which involves granulomatous inflammation and intimal hyperplasia. The lumen is sometimes occluded by thrombi (<15%), suggesting that embolic lesions may also occur, although imaging studies have not provided strong evidence for this. Moreover, persistence of intimal hyperplasia might explain persisting arterial stenosis, which may account for delayed stroke occurring in watershed areas. Other possible mechanisms of stroke are also discussed. Overall, GCA-related stroke mainly involves hemodynamic mechanisms. Besides early diagnosis and treatment initiation, future studies could seek to establish specific preventive or curative treatments using angioplasty or targeting intimal proliferation. [ABSTRACT FROM AUTHOR]

Introduction: The World Health Organization (WHO) definition of stroke is: “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular origin”. The pathological background for stroke may either be Thrombotic or hemorrhagic disturbances of the cerebral blood circulation. Thrombotic cerebral infarction results from the atherosclerotic obstruction of large cervical and cerebral arteries, with ischemia in all or part of the territory of the occluded artery. Hyperhomocysteinemia has been emerging as an independent risk factor for atherosclerosis. Several workers opined that moderately elevated plasma Homocysteine (Hcy) concentration might be an independent risk factor for cerebrovascular disease including stroke and transient ischaemic attack. Material and Methods: The study is a hospital based observational study was conducted in the Department of General Medicine at ACSR Government Medical College, Nellore from Dec 2022 to October 2023. 31 patients with thrombotic stroke(cases) and 31 subjects without thrombotic stroke (controls) and other comorbid conditions that affect serum homocysteine were included in the study. Venous blood samples were collected in tubes containing disodium EDTA. Homocysteine assay is based on the measurement of co-substrate conversion product. Results: In the present study, the mean age ± SD of cases was 55.03±14.51. The mean age of males was 51.68±13.45 and the mean age of females was 60.33±15.11. The mean age in control group was 51.22±13.77. The mean serum homocysteine level in the present study, in cases was 25.98±11.95. The mean homocysteine level in males was 7.83±14.29. The mean in females was 23.05±5.67. The mean homocysteine level in control group was 7.19±3.51. Mean homocysteine level of cerebral ischemic stroke females was 14.86 ± 5.34. The mean homocysteine level in controls was 7.428 ± 4.091. The mean homocysteine level in controls was 12.30± 4.68. The mean cholesterol of the cases was167.67±40.68. The mean LDL in the study was 89.74±27.38. The mean HDL was 38.48±10.92. Conclusions: Serum homocysteine levels were significantly higher in those patients with stroke when compared to those without stroke. Apparently, Serum homocysteine level is an independent risk factor for thrombotic stroke. [ABSTRACT FROM AUTHOR]

Stroke is a rare and severe complication of giant cell arteritis (GCA). Although early diagnosis and treatment initiation are essential, the mechanism of stroke is often related to vasculitis complicated by arterial stenosis and occlusion. Its recurrence is often attributed to early steroid resistance or late GCA relapse, so immunosuppressive treatment is often reinforced. However, many questions concerning the mechanisms of stroke remain elusive, and no review to date has examined the whole data set concerning GCA-related stroke. We therefore undertook this scoping review. GCA-related stroke does not necessarily display general signs and inflammatory parameters are sometimes normal, so clinicians should observe caution. Ischemic lesions often show patterns predating watershed areas and are associated with stenosis or thrombosis of the respective arteries, which are often bilateral. Lesions predominate in the siphon in the internal carotid arteries, whereas all the vertebral arteries may be involved with a predominance in the V3-V4 segments. Ultrasonography of the cervical arteries may reveal edema of the intima (halo sign), which is highly sensitive and specific of GCA, and precedes stenosis. The brain arteries are spared although very proximal arteritis may rarely occur, if the patient has microstructural anatomical variants. Temporal artery biopsy reveals the combination of mechanisms leading to slit-like stenosis, which involves granulomatous inflammation and intimal hyperplasia. The lumen is sometimes occluded by thrombi (

