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Giriş: İnflamasyon ve oksidatif stres artmış kardiyovasküler risk ile ilişkilidir.Duke koşu bandı skoru ve kalp hızı toparlanması (KHT) gibi egzersizelektrokardiyografi (EKG) testinden türetilen parametreler prognostik önemesahiptir ve kardiyovasküler risk tahmini için kullanılabilir. Endokan vetiyol/disülfid dengesi, inflamatuvar ve oksidatif durumu yansıtan yenibiyolojik belirteçlerdir. Bu çalışmanın amacı, bir egzersiz EKG testi yapılanhastalarda serum tiyol/disülfid dengesi ve endokan düzeylerini araştırmak ve bubelirteçlerin Duke treadmill skoru ve KHT ile ilişkisini değerlendirmektir.Hastalar veYöntem: Tanısal egzersiz EKG testi yapılan hastalar Duke skoruve KHT’ye göre iki gruba ayrıldı. Yüksek Duke skoru-orta/düşük Duke skorugrupları ile künt ve normal KHT grupları arasında serum endokan düzeyleri vetiyol/disülfid dengesi karşılaştırıldı.Bulgular: Serum endokan düzeyleri, Duke treadmill skoru ve KHT’ye göre gruplararasında benzerdi. Tiyol /disülfid oranı, azalmış KHT’li hastalarda normalKHT’li hastalara göre anlamlı derecede düşüktü. Yüksek/Duke skoru olanhastalarda, düşük/orta Duke skoru olan hastalara göre, serum nativ tiyoldüzeyleri, total tiyol düzeyleri ve total tiyol/disülfid oranı anlamlı olarakyüksekti. Doğal tiyol düzeyleri ve total tiyol düzeyleri Duke skoru ile anlamlıkorelasyon göstermekteydi. Çok değişkenli regresyon analizinde, azalmışKHT’inin bağımsız öngördürücüleri hipertansiyon ve diyabet varlığı; düşük/ortaDuke skorunun bağımsız öngördürücüleri ise hipertansiyon varlığı ve düşükendokan düzeyleridir.Sonuç: Serum tiyol düzeyleri Dukeskoru ile ilişkilidir ve düşük endokan seviyeleri düşük/orta Duke skoru ileilişkilidir., Introduction:Inflammationand oxidative stress are associated with increased risk of cardiovasculardiseases. Parameters derived from exercise electrocardiography (ECG) test, suchas Duke treadmill score and heart rate recovery (HRR), have prognosticimportance and can be used to predict cardiovascular risk. Endocan andthiol/disulfide homeostasis are emerging biomarkers that reflect theinflammatory and oxidative status. The aim of this study was to investigateserum thiol/disulfide homeostasis and endocan levels in an exercise ECG testingpatient cohort and to evaluate the association of these markers with Duketreadmill score and HRR.Patientsand Methods: Patients who underwent diagnostic exercise ECG test weredivided into two groups according to Duke treadmill score and HRR. Serumendocan levels and thiol/disulfide homeostasis were compared between high andlow/intermediate Duke treadmill score groups and blunted and normal HRR groups.Results: Serumendocan levels were similar between the groups according to Duke treadmillscore and HRR. Thiol/disulfide ratio was significantly lower in patients withblunted HRR than in those with normal HRR. Serum native thiol levels, totalthiol levels, and total thiol/disulfide ratio were significantly elevated inpatients with a high Duke treadmill score than in those with low/intermediateDuke treadmill score. Native thiol levels and total thiol levels weresignificantly correlated with Duke treadmill score. Multivariate regressionanalysis revealed that hypertension and diabetes were independent predictors ofblunted HRR, whereas hypertension and low endocan levels were those oflow/intermediate Duke treadmill score.Conclusion: Serum thiol levels arecorrelated with Duke treadmill score, and low endocan levels are associatedwith low/intermediate Duke treadmill score.

