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Ischemic stroke is a leading cause of motor impairment and psychosocial disability. Although free fatty acids (FFA) have been proven to affect the risk of stroke and potentially dementia, the evidence of their impact on cognitive functions in stroke patients is lacking. We aimed to establish such potential relationships. Seventy-two ischemic stroke patients were prospectively analysed. Their cognitive functions were assessed seven days post-stroke and six months later as follow-up ( n = 41). Seven days post-stroke analysis of serum FFAs levels showed direct correlations between Cognitive Verbal Learning Test (CVLT) and the following FFAs: C20:4n6 arachidonic acid and C20:5n3 eicosapentaenoic acid, while negative correlations were observed for C18:3n3 linolenic acid (ALA), C18:4 n3 stearidonic acid and C23:0 tricosanoic acid. Follow-up examination with CVLT revealed positive correlations with C15:0 pentadecanoid acid, C18:3n6 gamma linoleic acid, SDA, C23:0 tricosanoic acid and negative correlations with C14:0 myristic acid and C14:1 myristolenic acids. Several tests (Trail Making Test, Stroop Dots Trail, Digit Span Test and Verbal Fluency Test) were directly correlated mainly with C14:0 myristic acid and C14:1 myristolenic acid, while corresponding negatively with C18:1 vaccinic acid, C20:3n3 cis-11-eicosatrienoic acid, C22:1/C20:1 cis11- eicosanic acid and C20:2 cis-11-eicodienoic acid. No correlations between Montreal Cognitive Assessment (MOCA) test performed on seventh day, and FFAs levels were found. Saturated fatty acids play a negative role in long-term cognitive outcomes in stroke patients. The metabolic cascade of polyunsaturated fatty acids (n3 PUFA) and the synthesis of (AA) can be involved in pathogenesis of stroke-related cognitive impairment.

Objective: The neurotrophin brain-derived neurotrophic factor (BDNF) affects poststroke functional outcome, neurogenesis, neuroprotection, and neuroplasticity. Its level is related to the diet and nutritional status, and more specifically, it is free fatty acids (FFAs) and eicosanoids that can have an impact on the BDNF level. The aim of this study was to analyze the potential impact of FFAs and eicosanoids on the BDNF level in stroke patients. Material and Methods . Seventy-three ischemic stroke patients were prospectively enrolled in the study. Laboratory tests were performed in all subjects, including the levels of FFAs, eicosanoids, and BDNF. FFAs and inflammatory metabolites were determined by gas chromatography and liquid chromatography, while BDNF was evaluated by the immune-enzymatic method (ELISA)., Results: The plasma level of BDNF negatively correlated with C22:1n9 13 erucic acid, C18:3n3 linolenic acid (ALA), and lipoxin A4 15-epi-LxA4. A direct association was observed in relation to BDNF and C16:1 palmitoleic acid and C20:3n6 eicosatrienoic acid (dihomo-gamma-linolenic acid (DGLA))., Conclusions: Saturated fatty acids and omega-3 and omega-9 erucic acids can affect signaling in the BDNF synthesis resulting in the decrease in BDNF. There is a beneficial effect of DGLA on the BDNF level, while the effect of ALA on BDNF can be inhibitory. Specialized proresolving lipid mediators can play a role in the BDNF metabolism. BDNF can interact with inflammation as the risk factor in the cardiovascular disorders, including stroke., Competing Interests: The authors declare no conflict of interest., (Copyright © 2020 Dariusz Kotlega et al.)

The study was designed to demonstrate the relationship of free fatty acids (FFAs) and eicosanoids levels with the severity of depressive symptoms in stroke. The ischemic stroke patients ( n = 74) were included in the prospective study. The risk of depression was evaluated by the Beck Depression Inventory-II (BDI-II) 7 days and 6 months after the stroke onset. FFAs and inflammatory metabolites were determined by gas chromatography and liquid chromatography. In the acute phase of stroke, BDI-II and FFAs inversely correlated with C13:0 tridecanoic acid, C15:1 cis-10-pentadecanoid acid, C17:1 cis-10- heptadecanoid acid, C18:0 stearic acid, C20:3n6 eicosatrienoic acid, C22:1cis13 docosenoic acid and C22:6n3 docosahexaenoic acid (DHA). DHA level was significantly lower in patients with low vs. high BDI-II score. In the follow-up examination, BDI-II score directly correlated with C16:0 palmitic acid. The changes in BDI-II score during 6-month observation inversely correlated with lipoxin A4 and protectin D1, and directly correlated with 5-oxo-ETE. Importantly, the severity of depressive symptoms was associated with n3 PUFA level. Diet-derived FFAs were observed to potentially affect the inflammatory pathways in pathogenesis of depression in stroke and reduced DHA levels can attenuate depressive symptoms in stroke patients.