Emerging literature suggests that after a stroke, the peri-infarct region exhibits dynamic changes in excitability. In rodent stroke models, treatments that enhance excitability in the peri-infarct cerebral cortex promote motor recovery. This increase in cortical excitability and plasticity is opposed by increases in tonic GABAergic inhibition in the peri-infarct zone beginning three days after a stroke in a mouse model. Maintenance of a favorable excitatory-inhibitory balance promoting cerebrocortical excitability could potentially improve recovery. Brevetoxin-2 (PbTx-2) is a voltage-gated sodium channel (VGSC) gating modifier that increases intracellular sodium ([Na+]i), upregulates N-methyl-D-aspartate receptor (NMDAR) channel activity and engages downstream calcium (Ca2+) signaling pathways. In immature cerebrocortical neurons, PbTx-2 promoted neuronal structural plasticity by increasing neurite outgrowth, dendritogenesis and synaptogenesis. We hypothesized that PbTx-2 may promote excitability and structural remodeling in the peri-infarct region, leading to improved functional outcomes following a stroke. We tested this hypothesis using epicortical application of PbTx-2 after a photothrombotic stroke in mice. We show that PbTx-2 enhanced the dendritic arborization and synapse density of cortical layer V pyramidal neurons in the peri-infarct cortex. PbTx-2 also produced a robust improvement of motor recovery. These results suggest a novel pharmacologic approach to mimic activity-dependent recovery from stroke.

Background: sodium disorders are the most common and least understood in patients with acute brain injury due to the major role played by the central nervous system in regulating sodium and water homeostasis, which can lead to serious complications and adverse outcomes, including death. Objective: to determine the hypernatremia contribution to mortality in patients with neurological conditions in critical state. Methods: longitudinal analytical observational study on 55 patients who were admitted to the acute care units at the Arnaldo Milián Castro University Hospital, between October 2020 and May 2022, regardless of the plasma sodium value upon admission to the service, as well as during their stay in the critical care units. Univariate and bivariate statistical methods were used in data analysis. Results: the average age was 60 ± 16 years. The most relevant diagnoses were intraparenchymal hemorrhage (56.37%), head trauma, and ischemic stroke (both 30%). Plasma sodium concentrations showed significant differences (pX2= 0.000), with the highest average at 24 hours of admission (174.2 ± 133.6) and the lowest at the 5th day (102.9 ± 72.9). There was a significant correlation between plasma sodium concentrations at admission, 24h and 72h with the state at discharge. In the individual bivariate analysis by period, there was only a significant relationship after 24 hours. In this period, hypernatremia contributed 1.78 times more to mortality than in those who did not have elevated sodium (OR=1.78 with CI: 1,39-3,4). Conclusions: hypernatremia in critically ill patients with neurological conditions is associated with increased mortality. [ABSTRACT FROM AUTHOR]

Background and Purpose The influence of stroke etiology on outcomes after endovascular thrombectomy (EVT) is not well understood. We aimed to investigate whether stroke etiology subgrouped as large artery atherosclerosis (LAA) and cardiac embolism (CE) influences outcomes in large artery occlusion (LAO) treated by EVT. Methods We included EVT treated LAO stroke patients registered in the Safe Implementation of Treatment in Stroke (SITS) thrombectomy register between January 1, 2014 and September 3, 2019. Primary outcome was successful reperfusion (modified Treatment in Cerebral Infarction 2b-3). Secondary outcomes were symptomatic intracranial hemorrhage (SICH), 3-month functional independence (modified Ranking Scale 0–2) and death. Multivariable logistic regression models were used for comparisons. In addition, a meta-analysis of aggregate data from the current literature was conducted (PROSPERO, ID 167447). Results Of 7,543 patients, 1,903 (25.2%) had LAA, 3,214 (42.6%) CE, and 2,426 (32.2%) unknown, other, or multiple etiologies. LAA patients were younger (66 vs. 74, P

Background: There is no consensus on the effect of opium on stroke yet. Some studies show the negative effects of opium on ischemic strokes. Here, we attempt to compare the volume of lesions in opium addict and non-addict patients with thrombotic stroke. Methods: This case-control study was conducted on patients with thrombotic stroke at Shafa Hospital in Kerman, Iran. The diagnosis was confirmed by clinical examinations, imaging, and laboratory tests. The volume of lesions was calculated by magnetic resonance imaging (MRI), and the data were analyzed by descriptive statistics, Mann-Whitney U test, Chi-square test, and linear regression analysis. Findings: A total of 60 patients were studied, 30 of whom were opium addicts and the rest were non-addicts. The mean volume of the lesion was 46.008350 ± 7.488990 (in the addict group) and 31.023335 ± 1.441570 (in the non-addict group), indicating a significant difference between the two groups (P = 0.005). Regression analysis results showed a significant relationship between the volume of stroke with opium addiction (P = 0.017), ischemic heart diseases (IHDs) (P = 0.006), hyperlipidemia (HLP) (P = 0.016), age (P = 0.035), and smoking (P = 0.044). Conclusion: The results of this study showed a higher volume of lesion in opium-addict patients compared to that in non-addicts as an indicator of stroke severity.

