Exploring the Versatility of Exosomes: A Review on Isolation, Characterization, Detection Methods, and Diverse Applications.

Extracellular vesicles (EVs) are crucial mediators of intercellular communication and can be classified based on their physical properties, biomolecular structure, and origin. Among EVs, exosomes have garnered significant attention due to their potential as therapeutic and diagnostic tools. Exosomes are released via fusion of multivesicular bodies on plasma membranes and can be isolated from various biofluids using methods such as differential ultracentrifugation, immune affinity capture, ultrafiltration, and size exclusion chromatography. Herein, an overview of different techniques for exosome characterization and isolation, as well as the diverse applications of exosome detection, including their potential use in drug delivery and disease diagnosis, is provided. Additionally, we discuss the emerging field of exosome detection by sensors, which offers an up-and-coming avenue for point-of-care diagnostic tools development. Overall, this review aims to provide a exhaustive and up-to-date summary of the current state of exosome research.

Neuroprotective effects of hemicraniectomy in malignant middle cerebral artery infarctions: experimental study.

BACKGROUND: Despite optimal medical therapy the mortality rate approaches 50% in MCA infarctions. Although recent studies have been showed life-saving effect of hemicraniectomy; there are a few data available in regard to neuroprotection effect of decompressive craniectomy (DC). We induced a malignant cerebral ischemia model by intraluminal permanent middle cerebral artery occlusion (MCAo) in male rats for defining the neuroprotective effects of early DC on brain-blood barrier (BBB) molecular changes, infarct size and cerebral edema. METHODS: A total of 48 male Spraque-Dawley rats were allocated to 4 groups; sham (N.=9), control (N.=9), experiment 1 (N.=15), experiment 2 (N.=15). DC was performed by creating a bone flap, after MCAo at 4 and 24 hours. After 28 hours of survival, all animals were sacrificed. Infarction volumes were calculated from TTC (2,3,5-triphenyl-2H-tetrazolium chloride)-stained brain sections. In all groups, cerebral edema was quantified as a change in the percentage of brain water content. Western Blot was used to analyze the expression of tight junction protein claudin-5 and occludin. RESULTS: Brain water content was calculated 75.18±0.75% in the early DC group and 77.76±0.71% in the late DC group. No significant difference was found between experiment groups (P=0.178). In the early DC group; occludin and claudin-5 were significantly expressed at higher levels compared to late DC group (occluding, P=0.013; claudin-5, P=0.034). At early DC group (73.38±23.11 mm3) the final infarct volumes were significantly smaller than in the late DC group (377.18±39.23 mm3) (P=0.013). CONCLUSIONS: The study results supported the neuroprotective effects of early DC in malignant MCA infarcts.

Assessment of the neuroprotective effects of the acetylcholinesterase inhibitor huperzine A in an experimental spinal cord trauma model.

BACKGROUND: Spinal cord injury is nowadays still a challenging disease, and a treatment option aimed at the primary site of injury does not currently exist. Therefore, the management of acute spinal cord injury has recently focused on the reasons behind the aggravation of the initial insult through secondary mechanisms, and the search for pharmacological treatment protocols is generally aimed at reducing and minimizing the neural injury and neurological sequela. The secondary spinal cord injury usually develops following a primary lesion induced by spinal cord contusion and the emergence of apoptotic cells has been found to play an important role in the development of secondary injury. We propose that huperzine A may induce a significant reduction in the number of apoptotic cells because it possesses the ability to protect cells against glutamate, ischemia and staurosporine-induced cytotocity and apoptosis. METHODS: Huperzine A was administered intraperitoneally to male Wistar Albino rats (220-340 g of body weight) after moderate static clip compression (70 g for 60 s) of the spinal cord at T7 level. Neurological functions were assessed using the Basso-Beattle-Breshanan (BBB) motor rating scale until 3th and 7th days before perfusion, following which the spinal cord was harvested for histopathological examinations and apoptotic cell counts. RESULTS: Histopathological evaluations of the spinal cord of the control, trauma and huperzine A treated groups were evaluated. Control group showed normal neuronal and vascular structures of the spinal cord. However, in both trauma groups 3rd- and 7th-day perfusion showed extensive cavitation and hemorrhage, areas of necrosis and edema in gray matter, and degeneration in motor neurons along with patchy areas of necrotic and apoptotic cells. In the group treated with huperzine A, an increased number of normal cells was observed, along with a lower number of necrotic cells, with a significant reduction in the apoptotic cells (P<0.01). The administration of huperzine A improved post-trauma motor performance. Furthermore, BBB scores of all groups showed that there was an improvement of locomotor abilities in the treatment group as compared with the control. CONCLUSIONS: When compared with controls, huperzine A treatment demonstrates a significant reduction in the number of apoptotic cells. In addition, the group treated with huperzine A showed significant and appreciable neurological improvement in rats.

