Loading [a11y]/accessibility-menu.js
Araştırma Makalesi
BibTex RIS Kaynak Göster

Evaluation of the oxidative stress index in patients with acute decompensate heart failure

Yıl 2019, Cilt: 16 Sayı: 2, 375 - 379, 29.08.2019
https://doi.org/10.35440/hutfd.520377

Öz

Background: Decompansated heart failure (HF) causes
various metabolic and physiological processes as a result of the failure to
meet the metabolic needs of the tissues. Reactive oxygen species produced in
this process cause harmful oxidative reactions. In this study, we aimed to investigate
the relationship between the oxidative stres parameters and the treatment of
acute decompensated patients with HF.

Methods: A total of 40 patients with decompensated HF
were included in the study. Anthropometric measurements, echocardiography, routine
biochemical parameters, total antioxidant capacity (TAC), total oxidative level
(TOL), and oxidative stres index (OSI) were obtained before admission and
discharge.

Results: Pulse rate, systolic blood pressure and
diastolic blood pressure decreased and left ventricular ejection fraction was
increased after standard HF treatment (p <0.05 for all ). Also post
treatment TAC, TOL and OSI values were found to significantly higher than those
pre-treatment values (p <0.05 for all). İn corelation analysis there was a
negative correlation between TAK and systolic and diastolic blood pressure (r:
-0,307, p: 0.014; r: -0,393, p: 0.001, respectively), and a negative
correlation was found between EF and CT and OSI (r: - 0.298, p: 0.011; r:
-0.332, p: 0.005, respectively).







Conclusions: It was observed that oxidative stres was high
in decompensated HF patients and these high levels were maintained in patients
who were compensated after treatment. As there are limited studies on the
effects of acute decompensated HF treatment on these parameters in the
literature, further studies are needed on this subject, since the results are
limited and the controversial.