Background: Zinc (Zn) is highly important for metabolism in humans and its deficiency is associated with various diseases. The present retrospective study has assessed the serum Zn level in cases of acute stroke. Methods: Study cohort included 47 patients (mean age, 73 years) with minor (N = 27), moderate (N = 13), and severe (N = 7) stroke. The National Institutes of Health Stroke Scale (NIHSS) score at admission varied from 1 to 40 (median, 3). Results: Serum Zn level ranged from 23 to 102 μg/dL (mean, 68.4 μg/dL). It inversely correlated with the NIHSS score (P = 0.0340), was associated with the stroke severity (P = 0.0133), was significantly lower in patients with thrombotic stroke (P = 0.0434), and inversely correlated with the age of patient (P = 0.0220). In those aged >74 years (N = 23), but not in younger individuals, serum Zn level inversely correlated with the NIHSS score (P = 0.0155) and was associated with the stroke severity (P = 0.0117). Conclusions: In patients with acute stroke the serum Zn level is frequently decreased. It is associated with the stroke severity, thrombotic type, and older age, and may contribute to more severe clinical course of the disease among the elderly.

Introduction: Hemichorea-hemiballism (HCHB) is an uncommon movement disorder involved unilateral extremities characterized by irregular, poorly patterned, a continual hyperkinetic involuntary movement disorder in the proximal or distal parts of the body. The acute development of HCHB depends on focal lesions on the contralateral basal ganglia and subthalamic nuclei. Various conditions such as cerebrovascular, neurodegenerative, neoplastic, immunologic, infectious, and metabolic diseases are known as secondary causes of HCHB. This paper aims to compare and discuss the HCHB in various etiologies. Case Reports: Here, we reported 5 cases of HCHB induced by non-ketotic hyperosmolar hyperglycemia (NKKH), thrombotic stroke, and toxoplasmosis cerebral. We compare the admission data, clinical course, imaging, treatment, and outcome of every case. Conclusion: Various hypotheses have been proposed to explain the pathophysiology of HCHB due to these conditions. Principally, the main management for these cases is to determine the etiology and correct the underlying disorder

Background: Oral tranexamic acid is effective for heavy menstrual bleeding, but the thrombosis risk with this treatment is largely not studied. Methods: Using nationwide registries, we assessed associations between use of oral tranexamic acid and risk of deep-vein thrombosis or pulmonary embolism and arterial thrombosis in heart or brain in a nationwide historical prospective cohort of Danish women aged 15 to 49 years in the period 1996–2017. Exclusion criteria included potential confounding factors such as history of thromboembolism, anticoagulation therapy, thrombophilia, and cancer. Findings: Among 2·0 million women followed for 13·8 million person-years, 3,392 venous thromboembolisms and 4,198 arterial thromboses occurred. A total of 63,896 women (3·2%) filled 146,729 prescriptions of oral tranexamic acid during follow-up with median filled prescription per user being one of 15 g. The age-standardised incidence rate of venous thromboembolism was 11·8 (95% CI 4·6 to 30·2) per 10,000 person-years in oral tranexamic acid use compared to 2·5 (2·4 to 2·6) per 10,000 person-years in non-use. For arterial thrombosis, the age-standardised incidence rate per 10,000 person-years was 3·4 (1·1 to 10·7) among exposed compared to 3·0 (2·9 to 3·1) in non-exposed. Comparing oral tranexamic acid use with non-use, the adjusted incidence rate ratio was 4·0 (1·8 to 8·8) for venous thromboembolism and 1·3 (0·4 to 4·2) for arterial thrombosis.Number needed to harm per five days of treatment was 78,549 women for venous thromboembolism. Interpretation: We found use of oral tranexamic acid to be positively associated with venous thromboembolism. However, number needed to harm per five days of treatment was high.