Protective Effect of Ischemic Preconditioning on Myocardium Against Remote Tissue Injury Following Transient Focal Cerebral Ischemia in Diabetic Rats / Efeito Protetor do Pré-Condicionamento Isquêmico no Miocárdio Contra Lesão Remota de Tecidos após Isquemia Cerebral Focal Transitória em Ratos Diabéticos

Abstract Background: Remote ischemic preconditioning (IPreC) could provide tissue-protective effect at a remote site by anti-inflammatory, neuronal, and humoral signaling pathways. Objectives: The aim of the study was to investigate the possible protective effects of remote IPreC on myocardium after transient middle cerebral artery occlusion (MCAo) in streptozotocin- induced diabetic (STZ) and non-diabetic rats. Methods: 48 male Spraque Dawley rats were divided into eight groups: Sham, STZ, IPreC, MCAo, IPreC+MCAo, STZ+IPreC, STZ+MCAo and STZ+IPreC+MCAo groups. We induced transient MCAo seven days after STZ-induced diabetes, and performed IPreC 72 hours before transient MCAo. Remote myocardial injury was investigated histopathologically. Bax, Bcl2 and caspase-3 protein levels were measured by Western blot analysis. Total antioxidant status (TAS), total oxidant status (TOS) of myocardial tissue were measured by colorimetric assay. Oxidative stress index(OSI) was calculated as TOS-to-TAS ratio. For all statistical analysis, p values < 0.05 were considered significant. Results: We observed serious damage including necrosis, congestion and mononuclear cell infiltration in myocardial tissue of the diabetic and ischemic groups. In these groups TOS and OSI levels were significantly higher; TAS levels were lower than those of IPreC related groups (p < 0.05). IPreC had markedly improved histopathological alterations and increased TAS levels in IPreC+MCAo and STZ+IPreC+MCAo compared to MCAo and STZ+MCAo groups (p < 0.05). In non-diabetic rats, MCAo activated apoptotic cell death via increasing Bax/Bcl2 ratio and caspase-3 levels. IPreC reduced apoptotic cell death by suppressing pro-apoptotic proteins. Diabetes markedly increased apoptotic protein levels and the effect did not reversed by IPreC. Conclusions: We could suggest that IPreC attenuates myocardial injury via ameliorating histological findings, activating antioxidant mechanisms, and inducing antiapoptotic activity in diabetic rats.

Resumo Fundamentos: O pré-condicionamento isquêmico remoto (IPreC) poderia fornecer efeito protetor de tecido em um local remoto por vias de sinalização anti-inflamatórias, neuronais e humorais. Objetivos: O objetivo do estudo foi investigar os possíveis efeitos protetores do IPreC remoto no miocárdio após a oclusão transitória da artéria cerebral média (MCAo) em ratos com diabetes induzida por estreptozotocina (STZ) e ratos não diabéticos. Métodos: 48 ratos Spraque Dawley machos foram divididos em oito grupos: grupos Sham, STZ, IPreC, MCAo, IPreC + MCAo, STZ + IPreC, STZ + MCAo e STZ + IPreC + MCAo. Induzimos MCAo sete dias após a diabetes induzida por STZ e realizamos IPreC 72 horas antes do MCAo. A lesão miocárdica remota foi investigada histopatologicamente. Os níveis de proteína Bax, Bcl2 e caspase-3 foram medidos pela análise Western Blot. O estado de antioxidante total (TAS), e o estado de oxidação total (TOS) do tecido miocárdico foram medidos por meio de um estudo colorimétrico. O índice de estresse oxidativo (OSI) foi calculado como a relação TOS-TAS. Para todas as análises estatísticas, os valores de p < 0,05 foram considerados significativos. Resultados: Observamos danos graves, incluindo necrose, congestão e infiltração de células mononucleares no tecido miocárdico dos grupos diabético e isquêmico. Nesses grupos os níveis de TOS e OSI foram significativamente maiores; os níveis de TAS foram inferiores aos dos grupos relacionados com IPreC (p < 0,05). O IPreC melhorou marcadamente as alterações histopatológicas e aumentou os níveis de TAS em IPreC + MCAo e STZ + IPreC + MCAo em comparação com os grupos MCAo e STZ + MCAo (p < 0,05). Em ratos não diabéticos, MCAo activou a morte celular apoptótica através do aumento da relação Bax / Bcl2 e dos níveis de caspase-3. IPreC reduziu a morte celular apoptótica pela supressão de proteínas pró-apoptóticas. O diabetes aumentou acentuadamente os níveis de proteína apoptótica e o efeito não foi revertido pelo IPreC. Conclusões: Podemos sugerir que o IPreC atenua a lesão miocárdica através da melhora dos achados histológicos, ativando mecanismos antioxidantes e induzindo atividade antiapoptótica em ratos diabéticos.

