Prostaglandin E2, 9S-, 13S-HODE and resolvin D1 are strongly associated with the post-stroke cognitive impairment.

BACKGROUND: Inflammatory derivatives of free fatty acids are involved in the development of neuroinflammation and cognitive dysfunctions. The study aim was to establish the influence of eicosanoids on the cognitive status of stroke patients. METHODS: 73 stroke patients were prospectively evaluated towards the neuropsychological cognitive functions on the 7th day after stroke and after follow-up of 6 months. Eicosanoids levels were measured in all patients and compared to stroke-free controls (n = 30). RESULTS: Prostaglandin E2 was negatively correlated with Montreal Cognitive Assessment (MOCA) test on the 7th day after stroke. The level of 9-hydroxyoctadecadienoic acid (9S-HODE) was significantly higher in patients with cognitive dysfunctions in MOCA test compared to the others (group I mean ± SD: 0.040 ± 0.035 vs. group II: 0.0271 ± 0.016). In the initial neuropsychological assessment maresin 1-, 5-hydroxyeicosatetraenoic acid (HETE), 12S-HETE and 15S-HETE were negatively correlated with California Verbal Learning Test (CVLT) and thus with cognitive functions, while in the follow-up examination negative correlations were identified for prostaglandin E2, meresin 1, leukotriene B4, 13S HODE, 9S-HODE; the only positive correlation was observed in 15S-HETE. Other neuropsychological tests showed a beneficial impact of resolvin D1 and a negative role of prostaglandin E2 was observed in the first examination and in the follow-up. Resolvin D1 and the group of all analyzed eicosanoids predict changes in cognitive functions. CONCLUSIONS: Eicosanoids can play a role in the neuroinflammation. They can affect the cognitive status at the stroke onset and have a predictive value for post-stroke cognitive decline. Prostaglandin E2, 9S-, 13S-HODE and resolvin D1 are the most important inflammatory free fatty acid derivatives in the cognitive functions in stroke. Eicosanoids predict post-stroke cognitive functions.

Could Lipoxins Represent a New Standard in Ischemic Stroke Treatment?

INTRODUCTION: Cardiovascular diseases including stroke are one of the most common causes of death. Their main cause is atherosclerosis and chronic inflammation in the body. An ischemic stroke may occur as a result of the rupture of unstable atherosclerotic plaque. Cardiovascular diseases are associated with uncontrolled inflammation. The inflammatory reaction produces chemical mediators that stimulate the resolution of inflammation. One of these mediators is lipoxins-pro-resolving mediators that are derived from the omega-6 fatty acid family, promoting inflammation relief and supporting tissue regeneration. AIM: The aim of the study was to review the available literature on the therapeutic potential of lipoxins in the context of ischemic stroke. MATERIAL AND METHODS: Articles published up to 31 January 2021 were included in the review. The literature was searched on the basis of PubMed and Embase in terms of the entries: 'stroke and lipoxin' and 'stroke and atherosclerosis', resulting in over 110 articles in total. Studies that were not in full-text English, letters to the editor, and conference abstracts were excluded. RESULTS: In animal studies, the injection/administration of lipoxin A4 improved the integrity of the blood-brain barrier (BBB), decreased the volume of damage caused by ischemic stroke, and decreased brain edema. In addition, lipoxin A4 inhibited the infiltration of neutrophils and the production of cytokines and pro-inflammatory chemokines, such as interleukin (Il-1ß, Il-6, Il-8) and tumor necrosis factor-α (TNF-α). The beneficial effects were also observed after introducing the administration of lipoxin A4 analog-BML-111. BML-111 significantly reduces the size of a stroke and protects the cerebral cortex, possibly by reducing the permeability of the blood-brain barrier. Moreover, more potent than lipoxin A4, it has an anti-inflammatory effect by inhibiting the production of pro-inflammatory cytokines and increasing the amount of anti-inflammatory cytokines. CONCLUSIONS: Lipoxins and their analogues may find application in reducing damage caused by stroke and improving the prognosis of patients after ischemic stroke.

The Role of Thromboxane in the Course and Treatment of Ischemic Stroke: Review.

