Oğuz YAVUZGİL, Yasemin DELEN, Cemil GÜRGÜN, Filiz ÖZERKAN, Mehdi ZOGHİ, Gülinnaz ALPER, Hakan KÜLTÜRSAY, Cüneyt TÜRKOĞLU

Perkutan koroner girişim sırasındaki venöz plazma anjiotensin II düzeyi değişiklikleri

Perkütan koroner girişimler (PKG) sırasında meydana gelen endotel hasarı, miyokard iskemisi/hasarı ve hemodinamik değişikliklerin sempato-adrenerjik ve nörohumoral sistem aktivasyonuna neden olabildiği gösterilmiştir. Bu çalışmada, PKG.esnasında ortaya çıkan plazma Anjiotensin-ll değişikliklerinin incelenmesi ve takip dönemindeki restenozla ilişkisinin incelenmesi hedeflenmiştir. Çalışmaya nativ koroner artere elektif PKG endikasyonu konan ve başarılı olarak işlem uygulanan toplam 76 olgu ve özellikleri benzer 15 sağlıklı olgu kontrol grubu olarak alındı. Olguların bazal, işlem sonrası ve 24.saatte venöz plazma Ang-ll düzeyleri için kan örnekleri alındıktan sonra,ortalama 5,8±1 ay süre ile izlendiler. Bazal plazma Ang-ll düzeyleri, çalışma olgularında kontrol grubuna göre daha yüksek saptanmakla birlikte bu fark anlamlı değildi (15±6pm/L'ye karşın 14±5pm/L, p=0.299). PKG sonrasında ise hemen yapılan ölçümlerde Ang-ll düzeylerinde ve 24. saat ölçümlerinde bir artış izlenmekteydi (Bazal Ang ll'ye göre hemen sonrasında 25±15pm/L, p

Anahtar Kelimeler:

Kalp damar cerrahi işlemleri, Koroner restenoz, Anjiyotensin II

Changes of venous plasma angiotensin II levels during percutaneous coronary intervention

It has been shown that during percutaneous coronary intervention (PCI), sympatho-adrenergic and neuro-humoral system activation can occur due to endothelial injury, myocardial ischemia/injury and hemodynamic changes. In this article, we aimed to investigate the changes öf plasma Anjiotensin - II levels during PCI and its relationship between restenosis at the follow-up. We enrolled 76 cases which was performed elective and succesful PCI to a native coronary artery and 15 healthy controls. Blood samples were withdrawn before, after PCI and at the 24. hour of PCI for venous plasma Ang-ll and they were followed-up 5,8+1 months. Basal plasma Ang-ll levels were insignificantly higher in the PCI group (15±6 pm/L vs 14±5 pm/L, p=0.299). Post-PCI and 24.hour measurements were significantly higher ( Basal 15±6 pm/L vs Post-PCI 25±15pm/L, p <0.0001, Basal 15±6 pm/L vs 24.hour21±13 pm/L, p<0.0001)We performed control angiography in 51 (67%) cases and there were 19 cases of restenosis (19?76, 25% for totally)Basal plasma Ang-II levels were higher in restenotic patients (p=0.032 in Mann-Whitney U test for basal Ang-II levels) As a result, we observed that venous plasma Ang-II levels were significantly increased after PCI. Furthermore basal plasma Ang-II levels were found higher in restenotic patients.

Keywords:

Cardiovascular Surgical Procedures, Coronary Restenosis, Angiotensin II,

PDF

___

1. de Feyter PJ, van den Brand M, Laarman GJ, et al. Acute coronary artery occlusion during and after percutaneous transluminal coronary angioplasty:frequency, prediction, clinical course, management, and followup.Circulation 1991;83:927-936.
2. Vaitkus PT, Laskey WK. Efficacy of adjunctive thrombolytic therapy in percutaneous transluminal coronary angiopiasty. J Am Coll Cardiol 1994;24:1415-1423.
3. Bourassa MG. Silent myocardial ischemia after coronary angiopiasty; distinguishing the shadow from the substance. J Am Coll Cardiol 1992; 19:1410-1411.
4. Capron L, Heudes D, Chajara A. Bruneval P. Effect of ramipril, an inhibitor of angiotensin converting enzyme, on the response of the rat thoracic aorta to injury with a balloon catheter. J Cardiovasc Pharmacol 1991; 18:207-211.
5. Holmes DR, Vlietstra RR, Smith HS, et al.Restenosis after percutaneous transluminal coronary angioplasty: a report from the PTCA registry of the National Heart, Lung, and Blood Institute. Am J Cardiol 1984;53:77C- 81C.
6. Nobuyoshi M, Kimura T, Nosaka H, et al Restenosis after successful percutaneous transluminal coronary angioplasty: serial angiographic follow-up of 229 patients. J Am Coll Cardiol 1988; 12:616-623.
7. Karthikeyan G, Bhargava B. Prevention of restenosis after coronary angioplasty. Curr Opin Cardiol. 2004;19(5):500-9.
8. Shironati M, Yui Y, Kawai C. Restenosis after coronary angioplasty:pathogenesis of neointimal thickening initiated by endotheiial loss. Endothelium 1993; 1:5-22.
9. Karthikeyan G, Bhargava B. Prevention of restenosis after coronary angioplasty: Curr Opin Cardiol. 2004 Sep;19(5):500-9.
10. Libby P, Schwartz D, Brogi E, et al. A cascade model for restenosis: a special case of atherosclerosis progression. Circulation 1992;86(Suppl3):47-52.
11. Weiss D, Sorescu D, Taylor WR. Angiotensin II and atherosclerosis. Am J Cardiol. 2001; 87(8A):25C-32C.
12. Williams B. Angiotensin II and and the Pathophysiology of Cardiovascular Remodeling Am J Cardiol. 2001; 87(8A):10C-17C.
13. Jain D, Schafer U, Dendorfer A, et al. Neurohumoral activation in percutaneous coronary interventions: apropos of ten vasoactive substances during and immediately following coronary rotastenting. Indian Heart J. 2001;53(3):301-7.
14. Hojo Y, Ikeda U, Katsuki T, et al. Release of endothelin 1 and angiotensin II induced by percutaneous transluminal coronary angioplasty. Catheter Cardiovasc Interv. 2000;51(1):42-9.