Protective Effect of Ischemic Preconditioning on Myocardium Against Remote Tissue Injury Following Transient Focal Cerebral Ischemia in Diabetic Rats.

BACKGROUND: Remote ischemic preconditioning (IPreC) could provide tissue-protective effect at a remote site by anti-inflammatory, neuronal, and humoral signaling pathways. OBJECTIVES: The aim of the study was to investigate the possible protective effects of remote IPreC on myocardium after transient middle cerebral artery occlusion (MCAo) in streptozotocin- induced diabetic (STZ) and non-diabetic rats. METHODS: 48 male Spraque Dawley rats were divided into eight groups: Sham, STZ, IPreC, MCAo, IPreC+MCAo, STZ+IPreC, STZ+MCAo and STZ+IPreC+MCAo groups. We induced transient MCAo seven days after STZ-induced diabetes, and performed IPreC 72 hours before transient MCAo. Remote myocardial injury was investigated histopathologically. Bax, Bcl2 and caspase-3 protein levels were measured by Western blot analysis. Total antioxidant status (TAS), total oxidant status (TOS) of myocardial tissue were measured by colorimetric assay. Oxidative stress index(OSI) was calculated as TOS-to-TAS ratio. For all statistical analysis, p values < 0.05 were considered significant. RESULTS: We observed serious damage including necrosis, congestion and mononuclear cell infiltration in myocardial tissue of the diabetic and ischemic groups. In these groups TOS and OSI levels were significantly higher; TAS levels were lower than those of IPreC related groups (p < 0.05). IPreC had markedly improved histopathological alterations and increased TAS levels in IPreC+MCAo and STZ+IPreC+MCAo compared to MCAo and STZ+MCAo groups (p < 0.05). In non-diabetic rats, MCAo activated apoptotic cell death via increasing Bax/Bcl2 ratio and caspase-3 levels. IPreC reduced apoptotic cell death by suppressing pro-apoptotic proteins. Diabetes markedly increased apoptotic protein levels and the effect did not reversed by IPreC. CONCLUSIONS: We could suggest that IPreC attenuates myocardial injury via ameliorating histological findings, activating antioxidant mechanisms, and inducing antiapoptotic activity in diabetic rats.

Neuroprotective Effects of Chronic Fenofibrate Treatment via Modulating the Immunoreactivity of Cleaved Caspase-3 in Stroke Induced by Transient Middle Cerebral Artery Occlusion Rat Model.

AIM: Current stroke therapies include lipid-lowering drugs, which reduce inflammation and serve to stabilize the atherosclerotic plaque to demonstrate better outcome and neuroprotection. Peroxisome proliferator activated receptors (PPAR) ? regulates lipid homeostasis and is a target of fibrates, which have a neuroprotective function by various mechanisms. In this study, we aimed to evaluate the role of the PPAR? agonist, fenofibrate, in the modulation of cleaved caspase-3 immunoreactivity and at the final infarct volume in an experimental ischemia/reperfusion rat model by induced transient proximal middle cerebral artery occlusion. MATERIAL AND METHODS: A total of 65 male Sprague Dawley rats were allocated into 4 groups; sham (n =5), experiment 1 (n=20), experiment 2 (n=20), experiment 3 (n=20). All experiment groups were divided to 3 subgroups in order to evaluate the final infarct volume at 24th hour (n=5) and the immunoreactivity of cleaved caspase -3 at different time periods [at first hour (n=5), at 6th hour (n=5), at 24th hour (n=5)] after transient middle cerebral artery occlusion (MCAo). At the study, the experiment groups (Experiment 1 and Experiment 2) were received the fenofibrate-diet during 14 days before ischemia procedure. All animals were sacrificed at 24th hours after MCAo. Infarction volumes were calculated from 2,3,5,triphenyltetrozolium chloride (TTC)- stained brain sections. RESULTS: We found that fenofibrate-therapy reduced significantly more body weight than the other experiment groups (p < 0.05). At the time intervals, a decrease of immunoreactivity of cleaved caspase-3 was significantly observed with fenofibrate therapy after MCAo (p < 0.05). Chronic fenofibrate treatment before cerebral ischemia significantly reduced the infarction size after MCAo compared with the other groups (respectively; p = 0.011 and p < 0.000). CONCLUSION: Fenofibrate treatment has neuroprotective effects on middle cerebral artery infarcts.

