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Akut ST Segment Elevasyonlu Miyokard İnfarktüsü Geçiren N-asetil Sistein Uygulanan Hastalarda Oksidatif Stres ve QT Dispersiyonu İlişkisi

Relationsip Between Oxidative Stress and QT Dispersion in Patients With Acute ST Segment Elevation Myocardial Infarction Treated With N-acetylcysteine

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Abstract (2. Language): 
The aim of this study was to assess the effect of N-acetylcysteine (NAC) treatment, as an adjunct therapy in myocardial infarction on oxidative stress, infarct size and dispersion of QT. Patients with acute myocardial infarction received either 15 mgc of NAC infused intravenously over 24 hours (n=15) or no NAC (n=15), combined along with streptokinase. In order to assess the oxidative stres, plasma malondialdehyde (MDA) level was measured at admission and after 4 and 24 hours. For all patients, QT dispersion (QTd) and Bazett rate corrected QTc dispersion (QTcd) were measured from a high quality 12 lead ECG recorded at 50 mm/s on admission, at 4 and 24 hours. Coronary angiography were performed to assess reperfusion. At admission, plasma MDA levels were not different between the groups. In the NAC treated patients percent plasma MDA changes according to the baseline decreased whereas in the NAC non-treated patients percent MDA changes increased at 4 and 24 hours (p=0.001 and p=0.0001, respectively). Significant decreases in the percent QTd (p=0,04) and QTcd (p=0.03) period changes were observed in patients treated with NAC compaired to patients treated without NAC at 24 hours. N-acetylcysteine treatment reduces lipid peroxidation during ischemia and reperfusion and decreases QT dispersion
Abstract (Original Language): 
Çalışmanın amacı, miyokard infarktüsünde ek tedavi olarak, N-asetil sisteinin (NAS) oksidatif stres, infarkt büyüklüğü ve QT dispersiyonu üzerine olan etkisinin değerlendirilmesidir. Akut miyokard infarktüsü (Mİ) geçiren hastalar, streptokinaz ile birlikte 24 saat süreyle intravenöz infüzyon şeklinde 15 gram N-asetil sistein alanlar (n=15) ve almayanlar (n=15) şeklinde iki gruba ayrıldı. Oksidatif stresin değerlendirilmesi için kabulde, 4 saatte ve 24. saatte plazma malondialdehid (MDA) düzeyleri ölçüldü. Tüm hastaların başlangıçta, 4. ve 24. saatte 50 mm/sn ile 12 derivasyonlu elektrokardiyografileri çekilerek QT dispersiyonları ve “Bazett” formülü ile hıza göre düzeltilmiş QT dispersiyonları hesaplandı. Reperfüzyonun değerlendirilmesi için koroner anjiyografi yapıldı. Kabulde her iki grup arasında plazma MDA düzeyleri arasında farklılık yoktu. N-asetil sistein ile tedavi edilen hastalarda, plazma MDA düzeyleri azalırken, NAS ile tedavi edilmeyen hastalarda, plazma MDA düzeyleri 4. saat ve 24. saatte artış gösterdi (sırasıyla p=0.001 ve p=0.0001). 24. saatte NAS alan hastalarda, NAS almayan hastalara göre, QT dispersiyonu (p=0,04) ve hıza göre düzeltilmiş QT dispersiyonunun yüzde değişiminde (p=0.03) anlamlı olarak azalma izlendi. NAS tedavisi, iskemi reperfüzyon sırasında lipid peroksidasyonunu ve sonucunda QT dispersiyonunu anlamlı olarak azaltabilmektedir.
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REFERENCES

References: 