Background: There is no consensus on the effect of opium on stroke yet. Some studies show the negative effects of opium on ischemic strokes. Here, we attempt to compare the volume of lesions in opium addict and non-addict patients with thrombotic stroke. Methods: This case-control study was conducted on patients with thrombotic stroke at Shafa Hospital in Kerman, Iran. The diagnosis was confirmed by clinical examinations, imaging, and laboratory tests. The volume of lesions was calculated by magnetic resonance imaging (MRI), and the data were analyzed by descriptive statistics, Mann-Whitney U test, Chi-square test, and linear regression analysis. Findings: A total of 60 patients were studied, 30 of whom were opium addicts and the rest were non-addicts. The mean volume of the lesion was 46.008350 ± 7.488990 (in the addict group) and 31.023335 ± 1.441570 (in the non-addict group), indicating a significant difference between the two groups (P = 0.005). Regression analysis results showed a significant relationship between the volume of stroke with opium addiction (P = 0.017), ischemic heart diseases (IHDs) (P = 0.006), hyperlipidemia (HLP) (P = 0.016), age (P = 0.035), and smoking (P = 0.044). Conclusion: The results of this study showed a higher volume of lesion in opium-addict patients compared to that in non-addicts as an indicator of stroke severity. [ABSTRACT FROM AUTHOR]

Stroke is a leading cause of death and disability in the United States. Most strokes are ischemic, resulting in both cognitive and motor impairments. Animal models of ischemic stroke such as the distal middle cerebral artery occlusion (dMCAO) and photothrombotic stroke (PTS) procedures have become invaluable tools, with their own advantages and disadvantages. The dMCAO model is clinically relevant as it occludes the artery most affected in humans, but yields variability in the infarct location as well as the behavioral and cognitive phenotypes disrupted. The PTS model has the advantage of allowing for targeted location of infarct, but is less clinically relevant. The present study evaluates phenotype disruption over time in mice subjected to either dMCAO, PTS, or a sham surgery. Post-surgery, animals were tested over 28 days on standard motor tasks (grid walk, cylinder, tapered beam, and rotating beam), as well as a novel odor-based operant task; the 5:1 Odor Discrimination Task (ODT). Results demonstrate a significantly greater disturbance of motor control with PTS as compared with Sham and dMCAO. Disruption of the PTS group was detected up to 28 days post-stroke on the grid walk, and up to 7 days on the rotating and tapered beam tasks. PTS also led to significant short-term disruption of ODT performance (1-day post-surgery), exclusively in males, which appeared to be driven by motoric disruption of the lick response. Together, this data provides critical insights into the selection and optimization of animal models for ischemic stroke research. Notably, the PTS procedure was best suited for producing disruptions of motor behavior that can be detected with common behavioral assays and are relatively enduring, as is observed in human stroke., Competing Interests: Conflict of interest statement The authors declare no competing financial interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Endothelial dysfunction and vascular injuries are the early processes in thrombogenesis leading to thrombotic stroke. These processes trigger platelet activation characterized by synthesis of Thromboxane A2, potent agonist in platelet aggregation. Acetosal (ASA) 100 mg usually given to thrombotic stroke patients exerts its pharmacological effect by inhibition of TxA2 synthesis, thus could prevent thrombus formation. Diabetes mellitus (DM) as risk factor of thrombotic stroke exhibits an increase in TxA2 synthesis. It is not known whether ASA 100 mg could inhibit TxA2 adequately in diabetic patients. This study aimed to analyze the differences of serum TxA2 level, which was measured by serum TxB2 level as stabile metabolite of TxA2, after taking ASA 100 mg in diabetic and non-diabetic thrombotic stroke patients. This prospective observational study was held in Neurology Department of Dr. Soetomo Hospital, Surabaya. Total 27 patients, consisted of 15 patients with DM and 12 patients with non-DM were enrolled. Serum TxB2 was measured before and after 5-7 days 100 mg ASA 100 administration. Mean value of serum TxB2 level before and after taking ASA was 16.43 ± 16.08 ng/mL and 2.93 ± 1.83 ng/mL in diabetic and 27.36 ± 21.04 ng/mL and 5.36 ± 4.06 ng/mL in non-diabetic group. Mean reduction of serum TxB2 level in diabetic and non-diabetic group was 13.49 ± 15.9 ng/mL and 22.00 ± 21.65 ng/mL. There were significant differences in serum TxB2 level after taking ASA 100 mg in diabetic and non-diabetic group but the mean reduction of serum TxB2 level were not significantly different.