Aim and Clinical Rationale for Study: In Poland, it is widely believed that the outlook for ischaemic stroke patients is gradually improving due to the development of a network of stroke wards and other dedicated hospital units throughout the country. However, a study by Shah et al., reporting a significant increase in mortality from ischaemic stroke in several European countries including Poland, contradicts this belief. Therefore, the aim of this study was to determine the risk factors for death in patients with recent ischaemic stroke among a population of patients from Western Pomerania, a region in north-western Poland., Materials and Methods: This retrospective study involved 2,374 patients with recent ischaemic stroke. Mortality was defined as death within 30 days of admission to hospital. Patients who died in hospital during this period were defined as deceased, while those who survived beyond this time were classified as alive., Results: We found that compared to ischaemic stroke patients who survived, the group of ischaemic stroke patients who died included a higher number of patients who smoked cigarettes (OR = 6.08 in univariable model; OR = 6.22 in adjusted model), had hypertension (OR = 2.57; OR = 1.85), had a history of previous stroke (OR = 2.63; OR = 2.14), had coronary heart disease (OR = 1.78; OR=1.36), and were older (OR = 1.06; OR = 1.05). For all these factors, p-value was lower than 0.001. Females had a higher risk of death (OR = 1.48, p < 0.001; OR = 1.35, p = 0.01). For dyslipidemia, only univariable model was statistically significant (OR = 1.38, p < 0.001)., Conclusion and Clinical Implications: Older age, female sex, dyslipidemia, hypertension, coronary heart disease, and smoking are not only recognised risk factors for ischaemic stroke, but also risk factors associated with an unfavourable prognosis following stroke.

Background: Endothelial Progenitor Cells (EPCs) are important players in neovascularization, mobilized through signalling by Angiogenic Growth Factors (AGFs) such as Vascular Endothelial Growth Factor (VEGF) and fibroblast growth factor (FGF). In vitro, inflammatory parameters impair the function and influence of EPCs on AGFs. However, this connection is not clear in vivo. To understand the mechanisms of augmented arteriogenesis and angiogenesis in acute ischemic stroke (AIS) patients, we investigated whether circulating stem cells (CD133+), early endothelial progenitor cells (CD133+/VEGFR2+), and endothelial cells (ECs; CD34¯/CD133¯/VEGFR2+) were increasingly mobilized during AIS, and whether there were correlations between EPC levels, growth factor levels and inflammatory parameters., Methods: Data on demographics, classical vascular risk factors, neurological deficit information (assessed using the National Institutes of Health Stroke Scale), and treatment were collected from 43 consecutive AIS patients (group I). Risk factor control patients (group II) included 22 nonstroke subjects matched by age, gender, and traditional vascular risk factors. EPCs were measured by flow cytometry and the populations of circulating stem cells (CD133+), early EPCs (CD133+/VEGFR2+), and ECs (CD34¯/CD133¯/VEGFR2+) were analysed. Correlations between EPC levels and VEGF and FGF vascular growth factor levels as well as the influence of inflammatory parameters on EPCs and AGFs were assessed., Results: Patient ages ranged from 54 to 92 years (mean age 75.2 ± 11.3 years). The number of circulating CD34¯/CD133¯/VEGF-R2+ cells was significantly higher in AIS patients than in control patients (p < 0.05). VEGF plasma levels were also significantly higher in AIS patients compared to control patients on day 7 (p < 0.05). FGF plasma levels in patients with AIS were significantly higher than those in the control group on day 3 (p < 0.05). There were no correlations between increased VEGF and FGF levels and the number of CD133+, CD133+/VEGFR2+, or CD34¯/CD133¯/VEGFR2+ cells. Leukocyte levels, FGF plasma levels, and the number of early EPCs were negatively correlated on day 3. High sensitivity C-reactive protein levels and the number of CD133+ and CD133+/VEGFR2+ cells were negatively correlated on day 7. In addition, there was a negative correlation between fibrinogen levels and FGF plasma levels as well as the number of early EPCs (CD133+/VEGFR2+)., Conclusion: AIS patients exhibited increased numbers of early EPCs (CD133+/VEGFR2+) and AGF (VEGF and FGF) levels. A negative correlation between inflammatory parameters and AGFs and EPCs indicated the unfavourable influence of inflammatory factors on EPC differentiation and survival. Moreover, these correlations represented an important mechanism linking inflammation to vascular disease., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Endothelial Progenitor Cells (EPCs) have been suggested to be a therapeutic option in Acute Ischemic Stroke (AIS). Statins modulate endothelial function and preserve blood flow to tissue exposed to an ischemic insult. We tested the hypothesis that statins therapy might augment circulating EPCs in patients with AIS., Methods: Demographic data, classical vascular risk factors, treatment and National Institutes of Health Stroke Scale data were prospectively collected from 43 consecutive AIS patients (group I), comprising - 30 treated with statins (group Statin(+)) and 13 untreated (group Statin (-)). Risk factor controls (group II) included 22 subjects matched by age, gender, and traditional vascular risk factors. EPCs were measured by flow cytometry - and the populations of circulating stem cells (CD133+), early EPCs (CD133+/VEGFR2+) and ECs CD34-/CD133-/VEGFR2+ cells were analyzed., Results: Patients ages ranged from 54 to 92 years (mean age 75.2 ± 11.3 years). The number of CD34-/CD133-/VEGF-R2+ cells was significantly lower in group I than II (p<0.05). In group Statin(+) neurological deficit on the 1st, 3rd and 7th day was significantly lower in comparison Statin(-) (p<0.05). We observed significantly more frequent "improvement> 50% or complete recovery" and less frequent death in the statin-treated group. The number of early EPCs and ECs was significantly higher in the treated group on the day 3rd (p < 0.05)., Conclusions: Statins treatment is likely to have a positive effect on spontaneous CD133+/ VEGFR2+ and CD34-/CD133-/VEGFR2+ cell mobilization triggered by a stroke., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

