Significant Alteration of Nitrogen Species in Acute Myocardial Infarction does not Relate to the Site of Infarction

Abstract

This study aimed to assess the level of nitrogen species in patients presented with acute myocardial infarction and to relate the levels of nitrogen species to the infarction site. A total number of 113 patients admitted to the intensive care unit at Diyala Teaching Hospital. The patients were presented within 6 hours of pain onset and diagnosed as acute myocardial infarction using electrocardiograph criteria and positive cardiac troponin test. The most common infarction site was anterior followed by inferior and lateral. Serum peroxynitrite level was significantly higher than healthy subjects by 100 folds and serum nitric oxide level is significantly reduced compared with healthy subjects by 50%. There were non significant differences in nitrogen species regarding the infarct sites. Associated risk factors e.g. hypertension, diabetes mellitus and smoking influenced the nitrogen species levels. It concludes that the significant alterations in nitrogen species not related to the site of acute infarction

Keywords

• Acute myocardial infarction, nitric oxide, peroxynitrite

Significant Alteration of Nitrogen Species in Acute Myocardial Infarction does not Relate to the Site of Infarction

Öz

Bu çalışmada akut miyokard infarktüsü ile başvuran hastalarda seviyesini ve enfarktüs bölgesi ile nitrojen türlerinin ilişkisi değerlendirmek amaçlanmıştır. Diyala Eğitim Hastanesi'nde yoğun bakım ünitesine başvuran 113 hasta çalışmaya alındı . Hastalar ağrı başlangıcından ilk 6 saat içinde sunulan elektrokardiyografi kriterleri ve pozitif troponin testi ile akut miyokard infarktüsü tanısı konuldu. En yaygın enfarktüs bölgesi anteriyor, inferiyor ve lateral idi. Serum peroksinitritlerin seviyesi 100 kez sağlıklı kontrol grubuna göre daha yüksekti. Serum nitrik oksit düzeyi %50 oranında sağlıklı bireylerle karşılaştırıldığında zalmıştı. Enfarktüs bölgelerine göre nitrojen türlerinin anlamlı olmayan farklılıklar vardı. Hipertansiyon, diabetes mellitus ve sigara gibi ilişkili risk faktörleri nitrojen türlerinin düzeylerini etkilemiştir. Bu azot türlerindeki değişiklikler akut enfarktüs bölgesi ile ilgili olmadığı sonucuna varılmıştır

Anahtar Kelimeler

• Akut miyokard infarktüsü, nitrik oksit, peroksinitrit

References

1. Thygesen K, Alpert JS, White HD. Universal definition of myocardial infarction. J Am Coll Cardiol 2007; 50:2173–95
2. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000; 36:959–69
3. Antman EM, Tanasijevic MJ, Thompson B, et al. Cardiac- specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996; 335:1342–9.
4. Lorgis L, Zeller M, Dentan G, et al. Prognostic value of N-terminal pro-brain natriuretic peptide in elderly peo- ple with acute myocardial infarction: prospective obser- vational study. BMJ 2009; 338:b1605.
5. Wollert KC, Kempf T, Lagerqvist B, et al. Growth differ- entiation factor 15 for risk stratification and selection of an invasive treatment strategy in non ST-elevation acute coronary syndrome. Circulation 2007; 116: 1540–8
6. Khan SQ, Dhillon O, Struck J, et al. C-terminal pro-endo- thelin-1 offers additional prognostic information in pa- tients after acute myocardial infarction: Leicester Acute Myocardial Infarction Peptide (LAMP) Study. Am Heart J 2007; 154: 736–42
7. Suleiman M, Khatib R, Agmon Y, et al. Early inflamma- tion and risk of long-term development of heart failure and mortality in survivors of acute myocardial infarction predictive role of C-reactive protein. J Am Coll Cardiol 2006; 47:962–8
8. Mocatta TJ, Pilbrow AP, Cameron VA, et al. Plasma concen- trations of myeloperoxidase predict mortality after myo- cardial infarction. J Am Coll Cardiol 2007; 49:1993–2000