COVID-19 disease caused by the SARS coronavirus has caused significant morbidity and mortality around the world ever since it was first declared as a pandemic by the World Health Organization (WHO) in March 2020. Acute neurological manifestations of this disease have also started emerging and being recognized around the world and acute ischemic stroke (AIS) or thrombotic stroke is becoming one of the major neurological illnesses related to COVID-19. The management of AIS is time-critical and major advances in its management over the recent years, such as bridging thrombolysis and mechanical thrombectomy (MT), are multidisciplinary activities requiring robust coordination and management in the acute setting. All these advances are severely challenged in the COVID-19 pandemic where severe pressures exist on the clinical resources and logistics required to deliver an effective stroke service. This is further compromised by legal and preventive measures during this pandemic like local lockdowns. Reporting of minor or initial symptoms has also been compromised due to the fear of approaching healthcare settings which are perceived as high-risk zones to catch the infection. The purpose of this document is to highlight these challenges and provide a guiding framework for the management of AIS under three principles: (a) Delivering an effective service, (b) Preventing infections within the healthcare setting, and (c) Optimizing resource utilization. [ABSTRACT FROM AUTHOR]

Antiplatelet agents are effective for secondary prevention of ischemic stroke and can reduce the severity of first-ever ischemic stroke. However, it is uncertain if prophylactic antiplatelet therapy reduces the severity of recurrent ischemic stroke. The aim of this study was to determine the effect of preceding antiplatelet treatment on the severity of thrombotic stroke (TS) in patients with a prior history of stroke. From a prospective hospital registry of 1338 consecutive patients with acute ischemic stroke, we identified patients with a prior history of stroke who were admitted for cardioembolic stroke (CE); TS including large-artery atherosclerosis, small vessel occlusion, and branch atheromatous disease; or other cause or cryptogenic stroke (OCS). Cases in each subtype were categorized based on preceding medication: antiplatelet agents (AP) and none (N). Severity of stroke (National Institutes of Health Stroke Scale: NIHSS) on admission was compared between AP and N cases. The total cohort of 252 patients included 83 with CE, 102 with TS, and 67 with OCS. After excluding those with prior anticoagulants, the median NIHSS on admission was lower in AP cases than in N cases (3 vs. 5, p = 0.002). In multivariate analysis, preceding AP treatment was independently associated with minor stroke (NIHSS ≤4) on admission in CE group (OR 8.48, 95% CI 1.71–62.9, p = 0.008) and TS group (OR 4.24, 95% CI 1.44–13.4, p = 0.009). Preceding antiplatelet treatment in patients with a prior history of stroke may reduce the severity of subsequent thrombotic and cardiogenic stroke. • Effects of prior antiplatelet agents on thrombotic stroke severity were examined. • The subjects were patients with ischemic stroke and a prior history of stroke. • Prior antiplatelet use was independently associated with minor stroke on admission. • Prior antiplatelet agents may reduce the severity of subsequent ischemic stroke. [ABSTRACT FROM AUTHOR]

Large cerebral infarctions have high morbidity and mortality. Patients with large cerebral infarctions may have recurrent ischemia as high as 8.1% within 7 days; highest among other types of strokes. Data regarding risk factors for large cerebral infarction in Asian populations are still scant. All adult (age ≥15 years old) patients with the diagnosis of thrombotic ischemic stroke who were treated at Srinagarind Hospital, Khon Kaen University, Thailand from January 2012 to December 2013 were studied. Large cerebral infarctions are defined by clinical criteria of having cerebral cortical impairment, brain stem or cerebellar dysfunction with infarction sizes of more than 1.5 cm. The association of various stroke risk factors and large infarction strokes were calculated using multiple logistic regression analysis. There were 276 thrombotic stroke patients who met the study criteria; classified as large cerebral infarctions in 59 patients (21.38%) and small cerebral infarctions in 217 patients (78.62%). Baseline characteristics and risk factors for stroke were comparable between both groups. The large cerebral infarction group had a significantly larger proportions of right internal carotid artery stenosis, plaques on the left side, left internal carotid artery stenosis, and internal carotid artery stenosis at any side than the small cerebral infarction group. Among various stroke risk factors, only internal carotid artery stenosis at any side was the only significant factor associated with large cerebral infarction with an adjusted odds ratio of 11.14 (95% CI: 3.46, 35.82). In conclusion, significant internal carotid artery stenosis is associated with large cerebral infarction.