1. Goldhaber JI, Weiss JN. Oxygen free radicals and cardiac
reperfusion abnormalities. Hypertension 1992;20:118-27.
2. Grech ED, Dodd NJ, Jackson MJ, et al. Evidence for free
radical generation after primary percutaneous transluminal
coronary angioplasty recanalization in acute myocardial
infarction. Am J Cardiol 1996;77:122-7.
3. Buechter DD. Free radicals and oxygen toxicity. Pharm Res
1988;5:253-60.
4. Bolli R, Patel BS, Jeroudi MO, Lai EK, McCay PB.
Demonstration of free radical generation in “stunned”
myocardium of intact dogs with the use of the spin trap alphaphenyl N-tert-butyl nitrone. J Clin Invest 1988;82:476-85.
5. Bolli R. Mechanism of myocardial “stunning”. Circulation
1990;82:723-38.
6. Suzuki S, Kaneko M, Chapman DC, Dhalla NS. Alterations in
cardiac contractile proteins due to oxygen free radicals.
Biochim Biophys Acta 1997;1074:95-100.
7. Dhalla NS, Golfman L, Takeda S, Takeda N, Nagano M
Evidence for the role of oxidative stress in acute ischemic
heart disease: a brief review. Can J Cardiol 1999;15:587-93.
8. Liu P, Hock CE, Nagele R, Wong PY. Formation of nitric
oxide, superoxide, and peroxynitrite in myocardial ischemiareperfusion injury in rats. Am J Physiol 1997;272:2327-36.
9. Singh A, Lee KJ, Lee CY, Goldfarb RD, Tsan MF. Relation
between myocardial glutathione content and extent of
ischemia-reperfusion injury. Circulation 1989;80:1795-1804.
10. Haramaki N, Stewart DB, Aggarwal S, et al. Networking
antioxidants in the isolated rat heart are selectively depleted
by ischemia-reperfusion. Free Radic Biol Med 1998;25:329-
39.
11. Bolli R, Jeroudi MO, Patel BS, et al. Marked reduction of free
radical generation and contractile dysfunction by antioxidant
therapy begun at the time of reperfusion. Evidence that
myocardial "stunning" is a manifestation of reperfusion injury.
Circ Res 1989;65:607-22.
12. Sethi R, Takeda N, Nagan M, Dhalla NS. Beneficial effects of
vitamin E treatment in acute myocardial infarction. J
Cardiovasc Pharmacol Ther 2000;5:51-58.
13. Ferrari R, Ceconi C, Curello S, et al. Oxygen free radicals and
myocardial damage: protective role of thiol-containing agents.
Am J Med 1991;91:95-105.
14. Sochman J, Kolc J, Vrana M, Fabian J. Cardioprotective
effects of N-acetylcysteine: the reduction in the extent of
infarction and occurrence of reperfusion arrhythmias in the
dog. Int J Cardiol 1990;28:191-6.
15. Forman MB, Puett DW, Cates CU, et al. Glutathione redox
pathway and reperfusion injury. Effect of N-acetylcysteine on
infarct size and ventricular function. Circulation 1988;78:202-
13.
16. Kloner R, Rude R, Carlson N, et al. Ultrastructural evidence
of microvascular damage and myocardial cell injury after
coronary artery occlusion: which comes first? Circulation
1980;62:945–52.
17. Claeys MJ, Bosmans J, Veenstra L, et al. Determinants and
prognostic implications of persistent ST-segment elevation
after primary angioplasty for acute myocardial infarction:
importance of microvascular reperfusion injury. Circulation
1999;99:1272–7.
18. Bourke JP, Young AA, Richards DAB, et al. Reduction in
incidence of inducible ventricular tachycardia after
myocardial infarction by treatment with streptokinase during
infarct evolution. J Am Coll Cardiol 1990;16:1703–10.
19. Zareba W, Moss A, le Cessie S. Dispersion of ventricular
repolarization and arrhythmic cardiac death in coronary artery
disease. Am J Cardiol 1994;74:550–3.