The Relationship of Hematoma Growth to Red Blood Cell Distribution Width in Patients with Hypertensive Intracerebral Hemorrhage.

AIM: Hypertension is a primary risk factor for intracerebral hemorrhage (ICH) and is thought to be responsible for about 55% of all ICH cases. Thus, the primary goal of the study was to examine whether the status of vascular rheological factors upon admission to the hospital was associated with hypertensive ICH growth and early outcomes. MATERIAL AND METHODS: Over a 2-year period, the present study evaluated 60 ICH patients who were admitted within the first 12 hours of symptom onset. Brain computed tomography scans were performed at admission and then 24 hours later as a control. Hematoma growth was classified as an volume increase more than 6.5 ml or > 33%, and good outcome was defined using the modified Rankin Scale (mRS) score (? 2 at 3 months). RESULTS: The mean age of the study population was 65.07 ± 11.659 years, with 34 men and 26 women. The leading vascular risk factor was hypertension (86.7%). There were significant associations between the initial red blood cell distribution width (RDW) and hematoma growth (p=0.038). Therefore, hematoma growth in the first 24 hours after symptom onset was significantly related to a poor clinical outcome at 3 months (p = 0.050). CONCLUSION: The study identified significant relationships between the initial RDW and poor outcome as well as the initial RDW and hypertensive hematoma growth. Additionally, this study demonstrated that these parameters are easily obtainable and could be used to effectively evaluate outcomes in ICH patients.

Neuroprotective effect of ischemic preconditioning via modulating the expression of cerebral miRNAs against transient cerebral ischemia in diabetic rats.

OBJECTIVES: In this study, we aimed to evaluate the effect of the Ischemic preconditioning (IPreC) on the expression profile of cerebral miRNAs against stroke by induced transient middle cerebral artery occlusion (MCAo) in diabetic rats. METHODS: Eighty male Spraque Dawley rats were allocated to eight groups. In order to evaluate the expression profile of miRNAs, we induced transient MCAo seven days after STZ-induced diabetes (DM). Also we performed IPreC 72 h before transient MCAo to assess whether IPreC could have a neuroprotective effect against ischemia-reperfusion injury. RESULTS: The general characteristics of STZ-treated rats included reduced body weight and elevated blood glucose levels compared to non-diabetic ones. We demonstrated that miRNA expression profiles, which are determined for biological functions such as aquaporin 4 formation (miR-29b-2, miR-124a-3p, miR-130a, miR-223 and miR-320a), glutamate toxicity (miR107, miR-145, miR-223), salvageable ischemic area (miR-9a, miR-19b, miR-29b-2, miR-341, miR-339-5p, miR-15-5p, miR-99b-5p), and neoangiogenesis (let-7f-5p, miR-126a and miR-322-3p), were regulated following IPreC. Ischemic preconditioning before cerebral ischemia significantly reduced infarction size compared with the other groups [IPreC + MCAo (27 ± 11 mm3) vs. MCAo (109 ± 15 mm3) p < 0.001; DM + IPreC + MCAo (38 ± 9 mm3) vs. DM + MCAo (165 ± 41 mm3) p < 0.001, respectively]. DISCUSSION: The study results revealed the neuroprotective effects of ischemic preconditioning, supported with the upregulated pro-survival miRNAs in MCA infarcts.

The relationship of platelet-to-lymphocyte ratio with clinical outcome and final infarct core in acute ischemic stroke patients who have undergone endovascular therapy.

