Akut koroner sendromlu hastalarda endotelyal progenitör hücre sayımı

Amaç. Endotelyal progenitör hücreler mekanik olarak endotel hücrelerinin hasarlanarakuzaklaştırılması ile ya da sitokinlerin uyarımı ile kemik iliğinden periferik kana göç ederek hasarbölgesindeki endotel hücrelerinin yerine geçerek ilgili alanı onarmaktadırlar. Daha önce buhücrelerin stabil koroner arter hastalarında kronik süreçte azaldığı, akut koroner sendromhastalarında ise sayıca arttığı gösterilmişti. Bu çalışmanın amacı akut koroner sendrom tanısı ilekoroner yoğun bakım ünitesine yatırılan hastalarda hastalığın alt grupları arasında (ST elevasyonlumiyokard 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 yeralan üç alt grup (n=112) arasında endotelyal progenitor hücre sayıları arasında fark olup olmadığıaraştırıldı. Analizin ikinci aşamasında ise unstabil angına pektoris ön tanısı ile hospitalize edilenfakat enzim yüksekliği olmayan, koroner anjiografi ve ekokardiyografileri normal olarak saptanan13 hasta daha değerlendirmeye alındı. Hastalar, enzim yüksekliği saptanmayan yani kardiyakhasarın olmadığı unstabil angına pektoris hastaları ve koroner anjiografide normal koronerarterlerin saptandığı hastalar bir grup (Grup A, n=41), kardiyak enzim yüksekliği saptanan yanikardiyak hasarın dökümente olduğu, ST elevasyonlu miyokard enfarktüsü ve ST elevasyonsuzmiyokard enfarktüsü hastaları diğer bir grup (Grup B, n=84) olmak üzere iki gruba ayrıldı ve buiki grup arasında endotelyal progenitor hücreler sayıları açısından fark olup olmadığına bakıldı.Bulgular. Çalışma bulgularımız iç grup arasında arasında endotelyal progenitor hücre sayısıaçısından 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 arasındada endotelya progenitor hücre sayıları açısından anlamlı farklılık saptanmadı (3,89 ± 2,81ekarşılık 4,80 ± 5,22; p=0,302). Sonuç. Bu bilgiler ışığında, tedavi modalitelerindeki gelişmelererağmen halen tedavi direnci sorununun gündemde olduğu koroner arter hastalığında bu hücrelerinterapötik yaklaşımlarda kullanılması için kemik iliğinde ve periferik kandaki sayı ve fonksiyonları,hedef dokudaki etkileri ve bu hücreleri etkileyen düzenleyici faktörler konusunda daha ileri klinikçalışmalara ihtiyaç duyulmaktadır.

Endothelial progenitor cell count in patients with acute coronary syndrome

Aim. Endothelial progenitor cells repair related region by removal of damaged endothelial cellsmechanically or replacing endothelial cells via migration from bone marrow to peripheric bloodpool with stimulus of cytokines. Previously, it has been shown that number of these cells decreasein chronic stage of stable coronary heart disease, whereas they increase in number in acutecoronary syndromes. The aim of this study is to investigate the difference in the number ofendothelial progenitor cells among subgroups of acute coronary syndrome (ST elevationmyocardial infarction, non-ST elevation myocardial infarction and unstable angina pectoris ) inpatients hospitalized in coronary intensive care unit. Method. The study data were analysed in twosteps. In the first step, it has been investigated whether there were any differences regardingendothelial progenitor cell count among three subgroups of acute coronary syndrome (n=112). Inthe second step, a further 13 patients who were hospitalized with a prediagnosis of unstabil anginapectoris and subsequently reported to have normal echocardiography and coronary angiographywere also enrolled. The patients were divided into two groups; the patients with unstabil anginapectoris of whom no increase in cardiac enzymes detected indicating the absence of any cardiacdamage and patients with normal coronary angiography findings constituted the first group (GrupA, n=41) and the patients with ST elevation myocardial infarction and non-ST elevationmyocardial infarction of whom an increase in cardiac enzymes detected indicating a documentedcardiac damage constituted the second group (Grup B, n=84). We investigated whether there wereany differences regarding endothelial progenitor cell count between these two groups. Results.Our results indicate that the number of endothelial progenitor cells did not differ significantlyamong 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 andGrup B regarding EPC counts (3.89 ± 2.81 vs 4.80 ± 5.22; p=0.302). Conclusion. In the light ofthese data, in coronary heart disease in which resistance to treatment is a topical problem despiteimprovements in therapeutic modalities, further clinical studies are needed about the number andthe functions of these cells in the bone marrow and peripheric blood, their effects on target tissuesand the factors regulating them, for theurapeutic use of these cells.

