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Dergiler / Harran Üniversitesi Tıp Fakültesi Dergisi / 2015 / Cilt: 12 Sayı: 3

Tedavi Dekompanse Kalp Yetersizliğinde Lipit Peroksidasyonunu Azaltmaz

Treatment Does Not Decrease Lipid Peroxidation In Decompansated Heart Failure

Emin Şavik
Hatice Sezen
Hasan Bilinç
Musluhittin Emre Erkuş
İbrahim Halil Altıparmak
Yusuf Sezen
Nurten Aksoy
Sayfa
342–347
Yayın Tarihi
2015-12-30
DOI
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Yapay Zeka Hızlı Bakış & Çıkarımlar

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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

Bulgular En yüksek LOOH düzeyleri KKY grubunda en düşük LOOH düzeyleri kontrol grubunda idi.

📌 3 Maddede Bu Makale

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Amaç & Hipotez:Giriş Literatürde lipit peroksidasyonunun kalp yetersizliğinde (KY) arttığı gösterilmiş ancak dekompanse kalp yetersizliğinde (DKY) durumu hala açık değildir.
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Temel Bulgular & Veri:Bu yüzden çalışmanın amacı, dekompanse kalp yetersizliğinde lipit hidroperoksit'in (LOOH) serum düzeyini ve tedavinin LOOH düzeyleri üzerine etkisini araştırmaktır.
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Sonuç & Katkı:Bulgular En yüksek LOOH düzeyleri KKY grubunda en düşük LOOH düzeyleri kontrol grubunda idi.
🔬Tür:Literatür & Derleme Çalışması
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Lipit Hidroperoksit · Oksidatif Stres · Kalp Dekompansasyonu

Özet

Giriş Literatürde lipit peroksidasyonunun kalp yetersizliğinde (KY) arttığı gösterilmiş ancak dekompanse kalp yetersizliğinde (DKY) durumu hala açık değildir. Bu yüzden çalışmanın amacı, dekompanse kalp yetersizliğinde lipit hidroperoksit'in (LOOH) serum düzeyini ve tedavinin LOOH düzeyleri üzerine etkisini araştırmaktır. Materyal ve Metod Bu amaçla 50 DKYnedeni ile koroner yoğun bakım ünitesine yatan ve sonrasında kompansasyon sağlanarak taburcu edilen hastalar (kompanse KY(KKY)) ve yaş ve cinsiyet özellikleri benzer kalp yetersizliği olmayan 50 sağlıklı gönüllü çalışmaya dahil edildi. Örnekler hastaların ve sağlıklı kontrollerin her ikisinin kan damarlarından alındıktan sonra santrifüj edildi. Sonra, LOOH düzeyleri enzimatik bir metotla elde edilen serumlarda çalışıldı. Bulgular En yüksek LOOH düzeyleri KKY grubunda en düşük LOOH düzeyleri kontrol grubunda idi. Ek olarak, LOOH düzeyleri, DKY grubunda kontrollere göre belirgin olarak yüksekti (p<0,0001) ve KKY grubunda DKY grubuna ve kontrollere göre de anlamlı derecede yüksekti (p<0,0001). Korelasyon analizinde LOOH düzeyleri ile yaş, sistolik ve diastolik kan basıncı, serum glikozu ve troponin T düzeyleri, LV diastolik ve sistolik çapları ile mitral yetersizliği varlığı pozitif olarak, ejeksiyon fraksiyonu ile negatif bir şekilde ilişkili idi. Lineer regresyon analizi bu parametrelerden sadece açlık kan şekerinin LOOH'u bağımsız olarak etkilediğini gösterdi. Sonuç Sonuç olarak akut DKY hastalarında LOOH yüksekti. Bu yükseklik hastaların yatırılarak kompansasyon sağlanmasına rağmen azalmamaktaydı.&nbsp;

