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Koroner Arter Hastalığı Şiddeti ve Trombosit Agregasyonu

Yıl 2021, Cilt: 4 Sayı: 1, 13 - 19, 10.02.2021
https://doi.org/10.26650/JARHS2021-843387

Öz

Amaç: Koroner Arter Hastalığı (KAH), çoğunlukla ateroskleroz sebebiyle kalbi besleyen damarların daralması veya tıkanması ile ortaya çıkmaktadır. Ateroskleroz patogenezinde aterosklerotik risk faktörlerinin yanı sıra inflamasyon, endotel disfonksiyonu ve buna bağlı olarak trombosit aktivasyonu sıklıkla görülmektedir. KAH’da trombosit fonksiyonlarını araştıran çalışmalar olmasına rağmen, hastalık şiddeti ile trombosit aktivasyonu arasındaki ilişkiye dair çalışmalar kısıtlıdır. Bu çalışmada, tıkalı damar sayısı ile trombosit fonksiyonları arasındaki ilişkiyi araştırmayı amaçladık. Gereç ve Yöntem: Koroner anjiyografi ile damar tıkanıklığı tespit edilen KAH olguları, hastalık şiddetine göre 3 alt gruba ayrıldı. Işık geçirgenliği agregometri (LTA) yöntemi ile KAH ve sağlıklı kontrollere adenozindifosfat (ADP) uyaranı ile trombosit agregasyon testi uygulandı. Trombosit agregasyon testinin sonuçları, agregasyon kurbu eğimi ohm (Ώ) ve agregasyonun maksimum kapsamı yüzde (%) Amplitüd olarak hesaplandı. Bulgular: Trombosit agregasyon testinde KAH agregasyon eğim değerleri (116,90±28,21a ) kontrole göre (113,90±35,16a ) yüksek olmasına rağmen aralarında istatistiksel olarak bir farklılık yoktur (p=0,526a ). (%) Amplitüd değerleri kontrol grubunda (74,73±30,71a ), KAH grubuna göre (66,51±25,18a ) yüksek olmasına rağmen aralarında istatistiksel olarak anlamlılık bulunmamaktadır (p=0,056a ). KAH alt gruplarının agregasyon eğim (Ώ) ve (%) Amplitüd değerleri arasında istatistiksel olarak bir fark saptanmamıştır (Eğim (Ώ) p=0,461b , (%) Amplitüd p=0,140c ). Sonuç: KAH olgularında, ADP aracılı agregasyon testi sonuçlarını hastalık şiddetine göre değerlendirdiğimiz bu çalışmada, damar tıkanıklığı sayısı ile agregasyon testi sonuçları arasında istatistiksel olarak anlamlı bir ilişki saptanmamıştır.

Destekleyen Kurum

Bu çalışma İstanbul Üniversitesi Bilimsel Araştırma Projeleri Koordinasyon Birimi