9. Szabo C. Hydrogen sulphide and its therapeutic potential. Nat Rev Drug Discov 2007; 6:917–35.
10. Sharp BR, Jones SP, Rimmer DM, Lefer DJ. Differential re- sponse to myocardial reperfusion injury in eNOS-deficient mice. Am J Physiol Heart Circ Physiol 2002; 282:H2422–6
11. Elrod JW, Greer JJ, Bryan NS, et al. Cardiomyocyte- specific overexpression of NO synthase-3 protects against myocardial ischemia-reperfusion injury. Arterioscler Thromb Vasc Biol 2006;26:1517–23.
12. Jones SP, Greer JJ, Kakkar AK, et al. Endothelial ni- tric oxide synthase overexpression attenuates myocar- dial reperfusion injury. Am J Physiol Heart Circ Physiol 2004;286:H276–H282.
13. Hataishi R, Rodrigues AC, Neilan TG, et al. Inhaled nitric oxide decreases infarction size and improves left ventric- ular function in a murine model of myocardial ischemia- reperfusion injury. Am J Physiol Heart Circ Physiol 2006; 291:H379–84
14. Bolli R. Cardioprotective function of inducible nitric ox- ide synthase and role of nitric oxide in myocardial isch- emia and preconditioning: an overview of a decade of research. J Mol Cell Cardiol 2001;33:1897–918
15. Kleinbongard P, Dejam A, Lauer T, et al. Plasma nitrite concentrations reflect the degree of endothelial dysfunc- tion in humans. Free Radic Biol Med 2006; 40:295–302
16. Newaz MA, Yousefipour Z, Nawal N, Adeeb N. Nitric oxide synthase activity in blood vessels of spontaneously hyper- tensive rats: Antioxidant protection by gamma-tocotri- enol. J Physiol Pharmacol 2003; 54 :319-27
17. Beckman JS, Ischiropoulos H, Zhu L, van der Woerd M, Smith C, Chen J. Kinetics of superoxide dismutase and iron -catalyzed nitration of phenolics by peroxynitrite. Arch Biochem Biophys 1992; 298: 438-45
18. VanUffelen BE, Van Der Zee J, De Koster BM, Vanstereninck J, Elferink JG. Intracellular but not extracellular conversion of nitroxyl anion into nitric oxide leads to stimulation of human neutrophil migration. Biochem J 1998;330: 719-22
19. Abdel-Aziz TA, Mohamed RH. Association of endothelial nitric oxide synthase gene polymorphisms with classical risk factors in development of premature coronary artery disease. Mol Biol Rep 2013;40(4):3065-71.
20. Djordjevic VB, Stojanovic I, Cosic V, et al. Serum neop- terin, nitric oxide, inducible nitric oxide synthase and tu- mor necrosis factor-alpha levels in patients with ischemic heart disease. Clin Chem Lab Med 2008; 46:1149-55.
21. Li JL, Yang Z, Wu S, Kong J. Relationship between en- dothelial nitric oxide synthase, insulin resistance and macrovascular disease in patients with acute myocardial infarction. J Int Med Res 2012;40: 687-93.
22. Bekpinar S, Gurdol F, Unlucerci Y, Develi S, Yilmaz A. Serum levels of arginase I are associated with left ven- tricular function after myocardial infarction. Clin Biochem 2011;44 :1090-3.
23. Cavalca V, Veglia F, Squellerio I, et al. Circulating levels of dimethylarginines, chronic kidney disease and long- term clinical outcome in non-ST-elevation myocardial in- farction. PLoS One 2012; 7:e48499.
24. Veeravalli KK, Akula A, Kota MK. Nitric oxide- and prosta- glandin-mediated cardioprotection by bradykinin in myo- cardial ischemia and reperfusion injury. Pol J Pharmacol 2003; 55: 1021-9
25. Bianchi C, Wakiyama H, Faro R, et al. A novel per- oxynitrite decomposer catalyst (FP-15) reduces myocar- dial infarct size in an in vivo peroxynitrite decomposer and acute ischemia-reperfusion in pigs. Ann Thorac Surg 2002;74:1201-7.
26. Huang C, Cui Y, Ji L, et al. Catalpol decreases peroxynitrite formation and consequently exerts cardioprotective effects against ischemia/reperfusion insult. Pharm Biol 2013 22.