The association of poor outcome and mortality with low levels of hemoglobin (Hb) and hematocrit (HcT) in patients admitted after acute Ischemic Stroke (IS) was recently demonstrated. The mechanisms behind this still remain unclear. Our study aims to find out whether mRNA expressions and plasma concentrations of endothelin-1 (ET-l), endothelin-2 (ET-2) and endothelin-3 (ET-3) remain different in IS sufferers with low HcT and Hb levels in comparison with those whose HcT i Hb levels during a severe IS episode remain within the norm. The study included 60 patients treated consecutively for first-time IS. The assessment of mRNA gene expression and plasma concentration of ET-1, ET-2, ET-3 was conducted in the first, third and seventh day following the onset of stroke using qRT-PCR method and ELISA tests. We demonstrated that patients whose initial HcT and Hb levels were below the norm presented a deeper neurologic deficit on 1, 3 and 7 day following stroke with noticeable improvement no earlier than between day 3 and 7. We also found a negative correlation between the initial HcT and Hb and concentration of plasma ET-1 on the same days. The patients whose HcT and Hb levels were within normal limits showed a significant improvement in their neurologic condition on each consecutive day of the observation. Reduced levels of Hb and HcT combined with an increased plasma concentration of vasoconstrictive endothelin-1 are strongly associated with poor outcome and high mortality in acute ischemic stroke., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Stroke is the second leading cause of death worldwide, and the leading cause of acquired disability in adults in most regions. There have been distinguished modifiable and non-modifiable risk factors of stroke. Among them the emotional stress was presented as a risk factor. The aim of this review was to present available data regarding the influence of acute and chronic mental stress on the risk of ischemic stroke as well as discussing the potential pathomechanisms of such relationship. There is an evident association between both acute and chronic emotional stress and risk of stroke. Several potential mechanisms are discussed to be the cause. Stress can increase the cerebrovascular disease risk by modulating symphaticomimetic activity, affecting the blood pressure reactivity, cerebral endothelium, coagulation or heart rhythm. The emotional stress seems to be still underestimated risk factor in neurological practice and research. Further studies and analyses should be provided for better understanding of this complex, not fully known epidemiological problem., (Copyright © 2016 Polish Neurological Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)

Statins are increasingly widely used in primary and secondary prevention of cardiovascular disorders, including ischemic stroke. The initial studies regarded mainly coronary heart disease, but recently more attention has been paid to statin use in ischemic stroke, including primary and secondary prevention as well as the acute phase treatment. Besides their main hypolipemic activity, statins have been proved to have immunomodulating properties that are called a pleiotropic effect. Drug metabolism is under genetic influence, exemplified by the single nucleotide polymorphisms (SNPs). This also applies to statins. Pharmacogenetic studies are conducted in many disorders including stroke. The aim of this study was to review selected common genetic variants in lipid or statin metabolism-related genes and indicate associations with cardiovascular disorders, especially with ischemic stroke. We present available data of SNPs in regard to the most significant and promising proteins such as cytochrome P450, ATPase superfamily, organic anion transporter family, apolipoprotein E, lipoprotein-associated phospholipase A2, lipoprotein(a), LDLR, proprotein convertase subtilisin/kexin type 9, HMGCR, and CETP. A presentation of particular SNPs may help in future studies to aim for individual and thus more effective statin therapy in stroke patients.

Background: Our objectives are to investigate whether the percentage of early emergency calls for stroke had increased and to assess current factors determining the time of deciding to seek medical help in the event of early stroke symptoms., Materials and Methods: We analyzed data concerning the decision to call for medical help in relation to observed stroke symptoms. Group I comprised 287 people who made the decision to call emergency medical service (EMS) in the first 10 minutes after observing stroke symptoms. Group II included 275 people who called EMS after that time. Data from the current database (2013-2014) were compared with relevant data from the period 2003-2005., Results: In 2013-2014, awareness of stroke signs was 2.5 times greater than in 2003-2005. Among the groups of early and delayed EMS calls during 2003-2005 and 2013-2014, there were no significant differences in the number of people who suspected stroke. Advanced patient age, young caller age, hemiparesis, facial weakness, and the severity of neurological deficit were independent factors that correlated strongly with an early EMS call, whereas feelings of numbness and dizziness correlated significantly with delayed EMS calls., Conclusions: In the West Pomeranian community, general knowledge of stroke is not a significant factor when making appropriate decisions at the onset of stroke symptoms. The education campaign regarding the initial symptoms of stroke and the possible fatal consequences appears to have been ineffective., (Copyright © 2015 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Introduction: Atherosclerotic changes in carotid arteries play an important role in the pathogenesis of ischaemic stroke. To a high extent there is evident asymmetry within the development of these changes, affecting just one artery. The aim of the study was to determine the impact of the cardiovascular risk factors on the presence of haemodynamically significant atherosclerotic changes or occlusion only in one compared to both of the carotid arteries in patients with ischaemic stroke., Material and Methods: Patients diagnosed with ischaemic stroke were retrospectively assessed towards stenosis of ≥70% or occlusion in at least one of the internal or common carotid arteries. There were 104 patients enrolled in the study. Group I consisted of individuals with haemodynamically significant (≥70%) stenosis or occlusion in one carotid artery (n = 48). Group II consisted of patients with bilateral significant (≥70%) stenosis or occlusion in carotid arteries (n = 56)., Results: There were no changes found in the presence of non- -modifiable stroke risk factors between the groups. In group I higher HDL level (45.7 vs 38.9 mg/dL, p = 0.038) and significantly more frequent calcifications in the atherosclerotic plaques of carotid arteries were found (p = 0.03). There were no differences in other tested factors between groups., Conclusions: The protective properties of HDL cholesterol and the slow formation of more stable, calcified plaques play an important role only in the development of unilateral advanced atherosclerosis in carotid arteries. The role of HDL cholesterol in stroke pathomechanism needs further studies.