Proje Numarası

T-7883/05072010

Kaynakça

  • 1. Timmis A, Townsend N, Gale C, Grobbee R, Maniadakis N, Flather M, et al. European Society of Cardiology: cardiovascular disease statistics 2017. Eur Heart J 2018;39(7):508-79.
  • 2. Popa LE, Petresc B, Cătană C, Moldovanu CG, Feier DS, Lebovici A, et al. Association between cardiovascular risk factors and coronary artery disease assessed using CAD-RADS classification: a cross-sectional study in Romanian population. BMJ Open 2020;10(1):e031799.
  • 3. Henein MY, Vancheri S, Bajraktari G, Vancheri F. Coronary Atherosclerosis Imaging. Diagnostics 2020;10(2):65.
  • 4. Ulutin ON, Akman N, Ozcan E. Thrombosis, arteriosclerosis and hypercoagulability. Turk Tıp Cemiy Mecm 1963;29:428-32.
  • 5. Hamilos M, Petousis S, Parthenakis F. Interaction between platelets and endothelium: from pathophysiology to new therapeutic options. Cardiovasc Diagn Ther 2018;8(5):568–80.
  • 6. Gawaz M, Borst O. The Role of Platelets in Atherothrombosis. In: Michelson A.D, Cattaneo M, Frelinger A, Newman P, editors. Platelets 4th edition. Massachusetts: USA 2019.p.459-67.
  • 7. Totani L, Evangelista V. Platelet–leukocyte interactions in cardiovascular disease and beyond. Arterioscler Thromb Vasc Biol 2010;30(12):2357-61.
  • 8. Weyrich AS, Zimmerman G.A. Platelets in Lung Biology. Ann Rev Physiol 2013;75:569-91.
  • 9. Lefrançais E, Ortiz-Muñoz G, Caudrillier A, Mallavia B, Liu F, Sayah D.M, et al. The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors. Nature 2017; 544(7648):105-09.
  • 10. Ulutin ON. The platelets: Fundamentals and clinical applications. İstanbul: Kâğit ve Basim İsleri AŞ, 1976:ss.1-344.
  • 11. Furie B, Furie BC, Flaumenhaft R. A journey with platelet P-selectin: the molecular basis of granule secretion, signalling and cell adhesion. Thrombosis Haemost 2001;86(07):214-21.
  • 12. Bayram Gürel Ç, Ayaz G, Tuncel H, Kalkan T, Kurşun N, Ulutin T. Statik Manyetik Alanın Trombosit Agregasyonuna Etkisi. SABİAD 2020;3(3):173-8.
  • 13. Vanhoutte PM. Endothelial dysfunction and coronary heart disease. Interaction of endothelium and thrombocytes. Schweiz Rundsch Med Prax 1993;82(42):1161-6.
  • 14. Fuchs B, Budde U, Schulz A, Kessler CM, Fisseau C, Kannicht C. Flow-based measurements of von Willebrand factor (VWF) function: binding to collagen and platelet adhesion under physiological shear rate. Thromb Res 2010;125(3):239-45.
  • 15. Selvadurai MV, Hamilton JR. Structure and function of the open canalicular system–platelet’s specialized internal membrane network. Platelets 2018;29(4):319-25.
  • 16. Suzuki Y, Sano H, Mochizuki L, Honkura N, Urano T. Activated platelet-based inhibition of fibrinolysis via thrombin-activatable fibrinolysis inhibitor activation system. Blood Adv 2020;4(21):5501-11.
  • 17. Güngör ZB, Ekmekçi H, Tüten A, Toprak S, Ayaz G, Çalışkan O, et al. Is there any relationship between adipocytokines and angiogenesis factors to address endothelial dysfunction and platelet aggregation in untreated patients with preeclampsia? Arch Gynecol Obstet 2017;296(3):495-502.
  • 18. Ekmekçi H, Ekmekçi O.B, Erdine S, Sönmez H, Ataev Y, Oztürk Z, et al. Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension. J Thromb Thrombolysis 2009;28(4):418-24.
  • 19. Sipahioglu NT, İlerigelen B, Gungor ZB, Ayaz G, Ekmekci H, Gurel ÇB, et al. Relation of biochemical parameters with flow-mediated dilatation in patients with metabolic syndrome. Chin Med J 2017;130(13):1564-9.
  • 20. Tutluoglu B, Gurel ÇB, Ozdas SB, Musellim B, Erturan S, Anakkaya AN, et al. Platelet function and fibrinolytic activity in patients with bronchial asthma. Clin Appl Thromb Hemost 2005;11(1):77-81.
  • 21. Tetik Ş, Koray AK. Kardiyovasküler hastalıklarda trombosit fonksiyon testleri: patofizyolojiden klinik yaklaşıma. Cumhuriyet Tıp Derg 2010;32(2):264-74.
  • 22. Born GVR. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962;194:927-29.
  • 23. Blanc JL, Mullier F, Vayne C, Lordkipanidzé M. Advances in platelet function testing light transmission aggregometry and beyond. J Clin Med 2020;9(8):2636.
  • 24. Kaptan K. Trombosit Hastalıklarında Temel Tanısal Yaklaşım. İlk Basamak Kursu. Ankara 2006: p.1-5.
  • 25. Ekmekci H, Isler I, Sonmez H, Gurel CB, Ciftci O, Ulutin T, et al. Comparison of platelet fibronectin, ADP-induced platelet aggregation and serum total nitric oxide (NOx) levels in angiographically determined coronary artery disease. Thromb Res 2006;117(3):249-54.