Abstract

Background In literature, increased lipid peroxidation in heart failure (HF) has been demostrated, however, it is stil not clear in the decompensated heart failure (DHF). The aim of this study, hence, is to investigate serum lipid hydroperoxide (LOOH) levels in the DHF patients and the effect of DHF treatment on serum LOOH levels. Materials and Methods For our experiment, 50 patients, who are DHF patients admitted to coroner intensive care unit and discharged patients providing compansation after their hospitalisation, and 50 healty volunteers, whose age and gender are similar to the 50 patients, were included. After samples venupunctured from blood vessel of both these patients and healty volunteers, they were sentrifugated. Afterwards, LOOH levels were studied in the obtained serums using an enzimatical method. Results The highest LOOH levels were in CHF group, and the lowest LOOH levels were in the control group. Additionally, LOOH levels were significantly in DHF patients higher than in the the controls (p <0.0001), and were significantly higher in the CHF group compared to both the DHF and control group (p <0.0001). In the correlation analyses, LOOH levels were possitively correlated with the different parameters such as age, systolic and diastolic blood pressures, serum glucose and troponin T levels, the left ventricule diastolic and systolic diameters in the positive presence of mitral regurgitation, but negatifly correlated with the ejection fraction. Linear regression analysis showed that only glucose level among these parameters affects the LOOH levels independently. Conclusions As a result, LOOH levels elaveted in acute DHF patients. This elevation did not decrease after treatment,which provides compansation, of the hospitalized patients.&nbsp;

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Bu Makaleye Atıf Yap

Şavik, E., Sezen, H., Bilinç, H., Erkuş, M. E., Altıparmak, İ. H., Sezen, Y., Aksoy, N. (2015). Tedavi Dekompanse Kalp Yetersizliğinde Lipit Peroksidasyonunu Azaltmaz. Harran Üniversitesi Tıp Fakültesi Dergisi, Cilt: 12 Sayı: 3, 342–347. https://ajindex.com/articles/1081639

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Kaynakça (32)