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  • 1. Hennekens CH. Risk factors for coronary heart disease in women. Cardiol Clin 1998; 16: 1-8.
  • 2. Onat A, Sansoy V, Soydan İ, Tokgözoğlu L, Adalet K. TEKHARF Oniki yıllık izlenimlerine göre Türk eriskinlerinde kalp sağlıgı. Argos iletisim hizmetleri reklamcılık ve ticaret AŞ. Temmuz İstanbul-2003.
  • 3. Sans S, Kesteloot H, Kromhout D. The burden of cardiovascular diseases mortality in Europe. Task Force of the European Society of Cardiology on Cardiovascular Mortality and Morbidity Statistics in Europe. Eur Heart J 1997; 18: 1231-48.
  • 4. Ross R, Glomset J, Harker L. Response to injury and atherogenesis. Am J Pathol 1977; 86: 675-84.
  • 5. Gulati R, Jevremovic D, Peterson TE, Witt TA, Kleppe LS, Mueske CS, Lerman A, Vile RG, Simari RD. Autologous culture-modified mononuclear cells confer vascular protection after arterial injury. Circulation 2003; 108: 1520-6.
  • 6. He T, Smith LA, Harrington S, Nath KA, Caplice NM, Katusic ZS. Transplantation of circulating endothelial progenitor cells restores endothelial function of denuded rabbit carotid arteries. Stroke 2004; 35: 2378-84.
  • 7. Rauscher FM, Goldschmidt-Clermont PJ, Davis BH, Wang T, Gregg D, Ramaswami P, Pippen AM, Annex BH, Dong C, Taylor DA. Aging, progenitor cell exhaustion, and atherosclerosis. Circulation 2003; 108: 457-63.
  • 8. Wassmann S, Werner N, Czech T, Nickenig G. Improvement of endothelial function by systemic transfusion of vascular progenitor cells. Circ Res 2006; 99: e74-83.
  • 9. Vasa M, Fichtlscherer S, Aicher A, Adler K, Urbich C, Martin H, Zeiher AM, Dimmeler S. Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease. Circ Res 2001; 89: E1-E7.
  • 10. Fadini GP, Coracina A, Baesso I, Agostini C, Tiengo A, Avogaro A, de Kreutzenberg SV. Peripheral blood CD34+KDR+ endothelial progenitor cells are determinants of subclinical atherosclerosis in a middle-aged general population. Stroke 2006; 37: 2277-82.
  • 11. Zhu S, Liu X, Li Y, Goldschmidt-Clermont PJ, Dong C. Aging in the Atherosclerosis Milieu May Accelerate the Consumption of Bone Marrow Endothelial Progenitor Cells. Arterioscler Thromb Vasc Biol 2007; 27: 113-9.
  • 12. Thijssen DH, Vos JB, Verseyden C, van Zonneveld AJ, Smits P, Sweep FC, Hopman MT, de Boer HC. Haematopoietic stem cells and endothelial progenitor cells in healthy men: effect of aging and training. Aging Cell 2006; 5: 495-503.
  • 13. Daub K, Langer H, Seizer P, Stellos K, May AE, Goyal P, Bigalke B, Schönberger T, Geisler T, Siegel-Axel D, Oostendorp RA, Lindemann S, Gawaz M. Platelets induce differentiation of human CD34+ progenitor cells into foam cells and endothelial cells. FASEB J 2006; 20: 2559-61.
  • 14. Nonaka-Sarukawa M, Yamamoto K, Aoki H, Nishimura Y, Tomizawa H, Ichida M, Eizawa T, Muroi K, Ikeda U, Shimada K. Circulating endothelial progenitor cells in congestive heart failure. Int J Cardiol 2007; 119: 344-8.