Background: Intravenous injection of alteplase, a recombinant tPA (tissue-type plasminogen activator) as a thrombolytic agent has revolutionized ischemic stroke management. However, tPA is a more complex enzyme than expected, being for instance able to promote thrombolysis, but at the same time, also able to influence neuronal survival and to affect the integrity of the blood-brain barrier. Accordingly, the respective impact of endogenous tPA expressed/present in the brain parenchyma versus in the circulation during stroke remains debated., Methods: To address this issue, we used mice with constitutive deletion of tPA (tPA Null [tPA-deficient mice]) or conditional deletion of endothelial tPA (VECad [vascular endothelial-Cadherin-Cre-recombinase]-Cre ∆tPA ). We also developed parabioses between tPA Null and wild-type mice (tPA WT ), anticipating that a tPA WT donor would restore levels of tPA to normal ones, in the circulation but not in the brain parenchyma of a tPA Null recipient. Stroke outcomes were investigated by magnetic resonance imaging in a thrombo-embolic or a thrombotic stroke model, induced by local thrombin injection or FeCl 3 application on the endothelium, respectively., Results: First, our data show that endothelial tPA, released into the circulation after stroke onset, plays an overall beneficial role following thrombo-embolic stroke. Accordingly, after 24 hours, tPA Null /tPA Null parabionts displayed less spontaneous recanalization and reperfusion and larger infarcts compared with tPA WT /tPA WT littermates. However, when associated to tPA WT littermates, tPA Null mice had similar perfusion deficits, but less severe brain infarcts. In the thrombotic stroke model, homo- and hetero-typic parabionts did not differ in the extent of brain damages and did not differentially recanalize and reperfuse., Conclusions: Together, our data reveal that during thromboembolic stroke, endogenous circulating tPA from endothelial cells sustains a spontaneous recanalization and reperfusion of the tissue, thus, limiting the extension of ischemic lesions. In this context, the impact of endogenous parenchymal tPA is limited., Competing Interests: Disclosures None.

Yuyun Yueniwati,1 Ni Komang Darmiastini,1 Eko Arisetijono2 1Radiology Department, Faculty of Medicine, Brawijaya University, Malang, Indonesia; 2Neurology Department, Faculty of Medicine, Brawijaya University, Malang, Indonesia Background and objectives: Atherosclerosis causes reduction of the oxygen supply to structures in the far arterial wall, provoking the release of factors that drive angiogenesis of vasa vasorum, including VEGF. Other studies have revealed the inflammatory response in atherosclerosis and the role of platelet factor 4 (PF4) as an anti-angiogenic chemokine through the inhibition of VEGF. This cross-sectional study aims at measuring the effect of atherosclerosis assessed through carotid intima-media thickness (CIMT) against plasma VEGF levels in patients with post-acute thrombotic stroke. Materials and methods: CIMT was assessed sonographically using GE Logiq S6 with 13 MHz frequency linear probe. VEGF-A plasma levels were measured using enzyme-linked immunosorbent assay (ELISA) method. Differences among variables were compared statistically. The data were analyzed using Pearson correlation. Results: A total of 25 patients with post-acute thrombotic stroke were identified in days 7 to 90. CIMT thickening was indicated in 88% of patients (1.202 ± 0.312 mm), while an increase in plasma VEGF was identified in all patients (178.28 ± 93.96 ng/mL). There was no significant correlation between CIMT and plasma VEGF levels in patients with post-acute thrombotic stroke (p=0.741). A significant correlation was recognized between CIMT and total cholesterol (p=0.029) and low-density lipoprotein (p=0.018). Conclusion: There were no significant correlations between CIMT and plasma VEGF levels in patients with post-acute thrombotic stroke. However, plasma VEGF increased in patients with thrombotic stroke. CIMT measurement is a promising noninvasive modality to assess the vascular condition of patients with stroke and diabetes, while plasma VEGF cannot specifically assess vascular condition as it can be triggered by ischemic conditions in tissues of the whole body. Keywords: atherosclerosis, CIMT, VEGF, thrombotic stroke