Inflammatory components play an important role in the pathogenesis of arteriosclerosis, one of the main causes of stroke. Blood C-reactive protein (CRP) level is connected with the severity of neurological deficit and disability after stroke. Production of CRP depends on CRP gene polymorphism. This study enrolled 125 patients with ischemic stroke. CRP 717A/G polymorphism was tested in all patients along with an assay of CRP levels measured on the first and tenth day after stroke onset. Neurological deficit on admission and before discharge from hospital was evaluated according to National Institutes of Health Stroke Scale (NIHSS), and then associated with CRP levels and the CRP polymorphism. The CRP 717AA genotype was the most frequent, observed in 53.6% of patients; AG genotype in 40%, and GG genotype in 6.4%. Carriers of the 717GG genotype had a significantly higher CRP level on the first day after stroke versus heterozygotes (p=0.023). The improvement in neurological state evaluated with the NIHSS was significantly better in CRP 717AA patients in comparison with other CRP 717 genotypes (p=0.035). A higher level of CRP on the first day after ischemic stroke was slightly associated with the CRP 717AG genotype. The CRP 717AA genotype promotes improvement of neurological state in patients with ischemic stroke., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Atrial fibrillation (AF) is an independent factor increasing the risk of an ischemic stroke (IS) fivefold. The objective of the study was to evaluate the frequency of coexistence of non-valvular AF and IS during the acute stroke and to analyze the attitude of AF patients to treatment. The study included 3712 successive patients presenting either an IS or a transient ischemic attack. The analysis revealed a significant increase in the rate of patients with AF and IS in the years 2010-2013 (31.9%) compared with 2002-2005 (20.2%). A rise in the proportion of AF and IS patients was recorded over the course of consecutive years in group II. The proportion of newly detected AF cases during hospital stay differed significantly between the groups (16.9% vs. 31.9%). Group I and II patients differed essentially with regards to hypertension incidence and female rates. Antiplatelet medications or OACs were taken by a significantly greater number of AF patients in group II. Low number of therapeutic levels of INR was recorded in both groups. IS and AF coexist more frequently than indicated by previous assessments and demographic data from other countries. Increase in the number of IS and AF patients may result from higher detectability of AF and older age of patients affected with stroke, women in particular. Despite a well grounded knowledge about the benefits of OACs use in the prophylaxis of thrombotic-embolic events in AF patients, they are rarely used. A surprisingly low proportion of patients taking OACs reaches a therapeutic INR level., (Copyright © 2014 Polish Neurological Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)

Background and Purpose: Some of the risk factors of ischaemic stroke influence the development of atherosclerosis, which is a significant cause of vascular incidents. An inflammatory component plays a role in pathogenesis of both atherosclerosis and atrial fibrillation, the most important risk factor of embolic strokes. C-reactive protein (CRP) concentration in blood reflects the inflammatory process. Concentration of this protein depends on the CRP gene polymorphism. The aim of the study was to assess the relationship between selected risk factors of stroke and variant of -717A>G (rs2794521) CRP gene polymorphism in population of West Pomerania Province of Poland., Materials and Methods: There were 125 consecutive patients with ischaemic stroke analysed, who met the inclusion and exclusion criteria. In all patients, -717A>G CRP gene polymorphism was genotyped and analysed in relation to selected stroke risk factors., Results: Prevalence of type 2 diabetes was lower in patients with AA genotype of -717A>G CRP gene polymorphism than in patients with other alleles (p=0.017). Subjects with GG genotype had significantly higher concentration of CRP comparing to AG genotype (p=0.023). No correlation was found between -717A>G CRP gene polymorphism and the lipid profile and other selected risk factors of stroke., Conclusions: In patients with ischaemic stroke in West Pomerania Province, the GG genotype of -717A>G CRP gene polymorphism is associated with significantly higher CRP concentration in relation to AG genotype. Patients with AA genotype may be characterised by lower prevalence of type 2 diabetes., (Copyright © 2014 Polish Neurological Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)

Objectives: The question about anti-oxidized low-density lipoprotein antibodies (anti-oxLDL Abs) involvement in the pathogenesis of atherosclerosis-related ischemic stroke is still open. The aim of this study was to determine how anti-oxLDL Abs are involved in the pathogenesis of atherosclerosis-related ischemic stroke and identify the main risk factors for stroke, such as arterial hypertension, diabetes mellitus type 2, dyslipidemia, and atherosclerotic changes in the common and internal carotid arteries., Material and Methods: A total of 40 stroke patients and 25 age- and sex-matched healthy individuals were included in the study. For each subject, IgG anti-oxLDL Abs expression in peripheral blood was assessed and analyzed in relation to clinical data, carotid Doppler ultrasonography results, and results of peripheral blood laboratory tests, including inflammatory parameters and lipid profile., Results: The blood level of assessed antibodies was significantly higher in stroke patients than in control group. It did not relate to stroke severity and stroke outcome. The relationship between anti-oxLDL Abs and carotid plaques hyperechogenicity was observed. The antibodies concentration was significantly higher in patients with diabetes mellitus type 2 and also positively correlated with C-reactive protein blood level. However, multiple regression method did not confirm their independent influence., Discussion: Patients with atherogenic ischemic stroke may have significantly higher anti-oxLDL Abs concentrations. This should be interpreted as an attempt to limit the consequences of oxLDL production; however, this phenomenon does not seem to protect patients against cerebrovascular events.