Kaynakça

  • 1. Cleland JG, Khand A, Clark A.The heart failure epidemic: Exactly how big is it? Eur Heart J 2001; 22: 623-6.
  • 2. Packer M, Carver JR, Rodeheffer RJ, Ivanhoe RJ, DiBianco R, Zeldis SM. Effect of oral milrinone on mortality in severe chronic heart failure. The PROMISE Study Research Group. N Engl J Med 1991; 325: 1468-75.
  • 3. Martin A, Foxall T, Blumberg JB, Meydani M. Alphatocopherol inhibits LDL-induced adhesion of monocytes to human aortic endothelial cells in vitro. Arterioscler Thromb Vasc Biol 1997; 17: 429-36.
  • 4. Jolly SR, Kane WJ, Bailie MB, Abrams GD, Lucchesi BR: Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase. Circ Res 1984;54:277-85.
  • 5. Nakamura H, Nakamura K, Yodoi J: Redox regulation of cellular activation. Annu Rev Immunol 1997;15: 351-69.
  • 6. Ceconi C, Curello S, Cargnoni A, Ferrari R, Albertini A, Visioli O: The role of glutathione status in the protection against ischaemic and reperfusion damage: effects of N-acetyl cysteine. J Mol Cell Cardiol 1988;20: 5-13.
  • 7. Singh A, Lee KJ, Lee CY, Goldfarb RD, Tsan MF: Relation between myocardial glutathione content and extent of ischemia-reperfusion injury. Circulation 1989;80:1795-804.
  • 8. Chen Z, Siu B, Ho YS, Vincent R, Chua CC, Hamdy RC, Chua BH: Overexpression of MnSOD protects against myocardial ischemia/reperfusion injury in transgenic mice. J Mol Cell Cardiol 1998;30:2281-9.
  • 9. Woo YJ, Zhang JC, Vijayasarathy C, Zwacka RM, Englehardt JF, Gardner TJ, Sweeney HL: Recombinant adenovirus-mediated cardiac gene transfer of superoxide dismutase and catalase attenuates postischemic contractile dysfunction. Circulation 1998;98:255-60.
  • 10. Cabigas EB, Somasuntharam I, Brown ME, Che PL, Pendergrass KD, Chiang B, Taylor WR, Davis ME: Overexpression of catalase in myeloid cells confers acute protection following myocardial infarction. Int J Mol Sci 2014;15:9036-50.
  • 11. Erel O. A novel automated method to measure total antioxidant response against potent free radical reactions. Clin Biochem 2004; 37: 112-9
  • 12. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989; 2: 358-67.
  • 13. Schiller NB, Acquatella H, Ports TA, Drew D, Goerke J, Ringertz H, et al. Left ventricular volume from paired biplane two-dimensional echocardiography. Circulation. 1979; 60: 547-55.
  • 14. LeLeiko RM, Vaccari CS, Sola S, Merchant N, Nagamia SH, Thoenes M, et al. Usefulness of elevations in serum choline and free F2)-isoprostane to predict 30-day cardiovascular outcomes in patients with acute coronary syndrome. Am J Cardiol. 2009;104: 638-43.
  • 15. Polidori MC, Pratico D, Savino K, Rokach J, Stahl W, Mecocci P. Increased F2 isoprostane plasma levels in patients with congestive heart failure are correlated with antioxidant status and disease severity. J Card Fail. 2004;10: 334-8.
  • 16. Hokamaki J, Kawano H, Yoshimura M, Soejima H, Miyamoto S, Kajiwara I, et al. Urinary biopyrrins levels are elevated in relation to severity of heart failure. J Am Coll Cardiol. 2004;43: 1880-5.
  • 17. Dhalla AK, Singal PK. Antioxidant changes in hypertrophied and failing guinea pig hearts. Am J Phys. 1994;266:1280-5.
  • 18. Hill MF, Singal PK. Right and left myocardial antioxidant responses during heart failure subsequent to myocardial infarction. Circulation. 1997;96: 2414-20.
  • 19. Shiomi T, Tsutsui H, Matsusaka H, Murakami K, Hayashidani S, Ikeuchi M, et al. Overexpression of glutathione peroxidase prevents left ventricular remodeling and failure after myocardial infarction in mice. Circulation. 2004;109: 544-9.
  • 20. Anker SD, Doehner W, Rauchhaus M, Sharma R, Francis D, Knosalla C, et al. Uric acid and survival in chronic heart failure: validation and application in metabolic, functional, and hemodynamic staging. Circulation. 2003;107: 1991-7.
  • 21. Kunsch C, Medford RM. Oxidative stress as a regulator of gene expression in the vasculature. Circ Res. 1999;85: 753-66.
  • 22. Baines CP, Goto M, Downey JM. Oxygen radicals released during ischemic preconditioning contribute to cardioprotection in the rabbit myocardium. J Mol Cell Cardiol. 1997;29: 207-16.
  • 23. Mehta JL, Li D. Epinephrine upregulates superoxide dismutase in human coronary artery endothelial cells. Free Radic Biol Med. 2001;30: 148-53.
  • 24. Muzakova V, Kandar R, Vojtisek P, Skalicky J, Vankova R, Cegan A, et al. Antioxidant vitamin levels and glutathione peroxidase activity during ischemia/reperfusion in myocardial infarction. Physiol Res. 2001;50: 389-96.

Akut dekompanse kalp yetersizliği hastalarında oksidatif stres indeksinin değerlendirilmesi

Yıl 2019, Cilt: 16 Sayı: 2, 375 - 379, 29.08.2019
https://doi.org/10.35440/hutfd.520377

Öz

Amaç:
Dekompanse kalp yetersizliği (KY), dokuların metabolik ihtiyacının
karşılanamaması sonucunda çeşitli metabolik ve fizyolojik süreçlere yol açar.
Bu süreçte üretilen reaktif oksijen türleri zararlı oksidatif reaksiyonlara yol
açar. Bu çalışmamızda, akut dekompanse KY hastalarında uygulanan tedavinin
oksidatif stres parametreleri ile ilişkisini ve bu parametrelerde düzelmeyi
sağlayıp sağlamadığını araştırmayı amaçladık.