Background: Cardiocerebral infarction (CCI) is a rare and life-threatening presentation of simultaneous acute myocardial infarction and acute ischemic stroke that requires prompt recognition and proper treatment. CCI is time sensitive and carries a high mortality rate. There is no standardized treatment algorithm that addresses both conditions simultaneously., Case Report: We present a 29-year-old man with simultaneous myocardial infarction and thrombotic stroke after coital activity. He presented to the Emergency Department with left-sided extremity weakness and numbness and radicular left-sided chest pain. He suffered a cardiac arrest during his evaluation and required emergent percutaneous coronary intervention with stent placement. He was resuscitated successfully and had an uncomplicated clinical course, with improved neurologic recovery prior to discharge. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: CCI is a rare condition that typically occurs in elderly patients with risk factors for cardiovascular disease. Management is challenging due to the time-sensitive nature of diagnosis and treatment of each condition. Treatment is not standardized, unlike individual evidence-based algorithms for thrombotic stroke and acute myocardial infarction. Risks and benefits for each treatment plan should be weighed and therapy should be directed toward the most immediate life-threatening process. This case would add to the literature surrounding this condition and help guide emergency physicians toward the most optimal treatment strategies for this patient population. This case also raises awareness of the existence of this condition and its potential presence in young, otherwise healthy patients., Competing Interests: Declaration of Competing Interest None to disclose., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Previous ischemic stroke (IS) is a risk factor for subsequent IS in the general population; it is unclear if this relationship remains true in patients with cancer. Our objective was to examine the association between previous IS and risk for future IS in individuals newly diagnosed with cancer., Methods: We conducted a retrospective population-based matched cohort study of newly diagnosed adult cancer patients (excluding nonmelanoma skin cancers and primary central nervous system tumors) in Ontario, Canada from 2010 to 2020; those with prior IS were matched (1:4) by age, sex, year of cancer diagnosis, cancer stage, and cancer site to those without a history of stroke. Cumulative incidence function curves were created to estimate the incidence of IS. Subdistribution adjusted hazard ratios (aHRs) and 95% CIs were calculated, where death was treated as a competing event. Multivariable analysis was adjusted for imbalanced baseline characteristics., Results: We examined 65 525 individuals with cancer, including 13 070 with a history of IS. The median follow-up duration was 743 days (interquartile range, 177-1729 days). The incidence of IS following cancer diagnosis was 261.3/10 000 person-years in the cohort with prior IS and 75.3/10 000 person-years in those without prior IS. Individuals with prior IS had an increased risk for IS after cancer diagnosis compared with those without a history (aHR, 2.68 [95% CI, 2.41-2.98]); they also had more prevalent cardiovascular risk factors. The highest risk for stroke compared with those without a history of IS was observed in the gynecologic cancer (aHR, 3.84 [95% CI, 2.15-6.85]) and lung cancer (aHR, 3.18 [95% CI, 2.52-4.02]) subgroups. The risk of IS was inversely correlated with lag time of previous stroke; those with IS 1 year before their cancer diagnosis had the highest risk (aHR, 3.68 [95% CI, 3.22-4.22])., Conclusions: Among individuals with newly diagnosed cancer, those with IS history were almost 3× more likely to experience a stroke after cancer diagnosis, especially if the prediagnosis stroke occurred within 1 year preceding cancer diagnosis., Competing Interests: Disclosures Dr Kapral holds the Lillian Love Chair in Women’s Health from the University Health Network and the University of Toronto, Canada. Dr Carrier is a consultant for Bayer, Bristol-Myers Squibb Canada, Pfizer, Sanofi US Services Inc, and Servier, and holds grants from LEO Pharma Inc and Pfizer. Dr Siegal discloses receiving honoraria paid indirectly to her institution from Astra Zeneca, Pfizer Canada, and Servier Pharmaceuticals LLC. The remaining authors have nothing to disclose.