Among patients with stroke, the phenomenon of resistance to treatment with low-dose aspirin acetylsalicylic acid (ASA) is quite common. The study included 133 patients hospitalized with acute ischemic stroke. Impedance platelet aggregometry (IPA) and levels of vWF and thromboxane (TXB2) were assessed - with the efficacy of aspirin in daily clinical investigation. Responses to treatment with doses of 150 and 300 mg/day were measured. In addition, we analyzed the response of proinflammatory factors [fibrinogen, C-reactive protein (CRP), white blood corpuscles (WBC)], lipids and hemoglobin A1c, which may alter platelet aggregation response to treatment. After a week of treatment at 150 mg/day, ASA patients were classified as laboratory resistant (42%) or sensitive (58%). Values of IPA in the resistant group were significantly higher (472 ± 150 vs. 222 ± 59 AUC, P < 0.0001). In resistant patients were also found higher levels of fibrinogen (3.90 ± 0.89 vs. 3.46 ± 0.74 g/l, P = 0.0046), CRP (6.97 ± 5.66 vs. 4.17 ± 4.03 mg/l, P = 0.0011), WBC (9.2 ± 2.4 vs. 8.3 ± 2.2 × 10/l, P = 0.0207) and lower HDL cholesterol (46 ± 12 vs. 52 ± 15 mg/dl, P = 0.016). This research shows that aspirin resistance assessment by IPA well reflects the clinical status of patients and should be used routinely. Resistance generally fails to 'break' at higher doses, hence our suggestion that patients resistant to low doses of the drug immediately switch to a thienopyridine class antiplatelet agent, for example, clopidogrel.

Background and Purpose: CD4⁺CD28⁻ lymphocytes can directly contribute to the instability of atherosclerotic plaque. This paper attempts to answer the question of the potential influence of the CD4⁺CD28⁻ lymphocyte population on the ultrasound image of atherosclerotic plaque in the common carotid artery (CCA) wall., Material and Methods: The study involved a group of 109 patients, aged 45 to 65 years, including 42 patients with first ever ischaemic stroke, experiencing symptoms resulting from disturbances of the anterior area of cerebral circulation, arterial hypertension and/or type 2 diabetes mellitus (group 1). Group 2 consisted of 34 patients with mentioned risk factors, without ischaemic stroke. The control group comprised 33 heal-thy individuals. The percentage of CD4⁺CD28⁻ lymphocytes was assessed with flow cytometry., Results: A significant difference in the incidence of heterogeneous plaques was noted between groups 1 and 3 (p = 0.0023) as well as between group 2 and 3 (p = 0.0005), whereas groups 1 and 2 did not differ from each other. The proportion of CD4⁺CD28⁻ lymphocytes was similar in groups 1 and 2 (p = 0.97), but it differed between groups 1 and 3 (p < 0.0001) and between groups 2 and 3 (p < 0.001). A correlation was found between the proportion of CD4⁺CD28⁻ lymphocytes in the blood and the number of CCA atherosclerotic plaques (Rs = 0.191, p = 0.046). The proportion of CD4⁺CD28⁻ lymphocytes in peripheral blood did not correlate with the ultrasound types of atherosclerotic plaques. No correlation between the proportion of CD4⁺CD28 ⁻lymphocytes and the area of atherosclerotic plaques was found., Conclusions: The correlation between the proportion of CD4⁺CD28⁻ lymphocytes and the number of atherosclerotic plaques within the CCA suggests that the cells are involved in the mechanism of carotid plaque formation. There is no proof of the involvement of the above-mentioned cells in the mechanism of plaque destabilization in those arteries.

Background and Purpose: More and more data point to the involvement of the CD4⁺CD28⁻ lymphocyte subpopulation in the pathogenesis of ischaemic stroke. This paper attempts to answer the question of whether an increase in the percentage of CD4⁺CD28⁻ lymphocytes in the blood may be associated with carotid artery intima-media thickness (IMT)., Material and Methods: The study involved a group of 109 patients, aged 45 to 65 years, including 42 patients with first-ever ischaemic stroke, experiencing symptoms resulting from disturbances of the anterior area of cerebral circulation, arterial hypertension and/or type 2 diabetes mellitus (group 1). Group 2 consisted of 34 patients with above-mentioned risk factors but without ischaemic stroke. The control group comprised 33 healthy individuals. Distribution of sex and mean age was comparable. The IMT of carotid arteries was measured by ultrasonography. Flow cytometry was applied to determine the percentage of CD4⁺CD28⁻ lymphocytes in the peripheral blood., Results: The IMT was significantly greater in patients with stroke than in patients without stroke. No significant correlation was found between the proportion of CD4⁺CD28⁻ lymphocytes in the blood and the IMT of carotid arteries., Conclusions: The significant proportion of CD4⁺CD28⁻ lymphocytes in patients with ischaemic stroke points to the involvement of the cells in the pathogenesis of stroke. The CD4⁺CD28⁻ lymphocytes are not involved in the pathomechanism of common carotid arteries IMT thickening in this group of patients.