  1. Heart disease and stroke statistics--2010 update: a report from the American Heart Association. Circulation. 2010;121(7):e46-e215.
  2. Heart failure in the 21st century: a cardiogeriatric syndrome. Rich MW J Gerontol A Biol Sci Med Sci. 2001;56(2):M88-96.
  3. Levy D, Kenchaiah S, Larson MG, Benjamin EJ, Kupka MJ, Ho KK, Murabito JM, Vasan RS. Long-term trends in the incidence of and survival with heart failure. N Engl J Med. 2002;347(18):1397-402.
  4. Stewart S, MacIntyre K, Hole DJ, Capewell S, McMurray JJ. More 'malignant' than cancer? Five-year survival following a first admission for heart failure. Eur J Heart Fail. 2001;3(3):315-22.
  5. Fang J, Mensah GA, Croft JB, Keenan NL. Heart failure-related hospitalization in the U.S., 1979 to 2004. J Am Coll Cardiol. 2008;52(6):428-34.
  6. Fonarow GC, Adams KF Jr, Abraham WT, Yancy CW, Boscardin WJ, ADHERE Scientific Advisory Committee, Study Group, and Investigators. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA. 2005;293(5):572-80.
  7. Imai H. [Biological significance of lipid hydroperoxide and its reducing enzyme, phospholipid hydroperoxide glutathione peroxidase, in mammalian cells]. Yakugaku Zasshi. 2004;124(12):937-57.
  8. Marnett LJ. Lipid peroxidation-DNA damage by malondialdehyde. Mutat Res. 1999;424(1-2):83-95.
  9. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18:499-502.
  10. Nourooz Zadeh J. Ferrous ion oxidation in presence of xylenol orange for detection of lipid hydroperoxides in plasma. Methods Enzymol 1999;300:58–62.
  11. ACC/AHAGuidelines for the Clinical Application of Echocardiography. Circulation. 1997;95:1686-1744.
  12. Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems in echocardiographic volume determinations: Echocardiographic– angiographic correlations in the presence of absence of asynergy. Am J Cardiol 1976;37:7–11.
  13. Blair IA. Lipid hydroperoxide-mediated DNA damage. Exp Gerontol. 2001;36(9):1473-81.
  14. Wang TG, Gotoh Y, Jennings MH, Rhoads CA, Aw TY. Lipid hydroperoxide-induced apoptosis in human colonic CaCo-2 cells is associated with an early loss of cellular redox balance. FASEB J. 2000;14(11):1567-76.
  15. Yanagawa K, Takeda H, Egashira T, Sakai K, Takasaki M, Matsumiya T. Age-related changes in alphatocopherol dynamics with relation to lipid hydroperoxide content and fluidity of rat erythrocyte membrane. J Gerontol ABiol Sci Med Sci. 1999;54(9):B379-83.
  16. Sugihara N, Arakawa T, Ohnishi M, Furuno K. Antiand pro-oxidative effects of flavonoids on metal-induced lipid hydroperoxide-dependent lipid peroxidation in cultured hepatocytes loaded with alpha-linolenic acid. Free Radic Biol Med. 1999;27(11-12):1313-23.
  17. Montoro-García S, Shantsila E, Wrigley BJ, Tapp LD, Abellán Alemán J, Lip GY. Small-size Microparticles as Indicators of Acute Decompensated State in Ischemic Heart Failure. Rev Esp Cardiol (Engl Ed). 2015 Mar 25.
  18. Hashem SI, Perry CN, Bauer M, Han S, Clegg SD, Ouyang K, Deacon DC, Spinharney M, Panopoulos AD, Izpisua Belmonte JC, Frazer KA, Chen J, Gong Q, Zhou Z, Chi NC, Adler ED. Oxidative Stress Mediates Cardiomyocyte Apoptosis in a Human Model of Danon Disease and Heart Failure. Stem Cells. 2015 Mar 31.
  19. La Vecchia L, Mezzena G, Zanolla L, Paccanaro M, Varotto L, Bonanno C, Ometto R. Cardiac troponin I as diagnostic and prognostic marker in severe heart failure. J Heart Lung Transplant. 2000;19(7):644-52.
  20. Sato Y, Yamada T, Taniguchi R, Nagai K, Makiyama T, Okada H, Kataoka K, Ito H, Matsumori A, Sasayama S, Takatsu Y. Persistently increased serum concentrations of cardiac troponin-t in patients with idiopathic dilated cardiomyopathy are predictive of adverse outcomes. Circulation. 2001;103(3):369-74.
  21. Cheng W, Li B, Kajstura J, Li P, Wolin MS, Sonnenblick EH, Hintze TH, Olivetti G, Anversa P. Stretch-induced programmed myocyte cell death. J Clin Invest. 1995;96(5):2247-59.
  22. Anversa P, Kajstura J. Myocyte cell death in the diseased heart. Circ Res. 1998;82(11):1231-3.
  23. Olivetti G, Abbi R, Quaini F, Kajstura J, Cheng W, Nitahara JA, Quaini E, Di Loreto C, Beltrami CA, Krajewski S, Reed JC, Anversa P. Apoptosis in the failing human heart. N Engl J Med. 1997;336(16):1131-41.
  24. Logeart D, Beyne P, Cusson C, Tokmakova M, Leban M, Guiti C, Bourgoin P, Solal AC. Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain. Am Heart J. 2001;141(2):247-53.
  25. Moe GW, Marin-Garcia J, Konig A, Goldenthal M, Lu X, Feng Q. In vivo TNF-alpha inhibition ameliorates cardiac mitochondrial dysfunction, oxidative stress, and apoptosis in experimental heart failure. Am J Physiol Heart Circ Physiol. 2004;287(4):H1813-20.
  26. Dalla Libera L, Sabbadini R, Renken C, Ravara B, Sandri M, Betto R, Angelini A, Vescovo G. Apoptosis in the skeletal muscle of rats with heart failure is associated with increased serum levels of TNF-alpha and sphingosine. J Mol Cell Cardiol. 2001;33(10):1871-8.
  27. Ueda T, Ueda T, Fukuda S, Browne R, Jenis E, Spengler R, Chou R, Buch P, Aljada A, Dandona P, Sasisekharan R, Dorey CK, Armstrong D. Lipid hydroperoxide-induced tumor necrosis factor (TNF)-alpha, vascular endothelial growth factor and neovascularization in the rabbit cornea: effect of TNF inhibition. Angiogenesis. 1998;1(2):174-184.
  28. Blair IA. Lipid hydroperoxide-mediated DNA damage. Exp Gerontol. 2001;36(9):1473-81.
  29. Campolo J, De Maria R, Caruso R, Accinni R, Turazza F, Parolini M, Roubina E, De Chiara B, Cighetti G, Frigerio M, Vitali E, Parodi O. Blood glutathione as independent marker of lipid peroxidation in heart failure. Int J Cardiol. 2007;117(1):45-50.
  30. Varga ZV, Giricz Z, Liaudet L, Haskó G, Ferdinandy P, Pacher P. Interplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic c a r d i o m y o p a t h y. B i o c h i m B i o p h y s A c t a. 2015;1852(2):232-42.
  31. Pall ML. The NO/ONOO-cycle as the central cause of heart failure. Int J Mol Sci. 2013;14(11):22274-330.
  32. Varga ZV, Giricz Z, Liaudet L, Haskó G, Ferdinandy P, Pacher P. Interplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic c a r d i o m y o p a t h y. B i o c h i m B i o p h y s A c t a. 2015;1852(2):232-42.