Cardiovascular diseases are currently among the leading causes of morbidity and mortality in many developed countries. They are distinguished by chronic and latent development, a course with stages of worsening of symptoms and a period of improvement, and a constant potential threat to life. One of the most important disorders in cardiovascular disease is ischemic stroke. The causes of ischemic stroke can be divided into non-modifiable and modifiable causes. One treatment modality from a neurological point of view is acetylsalicylic acid (ASA), which blocks cyclooxygenase and, thus, thromboxane synthesis. The legitimacy of its administration does not raise any doubts in the case of the acute phase of stroke in patients in whom thrombolytic treatment cannot be initiated. The measurement of thromboxane B2 (TxB2) in serum (a stable metabolic product of TxA2) is the only test that measures the effect of aspirin on the activity of COX-1 in platelets. Measurement of thromboxane B2 may be a potential biomarker of vascular disease risk in patients treated with aspirin. The aim of this study is to present the role of thromboxane B2 in ischemic stroke and to present effective therapies for the treatment of ischemic stroke. Scientific articles from the PubMed database were used for the work, which were selected on the basis of a search for "thromboxane and stroke". Subsequently, a restriction was introduced for works older than 10 years, those concerning animals, and those without full text access. Ultimately, 58 articles were selected. It was shown that a high concentration of TXB2 may be a risk factor for ischemic stroke or ischemic heart disease. However, there is insufficient evidence to suggest that thromboxane could be used in clinical practice as a marker of ischemic stroke. The inclusion of ASA in the prevention of stroke has a beneficial effect that is associated with the effect on thromboxane. However, its insufficient power in 25% or even 50% of the population should be taken into account. An alternative and/or additional therapy could be a selective antagonist of the thromboxane receptor. Thromboxane A2 production is inhibited by estrogen; therefore, the risk of CVD after the menopause and among men is higher. More research is needed in this area.

Free Fatty Acids and Their Inflammatory Derivatives Affect BDNF in Stroke Patients.

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.

The Role of Resolvins: EPA and DHA Derivatives Can Be Useful in the Prevention and Treatment of Ischemic Stroke.

INTRODUCTION: Most ischemic strokes develop as a result of atherosclerosis, in which inflammation plays a key role. The synthesis cascade of proinflammatory mediators participates in the process induced in the vascular endothelium and platelets. Resolvins are anti-inflammatory mediators originating from eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which may improve the prognosis related to atherosclerosis by inhibiting the production of proinflammatory cytokines, limiting neutrophil migration, or positively influencing phagocytosis. Although clinical trials with resolvin in humans after stroke have not been realized, they may soon find application. AIM: The aim of the study was to review the available literature on the scope of the possibilities of the prevention and treatment of stroke with the use of resolvins, EPA and DHA derivatives. MATERIALS AND METHODS: The review features articles published until 31 January 2020. The search for adequate literature was conducted using the keywords: stroke and resolvins. Over 150 articles were found. Studies not written in English, letters to the editor, conference abstracts, and duplicate information were excluded. RESULTS: In several studies using the animal model, the supplementation of resolvin D2 decreased brain damage caused by myocardial infarction, and it reversed the neurological dysfunction of the brain. A decrease in the concentration of proinflammatory cytokines, such as TNF-α, Il-6, and Il-1ß, was also observed, as well as a decrease in the scope of brain damage. In the context of stroke in animals, the treatment with resolvin D2 (RvD2) (injection) has a better effect than supplementation with DHA. CONCLUSIONS: Resolvins are characterised by strong anti-inflammatory properties. Resolvins improve prognosis and decrease the risk of developing cardiovascular disease, consequently lowering the risk of stroke, and may find application in the treatment of stroke.

The Association of Free Fatty Acids and Eicosanoids with the Severity of Depressive Symptoms in Stroke Patients.

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.

The role of brain-derived neurotrophic factor and its single nucleotide polymorphisms in stroke patients.

Stroke is the main cause of motoric and neuropsychological disability in adults. Recent advances in research into the role of the brain-derived neurotrophic factor in neuroplasticity, neuroprotection and neurogenesis might provide important information for the development of new poststroke-rehabilitation strategies. It plays a role as a mediator in motor learning and rehabilitation after stroke. Concentrations of BDNF are lower in acute ischemic-stroke patients compared to controls. Lower levels of BDNF are correlated with an increased risk of stroke, worse functional outcomes and higher mortality. BDNF signalling is dependent on the genetic variation which could affect an individual's response to recovery after stroke. Several single nucleotide polymorphisms of the BDNF gene have been studied with regard to stroke patients, but most papers analyse the rs6265 which results in a change from valine to methionine in the precursor protein. Subsequently a reduction in BDNF activity is observed. There are studies indicating the role of this polymorphism in brain plasticity, functional and morphological changes in the brain. It may affect the risk of ischemic stroke, post-stroke outcomes and the efficacy of the rehabilitation process within physical exercise and transcranial magnetic stimulation. There is a consistent trend of Met alleles' being connected with worse outcomes and prognoses after stroke. However, there is no satisfactory data confirming the importance of Met allele in stroke epidemiology and the post-stroke rehabilitation process. We present the current data on the role of BDNF and polymorphisms of the BDNF gene in stroke patients, concentrating on human studies.

Early Emergency Medical Service Calls for Stroke: Was the Long-Term Education Program Based on the Experience of West Pomerania Successful?

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.