Ischaemic stroke induces endothelial progenitor cell (EPC) mobilisation from bone marrow into peripheral blood. Circulating EPCs play an important role in post-injury regeneration of vasculature, whereas endothelial cells (ECs) have been shown to reflect endothelial damage and may be responsible for increased Endothelin-1 (ET-1) expression. We investigated herein the association between numbers of circulating ECs and EPCs, the levels of soluble factors regulating their migration and function, and the clinical outcome in patients with haemorrhagic (HS) or ischaemic stroke (IS). Sixteen patients with HS and eighteen with IS were assessed during the first 24h, day 3, and day 7 after stroke and compared them with twenty-three control subjects. We found elevated EPC and EC concentrations using flow cytometry and increase in VEGF, SDF-1, HGF, and ET-1 plasma levels by ELISA in the HS patients, while ET-1 mRNA expression in peripheral blood cells was elevated in the IS patients. Significant correlations were observed between EPCs or ECs and Big ET-1 protein or mRNA levels in HS but not in the IS patients. We suggest that ET-1 may play a role in pathophysiology of stroke and subsequent EPC mobilisation; however, further studies aimed at the precise elucidation of this issue are required., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Background: The question about the role of CD4+CD28- lymphocytes in the pathogenesis of atherosclerosis-related ischemic stroke is still open., Material and Methods: The study included patients, who underwent endarterectomy of internal carotid arteries. The group consisted of patients after stroke and ones without previous stroke. The histopathologic examination of obtained plaques has been performed. The percentage of CD4+CD28- lymphocytes in peripheral blood and their cytotoxicity has been assessed for each patient., Results: The global percentage of CD4+CD28- lymphocytes in blood was higher in the group of patients with plaques where connective tissue fibers consisted significantly of collagen fibers. The cytotoxicity of analysed cells related to less plaques calcification and presence of cholesterol crystals in the plaque. A multifactor regression of dependent variable presented the last relationship above as a only strong., Conclusions: CD4+CD28- cytotoxic lymphocytes seem to be involved in carotid atherosclerotic plaques development. Intraplaque cholesterol deposits may contribute to this process.

There is an inflammatory component in the pathogenesis of ischaemic stroke, which plays an important role in inducing atherothrombotic and embolic stroke. Statins, HMG-CoA (3-hydroxy-3-methyl-glutaryl-coenzyme A) reductase inhibitors are widely used in the primary and secondary prevention of ischaemic stroke. It has been proved that beyond their main effect on inhibition of endogenous cholesterol, they also modify the inflammatory process. Additional benefits from the use of statins result from their effect on the immune system. Increased risk of recurrent vascular episodes and risk of death after statin withdrawal in patients with vascular disorders is connected with termination of the anti-inflammatory effect of these drugs. The authors highlight that because of the anti-inflammatory effect of statins it is reasonable to use them in all patients at risk of ischaemic stroke, including those with atrial fibrillation.

Disorders of haemostasis which result in ischaemic stroke usually appear as thromboembolism in peripheral veins and the pulmonary circulation, and to a lesser extent as coagulopathy. The S-100 protein, a marker of stroke, correlates positively with the neurological deficit National Institutes of Health Stroke Scale (NIHSS). We adopted the hypothesis that early death of patients with acute ischaemic stroke can be explained by changes in blood coagulation and fibrinolysis. The study included 84 patients hospitalized with acute ischaemic stroke. Three groups were created: I (death between 1 and 2 days), II (death between 5 and 7 days) and III (with no deaths in hospital). We measured levels of fibrinogen, antithrombin, D-dimers, plasmin-antiplasmin complexes, plasminogen and clotting times (prothrombin time and activated partial thromboplastin time), platelet number, euglobulin clot lysis time (ECLTindex) and S-100 protein, C-reactive protein and white blood cells (WBCs). Group I had lower concentrations of fibrinogen compared to groups II (3.13 vs. 4.18, P<0.01) and III (3.13 vs. 3.77, P<0.02) and higher levels of D-dimers (3643 vs. 2278, P<0.05), higher concentrations of plasmin-antiplasmin complexes (1410 vs. 882, P=0.03) and a lower ECLTindex (152 vs. 219, P<0.02) when compared with group III. Group I also had higher concentrations of protein S-100 (2.09 vs. 0.61, P<0.001), higher NIHSS (18.0 vs. 13.2, P=0.073) and number of WBC (14.1 vs. 11.1, P<0.02) than in group III. The observed abnormalities in haemostasis, either found systemically or locally as cerebral microvascular thrombosis, may be factors potentially associated with death of patients with the shortest survival time.