Aim. Endothelial progenitor cells repair related region by removal of damaged endothelial cells mechanically or replacing endothelial cells via migration from bone marrow to peripheric blood pool with stimulus of cytokines. Previously, it has been shown that number of these cells decrease in chronic stage of stable coronary heart disease, whereas they increase in number in acute coronary syndromes. The aim of this study is to investigate the difference in the number of endothelial progenitor cells among subgroups of acute coronary syndrome (ST elevation myocardial infarction, non-ST elevation myocardial infarction and unstable angina pectoris ) in patients hospitalized in coronary intensive care unit. Method. The study data were analysed in two steps. In the first step, it has been investigated whether there were any differences regarding endothelial progenitor cell count among three subgroups of acute coronary syndrome (n=112). In the second step, a further 13 patients who were hospitalized with a prediagnosis of unstabil angina pectoris and subsequently reported to have normal echocardiography and coronary angiography were also enrolled. The patients were divided into two groups; the patients with unstabil angina pectoris of whom no increase in cardiac enzymes detected indicating the absence of any cardiac damage and patients with normal coronary angiography findings constituted the first group (Grup A, n=41) and the patients with ST elevation myocardial infarction and non-ST elevation myocardial infarction of whom an increase in cardiac enzymes detected indicating a documented cardiac damage constituted the second group (Grup B, n=84). We investigated whether there were any differences regarding endothelial progenitor cell count between these two groups. Results. Our results indicate that the number of endothelial progenitor cells did not differ significantly among these three groups in the first step (3.87 ± 2.74, 5.46 ± 6.38 and 3.95 ± 2.94, respectively; p=0.232). The results of the statistical analysis also revealed no differences between Grup A and Grup B regarding EPC counts (3.89 ± 2.81 vs 4.80 ± 5.22; p=0.302). Conclusion. In the light of these data, in coronary heart disease in which resistance to treatment is a topical problem despite improvements in therapeutic modalities, further clinical studies are needed about the number and the functions of these cells in the bone marrow and peripheric blood, their effects on target tissues and the factors regulating them, for theurapeutic use of these cells., Özet Amaç. Endotelyal progenitör hücreler mekanik olarak endotel hücrelerinin hasarlanarak uzaklaştırılması ile ya da sitokinlerin uyarımı ile kemik iliğinden periferik kana göç ederek hasar bölgesindeki endotel hücrelerinin yerine geçerek ilgili alanı onarmaktadırlar. Daha önce bu hücrelerin stabil koroner arter hastalarında kronik süreçte azaldığı, akut koroner sendrom hastalarında ise sayıca arttığı gösterilmişti. Bu çalışmanın amacı akut koroner sendrom tanısı ile koroner yoğun bakım ünitesine yatırılan hastalarda hastalığın alt grupları arasında (ST elevasyonlu miyokard infarktüsü, ST elevasyonlu olmayan miyokard infarktüsü ve anstabil angina pektoris ) endotelyal progenitor hücre sayıları bakımından fark olup olmadığının incelenmesidir. Yöntem. Çalışma verileri iki aşamada analiz edildi. İlk aşamada akut koroner sendrom sınıflamasında yer alan üç alt grup (n=112) arasında endotelyal progenitor hücre sayıları arasında fark olup olmadığı araştırıldı. Analizin ikinci aşamasında ise unstabil angına pektoris ön tanısı ile hospitalize edilen fakat enzim yüksekliği olmayan, koroner anjiografi ve ekokardiyografileri normal olarak saptanan 13 hasta daha değerlendirmeye alındı. Hastalar, enzim yüksekliği saptanmayan yani kardiyak hasarın olmadığı unstabil angına pektoris hastaları ve koroner anjiografide normal koroner arterlerin saptandığı hastalar bir grup (Grup A, n=41), kardiyak enzim yüksekliği saptanan yani kardiyak hasarın dökümente olduğu, ST elevasyonlu miyokard enfarktüsü ve ST elevasyonsuz miyokard enfarktüsü hastaları diğer bir grup (Grup B, n=84) olmak üzere iki gruba ayrıldı ve bu iki grup arasında endotelyal progenitor hücreler sayıları açısından fark olup olmadığına bakıldı. Bulgular. Çalışma bulgularımız iç grup arasında arasında endotelyal progenitor hücre sayısı açısından istatistiksel olarak anlamlı farklılık olmadığını göstermiştir (sırasıyla 3,87 ± 2,74, 5,46 ± 6,38 ve 3,95 ± 2,94, p=0,232). Yapılan istatistiksel analiz sonucunda Grup A ve Grup B arasında da endotelya progenitor hücre sayıları açısından anlamlı farklılık saptanmadı (3,89 ± 