Association between selected gene polymorphisms and statin metabolism, risk of ischemic stroke and cardiovascular disorders.

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.

The emotional stress and risk of ischemic stroke.

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.

Simultaneous acute shoulder arthritis and multiple mononeuropathy in a newly diagnosed type 2 diabetes patient - First case report.

Diabetes is a common disorder that leads to the musculoskeletal symptoms such as the shoulder arthritis. The involvement of peripheral nervous system is one of the troublesome for the patients as it provokes chronic sensory symptoms, lower motor neuron involvement and autonomic symptoms. In the course of the disease there has been several types of neuropathies described. A 41-year-old male patient was admitted to the internal medicine department because of the general weakness, malaise, polydypsia and polyuria since several days. The initial blood glucose level was 780mg/dl. During the first day the continuous insulin infusion was administered. On the next day when he woke up, the severe pain in the right shoulder with limited movement, right upper extremity weakness and burning pain in the radial aspect of this extremity appeared. On examination right shoulder joint movement limitation was found with the muscle weakness and sensory symptoms in the upper limbs. The clinical picture indicated on the right shoulder arthritis and the peripheral nervous system symptoms such as the right musculocutaneous, supraspinatus, right radial nerve and left radial nerve damage. We present a first case report of simultaneous, acute involvement of the shoulder joint and multiple neuropathy in a patient with newly diagnosed type 2 diabetes, presumably in the state of ketoacidosis.

Potential role of statins in the intracerebral hemorrhage and subarachnoid hemorrhage.

Statins are used in primary and secondary prevention of cardiovascular episodes. Most of recent studies regard ischemic stroke. There are more emerging results of studies suggesting usefulness of these drugs in the other types of stroke e.g. intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). Searching for new methods of treatment is important, because both ICH and SAH lead to poor prognosis and severe psychomotor disability. The unquestionable role of inflammatory factors in the pathogenesis of these disorders justifies considering statin treatment. Previous results are contradictory, thus in present study we review results of studies and try to explain the potential pathomechanism of statin use in hemorrhagic strokes.

Atrial fibrillation and stroke - Coexistence and attitude to preventive therapy on the basis of Szczecin and Szczecin region patients.

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.

Risk factors of stroke and -717A>G (rs2794521) CRP gene polymorphism among stroke patients in West Pomerania province of Poland.

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.

Quality of Life in Female Patients with Overactive Bladder after Botulinum Toxin Treatment.

BACKGROUND: Manifestations of OAB can considerably diminish the quality of life. Botulinum toxin has emerged as a valuable treatment option in diseases whose symptoms cannot be controlled adequately with other available therapies. The aim of the present study was to compare the subjective quality of life of patients with OAB before the injection of botulinum toxin and three and six months after the intervention. METHODS: This study was based on a diagnostic survey with three validated questionnaires, ICIQ-OAB, ICIQ-OABqol, and ICIQ-LUTSqol, and an additional questionnaire developed by the authors to collect sociodemographic characteristics and selected medical data. RESULTS: This study demonstrated significant differences between pre-treatment scores and those at three and six months post injection. At three and six months after the intervention, mean scores for all three instruments (ICIQ-OAB, ICIQ-OABqol, ICIQ-LUTSqol) were significantly lower than the respective pre-treatment values, implying a significant attenuation of OAB symptoms and their lower impact on the quality of life. However, the severity of OAB symptoms and their impact on the quality of life at six months post intervention were significantly higher than at three months, except for the social interaction domain. CONCLUSIONS: Botulinum toxin is an effective treatment for OAB.

[Pathogenetic justification of statin use in ischaemic stroke prevention according to inflammatory theory in development of atherosclerosis]. / Patogenetyczne uzasadnienie stosowania statyn w profilaktyce udaru niedokrwiennego mózgu w swietle zapalnej teorii rozwoju miazdzycy.

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.

Smoking Affects the Post-Stroke Inflammatory Response of Lipid Mediators in a Gender-Related Manner.