Coronary Artery Disease Severity and Platelet Aggregation

Yıl 2021, Cilt: 4 Sayı: 1, 13 - 19, 10.02.2021
https://doi.org/10.26650/JARHS2021-843387

Öz

Objective: Coronary Artery Disease (CAD) is caused by the narrowing or occlusion of the vessels feeding the heart, mostly due to atherosclerosis. In the pathogenesis of atherosclerosis, besides atherosclerotic risk factors, inflammation, endothelial dysfunction and related platelet activation are frequently observed. While there are studies investigating platelet functions in CAD, studies on the relationship between disease severity and platelet activation are limited. In this study, we aimed to investigate the relationship between the number of occluded vessels and platelet functions. Materials and Methods: The cases of CAD with vascular occlusion detected by coronary angiography were divided into 3 subgroups according to disease severity. The platelet aggregation test with Adenosindiphosphate (ADP) stimulation was applied to the CAD and healthy controls with the Light Transmittance Aggregometry (LTA) method. The results of that test were calculated as aggregation curve slope and % Amplitude. Results: In the platelet aggregation test, although the CAD aggregation slope values (116.90±28.21a) were higher than the control (113.90±35.16a) there was no statistically significant difference (p=0.526a). Although % Amplitude values were higher in the control group (74.73±30.71a) compared to the CAD group (66.51±25.18a) there was no statistical significance between them (p=0.056a). There was no statistically significant difference between aggregation slope and % Amplitude values of the CAD subgroups (Slope p=0.461b, % Amplitude p=0.140c). Conclusion: In this study, in which we evaluated the results of ADP-induced aggregation tests according to the severity of the disease in CAD cases, no statistically significant relationship was found between the number of vascular occlusion and the results of the aggregation test.