Introduction: Reports point to the significant role of inflammatory mechanisms in stroke. These mechanisms are activated in peripheral blood in response to acute ischemic injury of cerebral tissues. The aim of this study was to determine whether peripheral inflammatory response to acute ischemia of the nervous tissue develops during the first twenty-four hours of ischemic stroke., Material and Methods: We studied 53 persons divided into three groups: 25 patients with ischemic stroke, arterial hypertension, and/or type 2 diabetes mellitus, and/or dyslipidemia (group I); 17 patients with arterial hypertension, and/or type 2 diabetes mellitus, and/or dyslipidemia but without stroke (group II); 11 young, healthy individuals (group III). TNF-alpha concentrations in peripheral blood were measured in each group using a sandwich enzyme-linked immunosorbent assay (ELISA). Other markers of inflammation in peripheral blood--C-reactive protein, fibrinogen, and leukocyte count--were assayed as well. The results were analyzed in relation to age, gender, co-morbidities, and blood-brain barrier injury., Results: TNF-alpha concentrations in peripheral blood of stroke patients were similar as in the other two groups. No associations between TNF-alpha and other inflammatory parameters were found. Injury of the blood-brain barrier was not accompanied by a significant change in the concentration of TNF-alpha., Conclusion: No significant peripheral inflammatory response to brain ischemia develops during the first twenty-four hours of ischemic stroke. This finding suggests that early anti-inflammatory prevention protocols can be devised to limit further injury of ischemic nervous tissue caused by activation of inflammatory processes.

Background and Purpose: In a murine model of stroke, we identified a population of very small embryonic-like (VSEL) stem cells (SCs) in adult murine bone marrow that could be mobilized into peripheral blood (PB). This raised the question of whether a similar population of cells is mobilized in human stroke patients., Methods: We evaluated a number of cells that corresponded to VSEL SCs in the PB of 44 stroke patients and 22 age-matched controls. After each patient's stroke, PB samples were harvested during the first 24 hours, on day +3, and on day +7 and then compared with normal controls. The circulating human cells with the phenotype of VSEL SCs were evaluated in PB by real-time quantitative polymerase chain reaction, fluorescence-activated cell sorting analysis, and direct immunofluorescence staining. In parallel, we also measured the serum concentration of stromal derived factor-1 by ELISA., Results: In stroke patients, we found an increase in the number of circulating cells expressing SC-associated antigens, such as CD133, CD34, and CXCR4. More important, we found an increase in the number of circulating primitive cells expressing the VSEL phenotype (CXCR4(+)lin(-)CD45(-) small cells), mRNA for Octamer-4 and Nanog, and Octamer-4 protein. All changes were accompanied by an increased serum concentration of stromal derived factor-1. Additionally, we found a positive correlation between stroke extensiveness, stromal derived factor-1 concentration in serum, and the number of CXCR4(+) VSEL SCs circulating in the PB., Conclusions: We conclude that stroke triggers the mobilization of CXCR4(+) VSEL SCs that have potential prognostic value in stroke patients. However, the potential role of these mobilized cells in brain regeneration requires further study.

Objectives: The purpose of the present study was to evaluate whether blood flow in the middle cerebral arteries (MCAs) in patients with atrial fibrillation (AF) during acute ischemic stroke is disturbed, as well as to assess if potential disturbances result from arrhythmia rather than a consequence of an embolus within the cerebral circulation., Patients and Methods: A total of 180 subjects were included in the study; 90 consecutive patients with AF and 90 consecutive patients in sinus rhythm who were admitted to the Stroke Unit of the Department of Neurology at Pomeranian Medical University Hospital in Szczecin, Poland within 24h of the onset of ischemic stroke symptoms. During the acute phase of the stroke (24h), all patients underwent transcranial Doppler ultrasonography (TCD) with assessment of mean blood flow velocity (MV) in the MCAs., Results: We observed significantly lower values of MV in MCAs of both damaged and intact hemispheres in patients with AF as compared to patients in sinus rhythm., Conclusion: In patients with AF, hemodynamic disturbances occur within the cerebral circulation during acute ischemic stroke which can cause a more severe course and worse stroke outcome. AF patients need more appropriate prevention of stroke, as well as more efficient treatment during acute ischemic stroke.

Introduction: The current project was aimed at elucidating whether blood pressure fluctuations in hypertensive patients with ischemic stroke, not characterized by hemodynamically significant stenosis in carotid arteries and proximal segments of intracranial arteries lead to circulation disturbances in anterior cerebral arteries (ACAs) as visualized by transcranial Doppler ultrasound (TCD)., Material and Methods: Sixty two hypertensive patients with the first ever ischemic stroke were included in the study with the average age of 65.16 +/- 11.52 years. Systolic (SBP), diastolic (DBP) and mean (MBP) blood pressure values were analyzed. The following parameters were calculated based on the obtained blood flow velocity spectra: mean velocity (Vmean), pulsatility index (PI) and resistance index (RI)., Results: A significant decrease of SBP, DBP and MBP occurred between the first and second day of observation, and no correlation between a reduction in arterial pressure and ACAs blood flow parameters was observed., Conclusions: In hypertensive patients with ischemic stroke, not characterized by hemodynamically significant stenosis within carotid arteries and proximal segments of anterior cerebral arteries, fluctuations of arterial blood pressure do not cause substantial disturbances of circulation in the ACAs, as visualized by TCD.

Background: CD4+CD28- lymphocytes are implicated in the destabilization of atheromatous plaque, leading to acute coronary episodes. One may ask whether these cells play a similar role in ischemic stroke pathogenesis with an atherosclerotic background., Methods: Flow cytometry was applied to determine the percentage of CD4+CD28- lymphocytes in the peripheral blood of patients during the acute phase of their first ischemic stroke (group I) and in patients without a history of stroke but with two of the most important risk factors (hypertension, diabetes) for atherosclerosis-related ischemic stroke (group II). The results were compared with healthy controls., Results: The median percentages of CD4+CD28- lymphocytes in groups I and II did not differ significantly, but for each of these groups the percentage was higher than in the control group. The time of blood sampling from onset of stroke, presence of the ischemic focus in the CT brain scan and severity of neurological deficits did not correlate with the percentage of CD4+CD28- lymphocytes., Conclusions: We conclude that CD4+CD28- lymphocytes are implicated in mechanisms enhancing the risk of acute ischemic stroke and not a consequence of stroke., (Copyright 2007 S. Karger AG, Basel.)