The main goal of our study was to determine the effect of cigarette smoking on selected derivatives of arachidonic acid, linoleic acid, DHA, and EPA, which may be markers of post-stroke inflammation. The eicosanoid profile was compared in both smoking and non-smoking patients, without division and with division into gender. In the group of non-smokers, we observed higher levels of the linolenic acid derivative (LA) 9S HODE (p ≤ 0.05) than in smokers. However, after dividing the results by sex, it turned out that the level of this derivative was higher in non-smoking women compared to smoking women (p ≤ 0.01) and did not differentiate the group of men. Similarly, the level of the arachidonic acid metabolite LTX A4 (p ≤ 0.05) differed only in the group of women. In this group, we also observed a decreased level of 15S HETE in smoking women, but it was statistically insignificant (p ≤ 0.08). On the other hand, the level of this derivative was statistically significantly higher in the group of non-smoking women compared to male non-smokers. The group of men was differentiated by two compounds: TXB2 and NPD1. Male smokers had an almost two-fold elevation of TXB2 (p ≤ 0.01) compared with non-smokers, and in this group, we also observed an increased level of NPD1 compared with male non-smokers. On the other hand, when comparing female non-smokers and male non-smokers, in addition to the difference in 15S HETE levels, we also observed elevated levels of TXB2 in the group of non-smokers. We also analyzed a number of statistically significant correlations between the analyzed groups. Generally, men and women smokers showed a much smaller amount of statistically significant correlations than non-smokers. We believe that this is related to the varying degrees of inflammation associated with acute ischemic stroke and post-stroke response. On the one hand, tobacco smoke inhibits the activity of enzymes responsible for the conversion of fatty acids, but on the other hand, it can cause the failure of the inflammatory system, which is also the body's defense mechanism. Smoking cigarettes is a factor that increases oxidative stress even before the occurrence of a stroke incident, and at the same time accelerates it and inhibits post-stroke repair mechanisms. This study highlights the effect of smoking on inflammation in both genders mediated by lipid mediators, which makes smoking cessation undeniable.

High Levels of Thromboxane (TX) Are Associated with the Sex-Dependent Non-Dipping Phenomenon in Ischemic Stroke Patients.

BACKGROUND: Inflammation and high blood pressure (nondipping profile) during the rest/sleep period have been associated with an effect on the incidence of cardiovascular disorders and a more severe course in the ischemic cerebrovascular event. There are no available data on the relationship between dipping status and the pro-inflammatory metabolites of arachidonic acid (AA); therefore, we undertook a study to investigate the influence of thromboxane on the incidence of nondipping among patients after stroke. METHODS: Sixty-two patients with ischemic stroke (including 34 women and 28 men) were tested for the involvement of thromboxane in the nondipping phenomenon. Subjects were analyzed for the presence of the physiological phenomenon of dipping (DIP group) versus its absence-nondipping (NDIP group). Thromboxane (TX) measurements were performed using liquid chromatography, and blood pressure was measured 24 h a day in all subjects. RESULTS: The analysis of the thromboxane level in the plasma of patients after ischemic stroke showed significant differences in terms of sex (p = 0.0004). Among women in both groups, the concentration of TX was high, while similar levels were observed in the group of men from the NDIP group. However, when comparing men in the DIP and NDIP groups, a lower TX level was noticeable in the DIP group. CONCLUSIONS: A higher level of TX may be associated with a disturbance of the physiological phenomenon of DIP in men and women. However, in our opinion, TX is not the main determinant of the DIP phenomenon and, at the same time, other pro-inflammatory factors may also be involved in the occurrence of this singularity.

Fatty Acid Levels and Their Inflammatory Metabolites Are Associated with the Nondipping Status and Risk of Obstructive Sleep Apnea Syndrome in Stroke Patients.

BACKGROUND: This paper discusses the role of inflammation in the pathogenesis of nondipping blood pressure and its role in the pathogenesis of obstructive sleep apnea syndrome. The aim of the study was to assess the impact of free fatty acids (FAs) and their inflammatory metabolites on the nondipping phenomenon and the risk of sleep apnea in stroke patients. METHODS: Sixty-four ischemic stroke patients were included in the prospective study. Group I consisted of 33 patients with a preserved physiological dipping effect (DIP), while group II included 31 patients with the nondipping phenomenon (NDIP). All subjects had FA gas chromatography and inflammatory metabolite measurements performed with the use of liquid chromatography, their 24 h blood pressure was recorded, and they were assessed with the Epworth sleepiness scale (ESS). RESULTS: In the nondipping group a higher level of C16:0 palmitic acid was observed, while lower levels were observed in regard to C20:0 arachidic acid, C22:0 behenic acid and C24:1 nervonic acid. A decreased leukotriene B4 level was recorded in the nondipping group. None of the FAs and derivatives correlated with the ESS scale in the group of patients after stroke. Correlations were observed after dividing into the DIP and NDIP groups. In the DIP group, a higher score of ESS was correlated with numerous FAs and derivatives. Inflammation of a lower degree and a higher level of anti-inflammatory mediators from EPA and DHA acids favored the occurrence of the DIP. A high level of C18: 3n6 gamma linoleic acid indicating advanced inflammation, intensified the NDIP effect. CONCLUSIONS: We demonstrated potential novel associations between the FA levels and eicosanoids in the pathogenesis of the nondipping phenomenon. There are common connections between fatty acids, their metabolites, inflammation, obstructive sleep apnea syndrome and nondipping in stroke patients.

Free Fatty Acids Are Associated with the Cognitive Functions in Stroke Survivors.

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.