Proje Numarası

T-7883/05072010

Kaynakça

  • 1. Timmis A, Townsend N, Gale C, Grobbee R, Maniadakis N, Flather M, et al. European Society of Cardiology: cardiovascular disease statistics 2017. Eur Heart J 2018;39(7):508-79.
  • 2. Popa LE, Petresc B, Cătană C, Moldovanu CG, Feier DS, Lebovici A, et al. Association between cardiovascular risk factors and coronary artery disease assessed using CAD-RADS classification: a cross-sectional study in Romanian population. BMJ Open 2020;10(1):e031799.
  • 3. Henein MY, Vancheri S, Bajraktari G, Vancheri F. Coronary Atherosclerosis Imaging. Diagnostics 2020;10(2):65.
  • 4. Ulutin ON, Akman N, Ozcan E. Thrombosis, arteriosclerosis and hypercoagulability. Turk Tıp Cemiy Mecm 1963;29:428-32.
  • 5. Hamilos M, Petousis S, Parthenakis F. Interaction between platelets and endothelium: from pathophysiology to new therapeutic options. Cardiovasc Diagn Ther 2018;8(5):568–80.
  • 6. Gawaz M, Borst O. The Role of Platelets in Atherothrombosis. In: Michelson A.D, Cattaneo M, Frelinger A, Newman P, editors. Platelets 4th edition. Massachusetts: USA 2019.p.459-67.
  • 7. Totani L, Evangelista V. Platelet–leukocyte interactions in cardiovascular disease and beyond. Arterioscler Thromb Vasc Biol 2010;30(12):2357-61.
  • 8. Weyrich AS, Zimmerman G.A. Platelets in Lung Biology. Ann Rev Physiol 2013;75:569-91.
  • 9. Lefrançais E, Ortiz-Muñoz G, Caudrillier A, Mallavia B, Liu F, Sayah D.M, et al. The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors. Nature 2017; 544(7648):105-09.
  • 10. Ulutin ON. The platelets: Fundamentals and clinical applications. İstanbul: Kâğit ve Basim İsleri AŞ, 1976:ss.1-344.
  • 11. Furie B, Furie BC, Flaumenhaft R. A journey with platelet P-selectin: the molecular basis of granule secretion, signalling and cell adhesion. Thrombosis Haemost 2001;86(07):214-21.
  • 12. Bayram Gürel Ç, Ayaz G, Tuncel H, Kalkan T, Kurşun N, Ulutin T. Statik Manyetik Alanın Trombosit Agregasyonuna Etkisi. SABİAD 2020;3(3):173-8.
  • 13. Vanhoutte PM. Endothelial dysfunction and coronary heart disease. Interaction of endothelium and thrombocytes. Schweiz Rundsch Med Prax 1993;82(42):1161-6.
  • 14. Fuchs B, Budde U, Schulz A, Kessler CM, Fisseau C, Kannicht C. Flow-based measurements of von Willebrand factor (VWF) function: binding to collagen and platelet adhesion under physiological shear rate. Thromb Res 2010;125(3):239-45.
  • 15. Selvadurai MV, Hamilton JR. Structure and function of the open canalicular system–platelet’s specialized internal membrane network. Platelets 2018;29(4):319-25.
  • 16. Suzuki Y, Sano H, Mochizuki L, Honkura N, Urano T. Activated platelet-based inhibition of fibrinolysis via thrombin-activatable fibrinolysis inhibitor activation system. Blood Adv 2020;4(21):5501-11.
  • 17. Güngör ZB, Ekmekçi H, Tüten A, Toprak S, Ayaz G, Çalışkan O, et al. Is there any relationship between adipocytokines and angiogenesis factors to address endothelial dysfunction and platelet aggregation in untreated patients with preeclampsia? Arch Gynecol Obstet 2017;296(3):495-502.
  • 18. Ekmekçi H, Ekmekçi O.B, Erdine S, Sönmez H, Ataev Y, Oztürk Z, et al. Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension. J Thromb Thrombolysis 2009;28(4):418-24.
  • 19. Sipahioglu NT, İlerigelen B, Gungor ZB, Ayaz G, Ekmekci H, Gurel ÇB, et al. Relation of biochemical parameters with flow-mediated dilatation in patients with metabolic syndrome. Chin Med J 2017;130(13):1564-9.
  • 20. Tutluoglu B, Gurel ÇB, Ozdas SB, Musellim B, Erturan S, Anakkaya AN, et al. Platelet function and fibrinolytic activity in patients with bronchial asthma. Clin Appl Thromb Hemost 2005;11(1):77-81.
  • 21. Tetik Ş, Koray AK. Kardiyovasküler hastalıklarda trombosit fonksiyon testleri: patofizyolojiden klinik yaklaşıma. Cumhuriyet Tıp Derg 2010;32(2):264-74.
  • 22. Born GVR. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962;194:927-29.
  • 23. Blanc JL, Mullier F, Vayne C, Lordkipanidzé M. Advances in platelet function testing light transmission aggregometry and beyond. J Clin Med 2020;9(8):2636.
  • 24. Kaptan K. Trombosit Hastalıklarında Temel Tanısal Yaklaşım. İlk Basamak Kursu. Ankara 2006: p.1-5.
  • 25. Ekmekci H, Isler I, Sonmez H, Gurel CB, Ciftci O, Ulutin T, et al. Comparison of platelet fibronectin, ADP-induced platelet aggregation and serum total nitric oxide (NOx) levels in angiographically determined coronary artery disease. Thromb Res 2006;117(3):249-54.
Toplam 25 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Klinik Tıp Bilimleri
Bölüm Araştırma Makaleleri
Yazarlar

Gülsel Ayaz 0000-0003-3085-232X

Bilgehan Karadağ 0000-0002-1361-5229

Mehmet Güven Bu kişi benim 0000-0002-8749-1708

Gönül Kanıgür Bu kişi benim 0000-0001-9029-1910

Ahmet Dirican Bu kişi benim 0000-0001-8454-4547

Barış İlerigelen Bu kişi benim 0000-0002-2039-8090

Turgut Ulutin 0000-0002-0406-1746

Proje Numarası T-7883/05072010
Yayımlanma Tarihi 10 Şubat 2021
Gönderilme Tarihi 21 Aralık 2020
Yayımlandığı Sayı Yıl 2021 Cilt: 4 Sayı: 1

Kaynak Göster

MLA Ayaz, Gülsel vd. “Koroner Arter Hastalığı Şiddeti Ve Trombosit Agregasyonu”. Sağlık Bilimlerinde İleri Araştırmalar Dergisi, c. 4, sy. 1, 2021, ss. 13-19, doi:10.26650/JARHS2021-843387.