Objective: Thrombolysis is a time-dependent therapy. It is therefore very important how fast stroke patients can reach hospital. The present study was designed to assess which proportion of patients with stroke (from the population of Szczecin, the capital of West Pomerania Province, Poland) reaches hospital within the recommended time from the thrombolytic therapy point of view. The purpose of our study was also to elucidate which factors can influence the time before the ambulance service is called., Patients and Methods: The study involved 1,015 patients with stroke admitted to the Emergency Department of the University Hospital, Szczecin., Results: 235 patients (23.1%) were admitted to the hospital within the appropriate period for thrombolytic therapy. Hospital arrival time was significantly earlier in older patients and in patients with severer neurological deficits. We also observed a tendency for faster hospitalization of women, the highly educated, and patients regularly using antiplatelet drugs for cardiovascular disease prevention., Conclusions: The percentage of stroke patients hospitalized within 2 h after stroke onset should be increased. The most susceptible subpopulations in our country seem to be older patients, the highly educated and patients regularly using antiplatelet drugs for cardiovascular disease prevention., (2007 S. Karger AG, Basel)

Introduction: The stroke mortality rate in the Polish population is significantly higher than the average stroke mortality in Western Europe. It may prove a poor "initial" health condition of the Polish population which is afflicted with many life-threatening diseases which are at the same time the major risk factors for both: first ever and recurrent stroke. The aim of our study was to evaluate what is an attitude of Polish people with first-ever or recurrent stroke to keeping under control the most important risk factors for ischemic stroke., Material and Methods: 1282 consecutive patients with ischemic stroke were examined and categorized as individuals with first ever (group I - 980 patients) and recurrent stroke (group II - 302 patients). The data on the patients' previous history of stroke and vascular modifiable risk factors diagnosed before the onset of stroke: arterial hypertension (AH), type 2 diabetes mellitus (DM), ischemic heart disease (IHD), atrial fibrillation (AF), cigarette smoking and alcohol consumption were determined. The treatment with antiplatelet agents or oral anticoagulants was also taken into account., Results: More than one-third ofpatients, irrespective of group admitted that they had treated AH unsystematically or not treated at all. Based on initial blood pressure, it may be suspected, that also individuals declaring systematic AH treatment, did not do it effectively. It also concerned the type 2 DM - glycemic control remained unsatisfactory within the period preceding first-ever and recurrent stroke. After first stroke, the patients haven't changed their habits considering tobacco smoking and alcohol consumption. The anticoagulants were used relatively seldom in relation to recommendations in both group of patients., Conclusions: The main risk factors for ischemic stroke are poorly controlled by Polish patients before first ever stroke. After the first cerebrovascular event they usually don't change their habits, which lead to recurrent stroke. In Poland the educational strategies regarding repetitive public information on benefits resulting from stroke prevention and fatal stroke consequences should be centered around the general public and the groupof high-risk patients.

Atrial fibrillation, one of the most frequent heart rhythm disturbances and the most common source of embolic material in cerebral circulation, is associated with a fivefold increased risk of ischemic stroke. Except thromboembolic complications, atrial fibrillation affects hemodynamic activity of the heart, reduces cardiac output and might decrease cerebral blood flow. It is possible that atrial fibrillation disturbs autoregulation mechanisms of cerebral circulation in patients suffering from an acute stroke. This could be the reason of higher early mortality and more severe clinical outcome versus strokes in patients with the sinus rhythm. An ongoing increase of population with atrial fibrillation is observed. Such patients often need intensive antithrombotic prevention with oral anticoagulants. Worldwide prescribing effective anticoagulant therapy is insufficient in relation to the needs. The leading reason underlying the under-utilization of oral anticoagulation in patients with atrial fibrillation is the lack of knowledge about importance of this kind of stroke prevention and fear of bleeding among doctors, particularly among general practitioners.

The majority of strokes (85-90%) result from cerebral ischemia. In most cases extra - and intracranial vessel atherosclerotic changes are considered to be responsible for cerebral ischemia. A sudden failure of cerebral circulation is usually combined with instability of atherosclerotic plaques. Pathologic studies demonstrate that atherosclerosis simultaneously involves the whole arterial vessel tree. The mechanism of atherosclerotic plaque formation is similar in different regions of the arterial system, including the brain supplying arteries. The essence of atherosclerosis appears to be an excessive inflammatory-fibroproliferative response to various forms of the arterial wall injury. The development of unstable plaques is closely related to the inflammatory process involving the arterial wall. Immunological factors seem to play an important role in the development of atherosclerotic changes and their destabilization. Imaging techniques for arteries supplying the brain are known. None of them gives a clear answer about plaque instability. Taking into account the role of the inflammatory process in the pathogenesis and instability of atherosclerotic changes, measurement of serologic markers of plaque instability seems to be complementary to imaging methods for diagnosis of unstable atherosclerotic plaques. The inflammatory aspect of atherosclerosis should be reflected in the prophylaxis of the central nervous system vascular disorders.