  • 15. Güven H, Shepherd RM, Bach RG, Capoccia BJ, Link DC. The number of endothelial progenitor cell colonies in the blood is increased in patients with angiographically significant coronary artery disease. J Am Coll Cardiol 2006; 48: 1579-87.
  • 16. Boos CJ, Lip GY, Blann AD. Circulating endothelial cells in cardiovascular disease. J Am Coll Cardiol 2006; 48: 1538-47.
  • 17. Hill JM, Zalos G, Halcox JP, Schenke WH, Waclawiw MA, Quyyumi AA, Finkel T. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med 2003; 348: 593-600.
  • 18. Körbling M, Reuben JM, Gao H, Lee BN, Harris DM, Cogdell D, Giralt SA, Khouri IF, Saliba RM, Champlin RE, Zhang W, Estrov Z. Recombinant human granulocyte-colony-stimulating factor-mobilized and apheresis-collected endothelial progenitor cells: a novel blood cell component for therapeutic vasculogenesis. Transfusion 2006; 46: 1795-802.
  • 19. Gensini GG. A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol 1983; 51: 606.
  • 20. Chen JZ, Zhang FR, Tao QM, Wang XX, Zhu JH, Zhu JH. Number and activity of endothelial progenitor cells from peripheral blood in patients with hypercholesterolaemia. Clin Sci 2004; 107: 273-80.
  • 21. Chen YH, Lin SJ, Lin FY, Wu TC, Tsao CR, Huang PH, Liu PL, Chen YL, Chen JW. High glucose impairs early and late endothelial progenitor cells by modifying nitric oxide-related but not oxidative stress-mediated mechanisms. Diabetes 2007; 56: 1559-68.
  • 22. Imanishi T, Hano T, Nishio I. Angiotensin II potentiates vascular endothelial growth factor-induced proliferation and network formation of endothelial progenitor cells. Hypertens Res 2004; 27: 101-8.
  • 23. Kondo T, Hayashi M, Takeshita K, Numaguchi Y, Kobayashi K, Iino S, Inden Y, Murohara T. Smoking cessation rapidly increases circulating progenitor cells in peripheral blood in chronic smokers. Arterioscler Thromb Vasc Biol 2004; 24: 1442-7.
  • 24. Kränkel N, Adams V, Linke A, Gielen S, Erbs S, Lenk K, Schuler G, Hambrecht R. Hyperglycemia reduces survival and impairs function of circulating blood- derived progenitor cells. Arterioscler Thromb Vasc Biol 2005; 25: 698-703.
  • 25. Laufs U, Wassmann S, Czech T, Münzel T, Eisenhauer M, Böhm M, Nickenig G. Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis. Arterioscler Thromb Vasc Biol 2005; 25: 809-14.
  • 26. Loomans CJ, de Koning EJ, Staal FJ, Rookmaaker MB, Verseyden C, de Boer HC, Verhaar MC, Braam B, Rabelink TJ, van Zonneveld AJ. Endothelial progenitor cell dysfunction: a novel concept in the pathogenesis of vascular complications of type 1 diabetes. Diabetes 2004; 53: 195-9.
  • 27. Scheubel RJ, Zorn H, Silber RE, Kuss O, Morawietz H, Holtz J, Simm A. Age- dependent depression in circulating endothelial progenitor cells in patients undergoing coronary artery bypass grafting. J Am Coll Cardiol 2003; 42: 2073- 80.
  • 28. Tepper OM, Galiano RD, Capla JM, Kalka C, Gagne PJ, Jacobowitz GR, Levine JP, Gurtner GC. Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures. Circulation 2002; 106: 2781-6.
  • 29. Wang X, Zhu J, Chen J, Shang Y. Effects of nicotine on the number and activity of circulating endothelial progenitor cells. J Clin Pharmacol 2004; 44: 881-9.
  • 30. Van Craenenbroeck EM, Vrints CJ, Haine SE, Vermeulen K, Goovaerts I, Van Tendeloo VF, Hoymans VY, Conraads VM. A maximal exercise bout increases the number of circulating CD34+/KDR+ endothelial progenitor cells in healthy subjects. Relation with lipid profile. J Appl Physiol 2008; 104: 1006-13.