2,81’e karşılık 4,80 ± 5,22; p=0,302). Sonuç. Bu bilgiler ışığında, tedavi modalitelerindeki gelişmelere rağmen halen tedavi direnci sorununun gündemde olduğu koroner arter hastalığında bu hücrelerin terapötik yaklaşımlarda kullanılması için kemik iliğinde ve periferik kandaki sayı ve fonksiyonları, hedef dokudaki etkileri ve bu hücreleri etkileyen düzenleyici faktörler konusunda daha ileri klinik çalışmalara ihtiyaç duyulmaktadır. Anahtar sözcükler: Endotelyal progenitör hücre, akut koroner sendrom, ateroskleroz Abstract Aim. Endothelial progenitor cells repair related region by removal of damaged endothelial cells mechanically or replacing endothelial cells via migration from bone marrow to peripheric blood pool with stimulus of cytokines. Previously, it has been shown that number of these cells decrease in chronic stage of stable coronary heart disease, whereas they increase in number in acute coronary syndromes. The aim of this study is to investigate the difference in the number of endothelial progenitor cells among subgroups of acute coronary syndrome (ST elevation myocardial infarction, non-ST elevation myocardial infarction and unstable angina pectoris ) in patients hospitalized in coronary intensive care unit. Method. The study data were analysed in two steps. In the first step, it has been investigated whether there were any differences regarding endothelial progenitor cell count among three subgroups of acute coronary syndrome (n=112). In the second step, a further 13 patients who were hospitalized with a prediagnosis of unstabil angina pectoris and subsequently reported to have normal echocardiography and coronary angiography were also enrolled. The patients were divided into two groups; the patients with unstabil angina pectoris of whom no increase in cardiac enzymes detected indicating the absence of any cardiac damage and patients with normal coronary angiography findings constituted the first group (Grup A, n=41) and the patients with ST elevation myocardial infarction and non-ST elevation myocardial infarction of whom an increase in cardiac enzymes detected indicating a documented cardiac damage constituted the second group (Grup B, n=84). We investigated whether there were any differences regarding endothelial progenitor cell count between these two groups. Results. Our results indicate that the number of endothelial progenitor cells did not differ significantly among these three groups in the first step (3.87 ± 2.74, 5.46 ± 6.38 and 3.95 ± 2.94, respectively; p=0.232). The results of the statistical analysis also revealed no differences between Grup A and Grup B regarding EPC counts (3.89 ± 2.81 vs 4.80 ± 5.22; p=0.302). Conclusion. In the light of these data, in coronary heart disease in which resistance to treatment is a topical problem despite improvements in therapeutic modalities, further clinical studies are needed about the number and the functions of these cells in the bone marrow and peripheric blood, their effects on target tissues and the factors regulating them, for theurapeutic use of these cells. Keywords: Endothelial progenitor cell, acute coronary syndrome, atherosclerosis

Increased microvascular resistance due to chronic inflammation is assumed to be one of the mechanisms associated with coronary slow flow (CSF). Previous studies have shown that the platelet-to-lymphocyte ratio (PLR) and the neutrophil-lymphocyte ratio (NLR) are markers of inflammation for various diseases. In this study we aimed to evaluate the relationship between CSF and PLR-NLR.Seventy-eight patients with CSF and 50 patients with normal coronary flow were enrolled into this study. The study subjects underwent medical examination and testing, after which their platelet-to-lymphocyte ratios and NLR values were calculated. An independent observer measured the coronary flow rate by Thrombolysis in Myocardial Infarction Frame Count (TFC) method. The platelet-to-lymphocyte ratio and NLR values were compared between the groups and correlation analysis was performed to explore the relationship between mean TFC with PLR and NLR.Platelet-to-lymphocyte ratio and NLR values were significantly higher in patients with CSF (p0.001). There was a positive significant correlation between TFC with NLR and PLR (Spearman's Rho: 0.59, p0.001 and Spearman's Rho: 0.30, p = 0.001, respectively). Multivariate logistic regression analysis revealed that NLR is the one independent predictor for CSF.This study demonstrated an association between CSF and PLR-NLR. Although the exact mechanism could not be explained, our findings support the possible role of inflammation in CSF physiopathology.