Materyal ve Metot:
Dekompanse KY nedeniyle yatan toplamda 40 hasta çalışmaya alındı. Hastaların
yatışında tedavi öncesi ve taburculuk öncesinde tedavi sonrası antropometrik
ölçümleri, ekokardiyografileri, rutin biyokimyasal parametreler yanında total
antioksidan kapasite (TAK), total oksidatif seviye (TOS) ve bu ölçümlerin
oranlarından elde edilen oksidatif stres indeksi (OSİ) hesaplandı.

Bulgular:
KY tedavisi sonrası nabız, sistolik kan basıncı ve diyastolik kan basıncında
azalma, sol ventrikül ejeksiyon fraksiyonunda yükselme gözlendi (hepsi için
p<0.05). Ek olarak KY tedavisi sonrası alınan TAK, TOS ve OSİ değerlerinin
tedavi öncesi değerlere göre anlamlı olarak daha fazla olduğu izlendi (hepsi için
p<0.05). Yapılan korelasyon analizinde TAK ile sistolik ve diyastolik kan
basıncı arasında negatif bir ilişki olduğu (sırasıyla r: -0,307, p:0.014; r:
-0,393, p:0.001), EF ile de TAK ve OSİ arasında negatif bir ilişki olduğu
bulundu (sırasıyla r: -0,298, p:0.011; r:-0,326, p:0.005).







Sonuç:
Oksidatif stresin dekompanse KY hastalarında yüksek olduğu ve tedavi ile
kompansasyon sonrasında da bu yüksek seviyelerinin devam ettiği görüldü.
Literatürde akut dekompanse KY tedavisinin bu parametreleri ne düzeyde etkilediğini
gösteren çalışmalar sınırlı ve sonuçları tartışmalı olduğundan, bu konu ile
ilgili daha fazla çalışma yapılması gerekmektedir.