  • 31. Rehman J, Li J, Parvathaneni L, Karlsson G, Panchal VR, Temm CJ, Mahenthiran J, March KL. Exercise acutely increases circulating endothelial progenitor cells and monocyte-/macrophage-derived angiogenic cells. J Am Coll Cardiol 2004; 43: 2314-8.
  • 32. Steiner S, Niessner A, Ziegler S, Richter B, Seidinger D, Pleiner J, Penka M, Wolzt M, Huber K, Wojta J, Minar E, Kopp CW. Endurance training increases the number of endothelial progenitor cells in patients with cardiovascular risk and coronary artery disease. Atherosclerosis 2005; 181: 305-10.
  • 33. Heeschen C, Lehmann R, Honold J, Assmus B, Aicher A, Walter DH, Martin H, Zeiher AM, Dimmeler S. Profoundly reduced neovascularization capacity of bone marrow mononuclear cells derived from patients with chronic ischemic heart disease. Circulation 2004; 109: 1615-22.
  • 34. Massa M, Rosti V, Ferrario M, Campanelli R, Ramajoli I, Rosso R, De Ferrari GM, Ferlini M, Goffredo L, Bertoletti A, Klersy C, Pecci A, Moratti R, Tavazzi L. Increased circulating hematopoietic and endothelial progenitor cells in the early phase of acute myocardial infarction. Blood 2005; 105: 199-206.
  • 35. George J, Goldstein E, Abashidze S, Deutsch V, Shmilovich H, Finkelstein A, Herz I, Miller H, Keren G. Circulating endothelial progenitor cells in patients with unstable angina: association with systemic inflammation. Eur Heart J 2004; 25: 1003-8.
  • 36. Dimmeler S, Aicher A, Vasa M, Mildner-Rihm C, Adler K, Tiemann M, Rütten H, Fichtlscherer S, Martin H, Zeiher AM. HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI 3-kinase/Akt pathway. J Clin Invest 2001; 108: 391-7.
  • 37. Iwakura A, Luedemann C, Shastry S, Hanley A, Kearney M, Aikawa R, Isner JM, Asahara T, Losordo DW. Estrogen-mediated, endothelial nitric oxide synthase-dependent mobilization of bone marrow-derived endothelial progenitor cells contributes to reendothelialization after arterial injury. Circulation 2003; 108: 3115-21.
  • 38. Pellegatta F, Bragheri M, Grigore L, Raselli S, Maggi FM, Brambilla C, Reduzzi A, Pirillo A, Norata GD, Catapano AL. In vitro isolation of circulating endothelial progenitor cells is related to the high density lipoprotein plasma levels. Int J Mol Med 2006; 17: 203-8.
  • 39. Strehlow K, Werner N, Berweiler J, Link A, Dirnagl U, Priller J, Laufs K, Ghaeni L, Milosevic M, Böhm M, Nickenig G. Estrogen increases bone marrow-derived endothelial progenitor cell production and diminishes neointima formation. Circulation 2003; 107: 3059-65.
  • 40. Vasa M, Fichtlscherer S, Adler K, Aicher A, Martin H, Zeiher AM, Dimmeler S. Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease. Circulation 2001; 103: 2885-90.
  • 41. Walter DH, Rittig K, Bahlmann FH, Kirchmair R, Silver M, Murayama T, Nishimura H, Losordo DW, Asahara T, Isner JM. Statin therapy accelerates reendothelialization: a novel effect involving mobilization and incorporation of bone marrow-derived endothelial progenitor cells. Circulation 2002; 105: 3017- 24.
  • 42. Werner N, Priller J, Laufs U, Endres M, Böhm M, Dirnagl U, Nickenig G. Bone marrow-derived progenitor cells modulate vascular reendothelialization and neointimal formation: Effect of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibition. Arterioscler Thromb Vasc Biol 2002; 22: 1567-72.
  • 43. Bahlmann FH, de Groot K, Mueller O, Hertel B, Haller H, Fliser D. Stimulation of endothelial progenitor cells: a new putative therapeutic effect of angiotensin II receptor antagonists. Hypertension 2005; 45: 526-9.
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  • Yayın Aralığı: Yılda 4 Sayı
  • Yayıncı: Cumhuriyet Üniversitesi Tıp Fakültesi
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