OBJECTIVES: Of all strokes, 85% are ischemic and intracranial artery occlusion accounts for 80% of these ischemic strokes. Endovascular therapy for acute ischemic stroke was a new modality aiming at resolution of clots in occluded cerebral arteries. The platelet-to-lymphocyte ratio (PLR) was introduced as a potential marker to determine increased inflammation, which is a result of releasing many mediators from the platelets. In this study we aimed to evaluate whether the PLR had a prognostic role in stroke patients undergoing thrombectomy and attempted to determine the effect that this ratio had on their survival. METHODS: Over a three-year period, demographic, clinical, and angiographic findings of 57 consecutive patients with acute ischemic stroke who underwent mechanical thrombectomy were evaluated. RESULTS: The patients were divided into two groups on the basis of a PLR level cut-off value of 145 based on receiver operating characteristic (ROC) curve. Successful revascularization (mTICI 2b and 3) was achieved in 42 of 57 (73.7%) patients; a mTICI 3 state was observed in 21 of 23 patients with low-PLR values (p = .015). Patients with higher PLR values had significantly a score of less than six on the ASPECT scale compared to patients with lower PLR values (p = .005). The patients with low-PLR values had better functional outcomes (mRS ≤ 2) compared with the patients with high-PLR values [respectively, p = .004 (at first month) and p = .014 (at third month)]. DISCUSSION: The platelet-to-lymphocyte ratio could represent pro-thrombotic inflammatory state in acute ischemic stroke patients because having a high-PLR values increased the poor prognosis, the rate of insufficient recanalization, and the size of infarcted area.

Association of platelet-to-lymphocyte ratio with silent brain infarcts in patients with paroxysmal atrial fibrillation.

OBJECTIVES: In this study, we aimed to evaluate whether the inflammation as measured by increased platelet to lymphocyte ratio (PLR) predispose to silent infarcts in patients with paroxysmal atrial fibrillation (PAF). METHODS: The present study investigated a total of 48 new diagnosed patients with PAF who had no signs of stroke. PLR, which was calculated as the ratio of the platelet count to the lymphocyte count, C-reactive protein and erythrocyte sedimentation rate were measured due to evaluate inflammatory state. Magnetic resonance imaging (MRI) was performed to evaluate the presence of silent brain infarcts (SBIs) in patients. We calculated CHA2DS2-VASc scores for stratifying the stroke risk of patients. RESULTS: Among our study population, the mean age was 56.40 ± 8.99; 36 patients were female. The leading vascular risk factor was hypertension (45.8%). SBI was determined in 16 patients (33.3%) on MRI. It was found that a higher PLR is significantly associated with the presence of SBIs in patients with PAF (P = .001). High PLR group showed silent lesions predominantly multiple, greater than 5 mm, bilateral and in the subcortical region; though no statistically significant differences were found in each lesion areas (P = .214; P = .509; P = .746; P = .059, respectively). Of 16 patients who showed SBI, 1 (6.3%) patient had CHA2DS2-Vasc scores of 0; 7 (43.8%) patients had CHA2DS2-Vasc scores of 1; 6 (37.5%) patients had CHA2DS2 -Vasc scores of 2 and 2 (12.5%) patients had CHA2DS2-Vasc scores of 3. We did not find any significant relationship between CHA2DS2-Vasc scores and presence of SBI in the study patients (P = .850). DISCUSSION: High PLR might be a factor to induce inflammatory process on SBIs even with low CHA2DS2-VASc scores.

The evaluation of vitamin D levels in patients with carpal tunnel syndrome.

The aim of this study was to evaluate the relationship between 25-hydroxyvitamin D (25(OH)D) levels and carpal tunnel syndrome (CTS). 25(OH)D levels were checked in 108 consecutive patients with CTS symptoms and 52 healthy controls. All patients underwent nerve conduction studies and completed Boston Carpal Tunnel Questionnaire (BQ) symptom severity and functional status scales to quantify symptom severity, pain status and functional status. There were 57 patients with electrophysiological confirmed CTS (EP+ group) and 51 electrophysiological negative symptomatic patients (EP- group). 25(OH) D deficiency (25(OH)D < 20 ng/ml) was found in 96.1 % of EP- group, in 94.7 % of EP+ group and in 73.8 % of control group. 25(0H) D level was found significantly lower both in EP+ and EP- groups compared to control group (p = 0.006, p < 0.001, respectively). Although mean vitamin D level in EP- group was lower than EP+ group, statistically difference was not significant between EP+ and EP- groups (p = 0.182). BQ symptom severity and functional status scores and BQ pain sum score were not significantly different between EP+ and EP- groups. We found no correlation with 25(OH) D level for BQ symptom severity, functional status and pain sum scores. 25(OH) D deficiency is a common problem in patients with CTS symptoms. As evidenced by the present study, assessment of serum 25(OH)D is recommended in CTS patients even with electrophysiological negative results.

Endovascular therapy of acute ischaemic stroke by interventional cardiologists: single-centre experience from Turkey.