Kaynakça

  • 1. Cleland JG, Khand A, Clark A.The heart failure epidemic: Exactly how big is it? Eur Heart J 2001; 22: 623-6.
  • 2. Packer M, Carver JR, Rodeheffer RJ, Ivanhoe RJ, DiBianco R, Zeldis SM. Effect of oral milrinone on mortality in severe chronic heart failure. The PROMISE Study Research Group. N Engl J Med 1991; 325: 1468-75.
  • 3. Martin A, Foxall T, Blumberg JB, Meydani M. Alphatocopherol inhibits LDL-induced adhesion of monocytes to human aortic endothelial cells in vitro. Arterioscler Thromb Vasc Biol 1997; 17: 429-36.
  • 4. Jolly SR, Kane WJ, Bailie MB, Abrams GD, Lucchesi BR: Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase. Circ Res 1984;54:277-85.
  • 5. Nakamura H, Nakamura K, Yodoi J: Redox regulation of cellular activation. Annu Rev Immunol 1997;15: 351-69.
  • 6. Ceconi C, Curello S, Cargnoni A, Ferrari R, Albertini A, Visioli O: The role of glutathione status in the protection against ischaemic and reperfusion damage: effects of N-acetyl cysteine. J Mol Cell Cardiol 1988;20: 5-13.
  • 7. Singh A, Lee KJ, Lee CY, Goldfarb RD, Tsan MF: Relation between myocardial glutathione content and extent of ischemia-reperfusion injury. Circulation 1989;80:1795-804.
  • 8. Chen Z, Siu B, Ho YS, Vincent R, Chua CC, Hamdy RC, Chua BH: Overexpression of MnSOD protects against myocardial ischemia/reperfusion injury in transgenic mice. J Mol Cell Cardiol 1998;30:2281-9.
  • 9. Woo YJ, Zhang JC, Vijayasarathy C, Zwacka RM, Englehardt JF, Gardner TJ, Sweeney HL: Recombinant adenovirus-mediated cardiac gene transfer of superoxide dismutase and catalase attenuates postischemic contractile dysfunction. Circulation 1998;98:255-60.
  • 10. Cabigas EB, Somasuntharam I, Brown ME, Che PL, Pendergrass KD, Chiang B, Taylor WR, Davis ME: Overexpression of catalase in myeloid cells confers acute protection following myocardial infarction. Int J Mol Sci 2014;15:9036-50.
  • 11. Erel O. A novel automated method to measure total antioxidant response against potent free radical reactions. Clin Biochem 2004; 37: 112-9
  • 12. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989; 2: 358-67.
  • 13. Schiller NB, Acquatella H, Ports TA, Drew D, Goerke J, Ringertz H, et al. Left ventricular volume from paired biplane two-dimensional echocardiography. Circulation. 1979; 60: 547-55.
  • 14. LeLeiko RM, Vaccari CS, Sola S, Merchant N, Nagamia SH, Thoenes M, et al. Usefulness of elevations in serum choline and free F2)-isoprostane to predict 30-day cardiovascular outcomes in patients with acute coronary syndrome. Am J Cardiol. 2009;104: 638-43.
  • 15. Polidori MC, Pratico D, Savino K, Rokach J, Stahl W, Mecocci P. Increased F2 isoprostane plasma levels in patients with congestive heart failure are correlated with antioxidant status and disease severity. J Card Fail. 2004;10: 334-8.
  • 16. Hokamaki J, Kawano H, Yoshimura M, Soejima H, Miyamoto S, Kajiwara I, et al. Urinary biopyrrins levels are elevated in relation to severity of heart failure. J Am Coll Cardiol. 2004;43: 1880-5.
  • 17. Dhalla AK, Singal PK. Antioxidant changes in hypertrophied and failing guinea pig hearts. Am J Phys. 1994;266:1280-5.
  • 18. Hill MF, Singal PK. Right and left myocardial antioxidant responses during heart failure subsequent to myocardial infarction. Circulation. 1997;96: 2414-20.
  • 19. Shiomi T, Tsutsui H, Matsusaka H, Murakami K, Hayashidani S, Ikeuchi M, et al. Overexpression of glutathione peroxidase prevents left ventricular remodeling and failure after myocardial infarction in mice. Circulation. 2004;109: 544-9.
  • 20. Anker SD, Doehner W, Rauchhaus M, Sharma R, Francis D, Knosalla C, et al. Uric acid and survival in chronic heart failure: validation and application in metabolic, functional, and hemodynamic staging. Circulation. 2003;107: 1991-7.
  • 21. Kunsch C, Medford RM. Oxidative stress as a regulator of gene expression in the vasculature. Circ Res. 1999;85: 753-66.
  • 22. Baines CP, Goto M, Downey JM. Oxygen radicals released during ischemic preconditioning contribute to cardioprotection in the rabbit myocardium. J Mol Cell Cardiol. 1997;29: 207-16.
  • 23. Mehta JL, Li D. Epinephrine upregulates superoxide dismutase in human coronary artery endothelial cells. Free Radic Biol Med. 2001;30: 148-53.
  • 24. Muzakova V, Kandar R, Vojtisek P, Skalicky J, Vankova R, Cegan A, et al. Antioxidant vitamin levels and glutathione peroxidase activity during ischemia/reperfusion in myocardial infarction. Physiol Res. 2001;50: 389-96.
Toplam 24 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Klinik Tıp Bilimleri
Bölüm Araştırma Makalesi
Yazarlar

İdris Kırhan 0000-0001-6606-6078

Hakan Büyükhatipoğlu 0000-0002-9974-1081

Yayımlanma Tarihi 29 Ağustos 2019
Gönderilme Tarihi 31 Ocak 2019
Kabul Tarihi 1 Ağustos 2019
Yayımlandığı Sayı Yıl 2019 Cilt: 16 Sayı: 2

Kaynak Göster

Vancouver Kırhan İ, Büyükhatipoğlu H. Akut dekompanse kalp yetersizliği hastalarında oksidatif stres indeksinin değerlendirilmesi. Harran Üniversitesi Tıp Fakültesi Dergisi. 2019;16(2):375-9.

Harran Üniversitesi Tıp Fakültesi Dergisi  / Journal of Harran University Medical Faculty