20. Barr C,Waas A, FreemaM, et al. QT dispersion and sudden
unexpected death in chronic heart failure. Lancet
1994;343:327–9.
21. Oikatinen L, Viitasalo M,Toivonen L. Dispersion of the QT
interval in postmyocardial infarction patients presenting with
ventricular tachycardia or with ventricular fibrillation. Am J
Cardiol 1998;81:694–7.
22. Pye M, Quinn A, Cobbe A. QT interval dispersion: a noninvasive marker of susceptibility to arrhythmia in patients
with sustained ventricular arrhythmia. Br Heart J
1994;71:511–4.
23. Perkiömäki J, Koistimen M, Yli-Mäyry S, et al. Dispersion of
QT interval in patients with and without susceptibility to
ventricular tachyarrythmias after previous infarction. J Am
Coll Cardiol 1995;26:174–9.
24. Young IS, Trimble ER. Measurement of malondialdeyhde in
plasma by high performance liquid choromatography with
fluorimetric detection. Ann Clin Biochem 1991;28:504-8.
25. Bazzet HC. An analysis of time relation of electrocardiogram.
Heart 1920;28:67-73.
26. Tieleman RG, Crijns HJ, Wiesfeld AC, et al. Increased
dispersion of refractoriness in the absence of QT prolongation
in patients with mitral valve prolapse and ventricular
arrhythmias. Br Heart J 1995;73:37-40.
27. Higham PD, Furniss SS, Campbell RW. QT dispersion and
components of the QT interval in ischaemia and infarction. Br
Heart J 1995;73:32-6.
28. Glancy JM, Garratt CJ, Woods KL, de Bono DP. QT
dispersion and mortality after myocardial infarction. Lancet
1995 ;345:945-6.
29. Yunus A, Gillis AM, Duff HJ, Wyse DG, Mitchell LB.
Increased precordial QTc dispersion predicts ventricular
fibrillation during acute myocardial infarction. Am J Cardiol
1996;78:706-8.
30. Loo A, Arendts W, Hohnloser SH. Variability of QT
dispersion measurements in the surface electrocardiogram in
patients with acute myocardial infarction and in normal
subjects. Am J Cardiol 1994;74:1113-8
31. Day CP, McComb JM, Campbell RWF. Reduction in QT
dispersion by sotalol following myocardial infarction. Eur
Heart J 1991;12:423-7.
32. Moreno FL1, Villanueva MT, Karagounis LA, Anderson JL.
Reduction in QT interval dispersion by successful
thrombolytic therapy in acute myocardial infarction.
Circulation 1994;90:94-100.
33. Nielsen F, Mikkelsen BB, Nielsen JB, Andersen HR,
Grandjean P. Plasma malondialdehyde as biomarker for
oxidative stress: reference interval and effects of life-style
factors. Clinical Chemistry 1997;3:1209-1214.
34. Tripathi Y, Hegde BM. Effect of N-acetylcysteine on
myocardial infarct size following ischemia and reperfusion in
dogs. Indian J Physiol Pharmacol 1998;42:50-5.
35. Glancy JM, Garratt CJ, de Bono DP. Dynamics of QT
dispersion during myocardial infarction and ischemia. Int J
Cardiol 1996;57:55-60.
36. Cowan JC, Yusoff K, Moore M, et al. Importance of lead
selection in QT interval measurement. Am J Cardiol
1988;61:83– 7.
37. Akira T, Kimiaki N, Yoshiaki M, Masaru N. Relation of QT
dispersion to infarct size and left ventricular wall motion in
anterior wall acute myocardial infarction. Am J Cardiol
1999;83:1423–6.
38. Boesgaard S, Iversen HK, Wroblewski H, et al. Altered
peripheral vasodilator profile of nitroglycerin during longterm infusion of N-acetylcysteine. J Am Coll Cardiol
1994;23:163-9.
39. Horowitz JD, Henry CA, Syrjanen ML, et al. Combined use of
nitroglycerin and N-acetylcysteine in the management of
unstable angina pectoris. Circulation 1988;77:787-94.

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