Akut koroner sendromlu hastalarda endotelyal progenitör hücre sayımı
Akut koroner sendromlu hastalarda endotelyal progenitör hücre sayımı
Yazar: Karagöz, Ahmet; Kocaoğlu, İbrahim; Uçar, Özgül; Örnek, Ender; Serdar, Serkan; Ertürk, Emre; Yetiş Sayın, Begüm
Dergi: Cumhuriyet Tıp Dergisi, Vol. 35 No. 1, 2012
Anahtar kelimeler: Endothelial progenitor cell, acute coronary syndrome, atherosclerosis ; Endotelyal progenitör hücre, akut koroner sendrom, ateroskleroz

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

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.