The Relationship Between The Level of Serum Uric Acid and No-Reflow Phenomenon After Primary Percutaneous Coronary Intervention in Patients With St Segment Elevated Myocardial Infarction

Abstract

No-reflow phenomenon is the absence of myocardial perfusion despite adequate dilatation ofthe infarct related coronary artery during percutaneous coronary intervention. Uric acid (UA)release during ischemia and washout from the ischemic zone during reperfusion is adeninenucleotide breakdown product. Therefore uric acid may play reperfusion injury and no-reflow.İn this study, we aimed to compare serum uric acid value of ST segment elevated Mİ patientsgroups whith no-reflow phenomenon and normal miyocardial perfusion after primary coronaryintervention.47 patients was enrolled consecutively to this study. During hospital admission, patients bloodsamples were taken for serum uric acid value. Patients was grouped as no reflow and normalperfusion groups according to myocardial blush grades (MBG). Patient with myocardial blushgrades 0-1 were accepted as no-reflow group, patients with MBG 2-3 normal perfusion group.When the serum uric acid value of no-reflow and normal perfusion groups was compared, therewas statistificaly significant difference (respectively 6,680±1,11 mg/dl versus 5,066±0,68 mg/dl.p

Keywords

• No-reflow,Uric acid,Acute myocardial infarction,primary coronary intervention

St Elevasyonlu Miyokard İnfarktüslü Hastalarda Primer Perkütan Girişim Sonrası No-Reflow Fenomeni Gelişimi ile Serum Ürik Asit Düzeyleri Arasındaki İlişki

Abstract

Perkütan koroner girişimlerde, sorumlu arterin açılmasına rağmen, miyokardial perfüzyonunsağlanamaması “no-reflow” fenomeni olarak tanımlanır. Adenin nükleotit metabolitlerinden biriolan ürik asidin hem iskemi sırasında, hem de reperfüzyon sırasında iskemik dokulardansalındığı gösterilmiş ve iskemik hasar ile reperfüzyon hasarında rol oynayabileceğidüşünülmüştür. Biz çalışmamızda ST elevasyonlu akut miyokard infarktüsü tanısı alıp, primerperkütan girişim uygulanan hastalarımızda, işlem sonrası anjiyografik olarak no-reflowfenomeni gelişen ve gelişmeyen gruplarda ürik asit değerlerini karşılaştırdık. Çalışmaya 47 hasta alındı. Olguların hastaneye gelişinde kan örnekleri alınarak ürik asit sayımıyapıldı. Hastalar primer perkütan girişim sonrası Miyokardial Blush Grade (MBG) derecelerinegöre iki gruba ayrıldı. Buna göre MBG 0 ve 1 olan olgular no-reflow fenomeni var, MBG 2 ve3 olan olgular no-reflow fenomeni yok, olarak kabul edildi.İki grup mutlak ürik asit değerleri açısından karşılaştırıldı ve no-reflow fenomeni gözlenenhastaların ürik asit değerleri ortalaması 6,680±1,11 mg/dl iken, no-reflow gözlenmeyen grupta5,066±0,68 mg/dl idi. İki değer arasındaki fark istatistiksel olarak anlamlı kabul edildi.(p

Keywords

• No-reflow,Ürik asit,Akut miyokard infarktüsü,Primer koroner girişim

References

1. Swain J, Gutteridge JMC.Prooxidant iron and copper, with ferroxidase and xanthine oxidase activities in human atherosiclerosis material. FEBS Lett. 368:513-515, 1995.
2. Ross R. The pathogenesis of atherosclerosis-an update. N Engl J Med. 314:488-500, 1986.
3. Grines CL, Browne KF, Marco J, et al. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. N Engl J Med. 328: 673-9, 1993.
4. The GUSTO angiographic investigators. The effects of tissue plasminogen activator, streptokinase, or both on coronary- artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med. 329: 1615-22, 1993.
5. Morishima I, Sone T, Mokuno S, et al. Clinical significance of no-reflow phenomenon observed on angiography after successful treatment of acute myocardial infarction with percutaneous transluminal coronary angioplasty. Am Heart J. 130: 239-43, 1995.
6. Piana RN, Paik GY, Moscucci M, et al. Incidence and treatment of 'no-reflow' after percutaneous coronary intervention. Circulation. 89: 2514-8, 1994.
7. Hamada S, Nakamura S, Sugiura T, et al. Early detection of the no-reflow phenomenon in reperfused acute myocardial infarction using technetium-99m tetrofosmin imaging. Eur J Nucl Med. 26: 208-14, 1999.
8. Ragosta M, Camarano G, Kaul S, et al. Microvascular integrity indicates myocellular viability in patients with recent myocardial infarction. New insights using myocardial contrast echocardiography. Circulation. 89: 2562-9, 1994.