Endothelial dysfunction and vascular injuries are the early processes in thrombogenesis leading to thrombotic stroke. These processes trigger platelet activation characterized by synthesis of Thromboxane A2, potent agonist in platelet aggregation. Acetosal (ASA) 100 mg usually given to thrombotic stroke patients exerts its pharmacological effect by inhibition of TxA2 synthesis, thus could prevent thrombus formation. Diabetes mellitus (DM) as risk factor of thrombotic stroke exhibits an increase in TxA2 synthesis. It is not known whether ASA 100 mg could inhibit TxA2 adequately in diabetic patients. This study aimed to analyze the differences of serum TxA2 level, which was measured by serum TxB2 level as stabile metabolite of TxA2, after taking ASA 100 mg in diabetic and non-diabetic thrombotic stroke patients. This prospective observational study was held in Neurology Department of Dr. Soetomo Hospital, Surabaya. Total 27 patients, consisted of 15 patients with DM and 12 patients with non-DM were enrolled. Serum TxB2 was measured before and after 5-7 days 100 mg ASA 100 administration. Mean value of serum TxB2 level before and after taking ASA was 16.43 ± 16.08 ng/mL and 2.93 ± 1.83 ng/mL in diabetic and 27.36 ± 21.04 ng/mL and 5.36 ± 4.06 ng/mL in non-diabetic group. Mean reduction of serum TxB2 level in diabetic and non-diabetic group was 13.49 ± 15.9 ng/mL and 22.00 ± 21.65 ng/mL. There were significant differences in serum TxB2 level after taking ASA 100 mg in diabetic and non-diabetic group but the mean reduction of serum TxB2 level were not significantly different. [ABSTRACT FROM AUTHOR]

Background and Objectives: Disability after stroke occurs across ischemic stroke subtypes, with a suggestion that embolic strokes are more devastating. Whether this difference is as a result of differences in comorbidities or differences in severity at the time of the stroke event is not known. The primary hypothesis was that participants with embolic stroke would have more severe stroke at the time of admission and a higher risk of mortality, compared with thrombotic stroke participants even with consideration of confounders over time, with a secondary hypothesis that this association would differ by race and sex., Methods: Atherosclerosis Risk in Communities (ARIC) study participants with incident adjudicated ischemic stroke, stroke severity and mortality data, and complete covariates were included. Multinomial logistic regression models determined the association between stroke subtype (embolic vs thrombotic) and admission NIH Stroke Scale (NIHSS) category (minor [≤5], mild [6-10], moderate [11-15], severe [16-20], and very severe [>20]) adjusted for covariates from visits most proximal to the stroke. Separate ordinal logistic models evaluated for interaction by race and sex. Adjusted Cox proportional hazard models estimated the association between stroke subtype and all-cause mortality (through December 31, 2019)., Results: Participants (N = 940) were mean age 71 years (SD = 9) at incident stroke, 51% female, and 38% Black. Using adjusted multinomial logistic regression, the risk of having a more severe stroke (reference NIHSS ≤5) was higher among embolic stroke vs thrombotic stroke patients, with a step-wise increase for embolic stroke patients when moving from mild (odds ratio [OR] 1.95, 95% CI 1.14-3.35) to very severe strokes (OR 4.95, 95% CI 2.34-10.48). After adjusting for atrial fibrillation, there was still a higher risk of having a worse NIHSS among embolic vs thrombotic strokes but with attenuation of effect (very severe stroke OR 3.91, 95% CI 1.76-8.67). Sex modified the association between stroke subtype and severity (embolic vs thrombotic stroke, p interaction = 0.03, per severity category, females OR 2.38, 95% CI 1.55-3.66; males OR 1.75, 95% CI 1.09-2.82). The risk of death (median follow-up 5 years, interquartile range 1-12) was also increased for embolic vs thrombotic stroke patients (hazard ratio 1.66, 95% CI 1.41-1.97)., Discussion: Embolic stroke was associated with greater stroke severity at the time of the event and a higher risk of death vs thrombotic stroke, even after careful adjustment for patient-level differences., (Written work prepared by employees of the Federal Government as part of their official duties is, under the U.S. Copyright Act, a “work of the United States Government” for which copyright protection under Title 17 of the United States Code is not available. As such, copyright does not extend to the contributions of employees of the Federal Government.)