AIMS: We report our single-centre experience with the Solitaire AB self-expanding retrievable stent system in patients with acute ischaemic stroke. METHODS AND RESULTS: Demographic, clinical, and angiographic findings of thirty-eight consecutive patients with acute ischaemic stroke who underwent mechanical thrombectomy were evaluated retrospectively. The mean initial National Institutes of Health Stroke Scale (NIHSS) score was 17.8±4.6. Nearly half of the patients had a middle cerebral artery (MCA) occlusion (45%). Both internal carotid artery and MCA occlusions were detected in five patients. Successful revascularisation (Thrombolysis in Cerebral Infarction [TICI] 2b and 3) was achieved in 34 of 38 (89%) patients; a TICI 3 state was observed in 24 (63%) patients. Almost three quarters of the patients (74.3%) improved by >5 points on the NIHSS at discharge, and 57.9% showed a modified Rankin Scale (mRS) score of ≤2 at 90 days. CONCLUSIONS: This single-centre experience with mechanical thrombectomy devices demonstrated that the procedure could be performed safely with high success rates by experienced interventional cardiologists in suitably equipped cathlabs.

Bilateral jugular vein and sigmoid sinus thrombosis related to an inherited coagulopathy: an unusual presentation.

Internal jugular vein thrombosis (IJVT) is a rare condition associated with malignancy, coagulopathy, and trauma. The optimal management of any IJVT must be individualized and depends on the condition of the patient. Case Presentation. We report the case of a 42-year-old woman with a history of a first trimester spontaneous abortion. Apart from a tension-type headache, she had no neurological symptoms. She reported an incidental diagnosis of right-sided IJVT when she was evaluated for hyperthyroidism ultrasonographically. On ultrasonography, we observed bilateral jugular vein thrombosis. The patient was started on oral warfarin. Seven months later, when she was adequately anticoagulated, she developed a second thrombosis. According to the etiological workup, she had a mutation in the homozygous methylene tetrahydrofolate reductase (MTHFR) gene and reduced protein C levels and activity. Conclusion. This report illustrates an unusual presentation of a rare condition. In this case, the etiology was associated with the coagulopathy, which occurred despite adequate anticoagulation.

Reversible conduction failure in overlap of Miller Fisher syndrome and pharyngeal-cervical-brachial variant of Guillain-Barré syndrome in the spectrum of nodo-paranodopathies.

Patients with an overlap of the pharyngeal-cervical-brachial variant of Guillain-Barré syndrome and Miller Fisher syndrome (PCB/MFS) have rarely been reported. The electrophysiological findings in PCB/MFS are of great interest and may provide insight into the pathophysiology of the disorder. We report the clinical features and nerve conduction study findings in a patient with PCB/MFS with high titers of antiganglioside antibodies against GQ1b, GD1a, and GD1b. In serial nerve conduction studies, compound muscle action potential amplitudes normalised without development of temporal dispersion within 3 weeks, and absent median, ulnar, and sural sensory nerve action potentials became recordable within 4 months. These findings are consistent with reversible conduction failure in both motor and sensory fibres, and PCB/MFS could be classified in the recently described nodo-paranodopathy spectrum of acute neuropathies associated with anti-ganglioside antibodies.

Neutrophil/lymphocyte ratio is associated with thromboembolic stroke in patients with non-valvular atrial fibrillation.

BACKGROUND: Neutrophil/lymphocyte ratio (NLR) has been associated with poor outcomes in patients with cardiovascular diseases. However, little is known about the role of NLR in patients with thromboembolic stroke due to atrial fibrillation (AF). We aimed to compare the NLR ratios between non-valvular AF patients with or without thromboembolic stroke. METHODS: A total of 126 non-valvular AF patients with or without stroke were included in the study; 126 consecutive patients (52 males and 74 females), mean age, 70 ± 10.2 years old. No patient had a recent history of an acute infection or an inflammatory disease. Baseline NLR was measured by dividing neutrophil count to lymphocyte count. WBC count>12.000 cells per µL or <4.000 cells per µL and high body temperature>38 º are excluded from the study. RESULTS: Mean NLR was significantly higher among persons with stroke compared to individuals without a stroke (5.6 ± 3.4 vs. 3.1 ± 2.1, p=0.001). There were no significant differences in RDW levels between the two groups (p>0.05). HAS-BLED and CHADS(2) scores were significantly higher in the stroke group. CONCLUSION: Higher NLR, an emerging marker of inflammation, is associated with thromboembolic stroke in non-valvular AF patients.