9. Van't Hof A.W.J., Liem A., Suryapranta H.: Angiographic Assessment of Myocardial Reperfusion in patients treated with primary coronary angioplasty for acute myocardial infarction. Myocardial blush grade. Circulation. 97, 2302-2306, 1998.
10. Kuzmin AI, Tskitishvili OV, Serebryakova LI, Kapelko VI, Majorova IV, Medvedev OS. Allopurinol: kinetics, inhibition of xanthine oxidase activity, and protective effect in ischemic- reperfused canine heart as studied by cardiac microdialysis. J Cardiovasc Pharmacol. 25(4):564-71, 1995.
11. DeWall RA, Vasko KA, Stanley EL, Kezdi P. Responses of the ischemic myocardium to allopurinol. Am Heart J. 82:362-370, 1971.
12. Bando K, Tago M, Teramoto S. Prevention of free radical- induced myocardial injury by allopurinol. Experimental study in cardiac preservation and transplantation. J Thorac Cardiovasc Surg. 95:465-473, 1988.
13. Gertler MM, Garn SM, Levine SM. Serum uric acid in relation to age and physique in health and in coronary heart disease. Ann Intern Med. 34:1421-1431. 1951.
14. Klein R, Klein BE, Cornoni JC, Maready J, Cassel JC, Tyroler HA. Serum uric acid: its relationship to coronary heart disease risk factors and cardiovascular disease, Evans County, Georgia. Arch Intern Med. 132:401-410, 1973.
15. The Coronary Drug Project Research Group. Serum uric acid: its association with other risk factors and with mortality in coronary heart disease. J Chronic Dis. 29:557-569, 1976.
16. Bengtsson C, Lapidus L, Stendahl C, Waldenstrom J. Hyperuricemia and risk of cardiovascular disease and overall death: a 12-year follow-up of participants in the population study of women in Gothenburg, Sweden. Acta Med Scand. 224:549-555. 1988.
17. Freedman DS, Williamson DF, Gunter EW, Byres T. Relation of serum uric acid to mortality and ischemic heart disease: The NHANES I epidemiologic follow-up study. Am J Epidemiol. 141:637-644, 1995.
18. Kannel WB. Metabolic risk factors for coronary heart disease in women: perspective from the Framingham Study. Am Heart J. 114:413-419, 1987.
19. Tuttle KR, Short RA, Johnson RJ. Sex differences in uric acid and risk factors for coronary artery disease. Am J Cardiol. 87:1411-1414, 2001.
20. Newland H. Hyperuricemia in coronary, cerebral and peripheral arterial disease: an explanation. Med Hypotheses. 1:152-155, 1975.
21. Emmerson BT. Atherosclerosis and urate metabolism. Aust NZ J Med. 9:451-454, 1979.
22. Ginsberg MH, Kozin F, O’Malley M, McCarty DJ. Release of platelet constituents by monosodium urate crystals. J Clin Invest. 60:999-1007, 1977.
23. Rao GN, Corson MA, Berk CB. Uric acid stimulates vascular smooth muscle cell proliferation by increasing platelet-derived growth factor A-chain expression. J Biol Chem. 266:8604- 8608, 1991.
24. Boogaerts MA, Hammerschmidt DE, Roelant C, Verwilghen RL, Jacob HS. Mechanisms of vascular damage in gout and oxalosis crystal induced, granulocyte mediated, endothelial injury. Thromb Haemostas. 50:576-580, 1983.
25. DeScheeder IK, van de Kraay AM, Lamers JM, Koster JF, deJong JW, Serruys PW. Myocardial malodialdehyde and uric acid release after short-lasting coronary occlusions during angioplasty: potential mechanisms for free radical generation. Am J Cardiol. 68:392-395, 1991.
26. Leyva F, Anker S, Swan JW, et al. Serum uric acid as an index of impaired oxidative metabolism in chronic heart failure. Eur Heart J. 18:858-865, 1997.
27. Puig JG, Ruilope LM. Uric acid as a cardiovascular risk factor in arterial hypertension. J Hypertens. 17:869-872.
28. Patetsios P, Song M, Shutze WP, et al. Identification of uric acid and xanthine oxidase in atherosclerotic plaque. Am J Cardiology. 88:188-191, 2001.
29. Morishima I, Sone T, Okumura K, et al. Angiographic no- reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol. 36:1202-9, 2000.
30. Kloner RA, Ganote CE, Jennings RB. The ‘’no-reflow’’ phenomenon after temporary coronary occlusion in the dog. J Clin Invest. 54:1496-508, 1974.
31. Meisel SR, Shapiro H, Radnay J, et al. Increased expression of neutrophil and monocyte adhesion molecules LFA-1 and Mac-1 and their ligand ICAM-1 and VLA-4 throughout the acute phase of myocardial infarction. Possible implications for leukocyte aggregation and microvascular plugging. J Am Coll Cardiol. 31:120-5, 1998.