Aydın Rodi Tosu, Mustafa Yurtdaş, Mahmut Özdemir, Murat Selçuk, Nesim Aladağ, Yemlihan Ceylan, Tayyar Akbulut, Yüksel Kaya

İzole Koroner Arter Ektazilerinde Serum Ürik Asit ve C-reaktif Protein Düzeylerinin Değerlendirilmesi

Giriş: İzole koroner arter ektazileri (KAE) ciddi koroner arter darlığı olmaksızın normal koroner arter bölgesine göre 1,5 kat veya daha fazla arter genişlemesi olarak tanımlanır. KAE'nin nedeni tam olarak bilinmemekle beraber patogenezinde en çok artmış inflamasyon suçlanmaktadır. Serum ürik asit (SÜA) ve C-reaktif protein (CRP) inflamasyonun yaygın kullanılan belirteçleridir. Biz bu çalışmada SÜA ve CRP ile izole KAE arasındaki muhtemel ilişkiyi araştırdık.Hastalar ve Yöntem: Bu çalışmada bilinen veya süpheli iskemik kalp hastalığı nedeniyle Ocak 2011-Ağustos 2012 tarihleri arasında hastanemizde koroner anjiyografi yapılan 4600 hasta geriye dönük olarak değerlendirildi. Dışlanma kriterleri sonrası, çalışma popülasyonumuz 110 (Erkek, 63,6%; ort. yaş, 55,1±2,5 yıl) izole KAE hastası, bu grupla yaş, cinsiyet ve kardiyovasküler risk faktörleri (vücut kütle indeksi, hipertansiyon, diyabet, hiperlipidemi ve sigara içiciliği) olarak eşlenmiş 110 koroner arter hastası (KAH) (Erkek, 63,6%, ort. yaş, 55,2±2,3 yıl) ve 100 anjiyografik olarak normal koroner arterlere sahip hastayı (Erkek, 63,6%, ort. yaş, 55,2±2,5 yıl) kapsadı.Bulgular: Serum ürik asit düzeyi KAE ve KAH grupları arasında anlamlı fark göstermezken (6,5±0,5 mg/dl ve 6,4±0,5 mg/dl; p>0,05), kontrol grubuna (5,1±0,5 mg/dl) göre her iki grupta da anlamlı derecede yüksek bulundu (p<0,001). Benzer şekilde serum CRP düzeyi KAE ve KAH grupları arasında anlamlı fark göstermezken (1,8±0,0 mg/dl ve 1,7±0,3 mg/dl; p>0,05), kontrol grubuna (1,1±0,4 mg/dl) göre her iki grupta da anlamlı derecede yüksek bulundu (p<0,01).Sonuç: KAE olanlarda, normal koroner arterlere sahip olanlar ile karşılaştırıldığında, SÜA ve CRP seviyelerinin yüksek olduğunu ancak KAH ile karşılaştırıldığında anlamlı farklılık olmadığını saptadık. Bu veriler, KAE ve KAH'ın ortak patofizyolojik mekanizmaya sahip olduğunu düşündürmektedir.

Anahtar Kelimeler:

Koroner ektazi, koroner arter hastalığı; serum ürik asit; C-reaktif protein

Evaluation of the Serum Levels of Uric Acid and C-reactive Protein in Isolated Coronary Artery Ectasia

Introduction: Isolated coronary artery ectasia (CAE) is defined as the arterial enlargement of 1.5 times or more compared to the adjacent normal arterial portion without significant coronary artery stenosis. Although the exact cause is not clearly known, increased inflammation is the most responsible factor in pathogenesis of CAE. Serum uric acid (SUA) and C-reactive protein (CRP) are the most widely used markers of inflammation. In this study, we aimed to investigate the possible association of isolated CAE with SUA and CRP levels.Patients and Methods: In this study, 4.600 patients undergoing coronary angiography in our hospital due to a known or suspected ischemic heart disease between January 2011 and August 2012 were retrospectively evaluated. Following the exclusion criteria, our study population consisted of 110 (63.6% males, mean age: 58.1±9.5 years) isolated CAE patients, 110 patients (63.6% males, mean age: 55.2.4±2.3 years) with coronary artery diseases (CAD) who were matched with this group in age, gender and cardiovascular risk factors (body mass index, hypertension, diabetes, hyperlipidemia and smoking status) and 100 patients with angiographically normal coronary arteries (51.0% males; mean age: 57.6±10.1 years). Basal SUA and CRP are routinely measured in our clinic before the coronary angiography.Results: Serum level of uric acid did not show a significant difference between CAE and CAD groups (6.5±0.5 mg/dL and 6.4±0.5 mg/dL; p>0.05), while this value was found significantly higher in both groups compared to the controls (5.1±0.5 mg/dL; p<0.001). Similarly, there was not a significant difference between CAE and CAD groups in terms of the serum level of CRP (1.8±0.0 mg/dL and 1.7±0.3 mg/dL; p>0.05), while CRP values were significantly higher in both groups compared to the controls (1.1±0.4 mg/dL; p<0.001).Conclusion: We found that levels of SUA and CRP were higher in the patients with CAE than in subjects with normal coronary artery, but no significant different was found compared to patients with CAD. These data suggest that both CAE and CAD shared common pathophysiological mechanisms.

Keywords:

Coronary ectasia, coronary artery disease; serum uric acid; C-reactive protein,

PDF

___

Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG, et al. Aneurysmal coronary artery disease. Circulation 1983;67:134-8.
Tunick PA, Slater J, Kronzon I, Glassman E. Discrete atherosclerotic coronary artery aneurysms: a study of 20 patients. J Am Coll Cardiol 1990;15:279-82.
Kruger D, Stierle U, Herrmann G, Simon R, Sheikhzadeh A. Exercise- induced myocardial ischemia in isolated coronary artery ectasias and aneurysms (“dilated coronopathy”). J Am Coll Cardiol 1999;34:1461-70.
Alford WC Jr, Stoney WS, Burrus GR, Frist RA, Thomas CS Jr. Recognition and operative management of patients with arteriosclerotic coronary artery aneurysms. Ann Thorac Surg 1976;22:317-21.
Freedman DS, Williamson DF, Gunter EW, Byers T. Relation of serum uric acid to mortality and ischemic heart disease. The NHANES I Epidemiologic Follow-up Study. Am J Epidemiol 1995;141:637-44.
Fessel WJ. High uric acid as an indicator of cardiovascular disease. Independence from obesity. Am J Med 1980;68:401-4.
Culleton BF, Larson MG, Kannel WB, Levy D. Serum uric acid and risk for cardiovascular disease and death: the Framingham Heart Study. Ann Intern Med 1999;131:7-13.
Ruggiero C, Cherubini A, Ble A, Bos AJ, Maggio M, Dixit VD, et al. Uric acid and inflammatory markers. Eur Heart J 2006;27:1174-81.
Many A, Hubel CA, Roberts JM. Hyperuricemia and xanthine oxidase in preeclampsia, revisited. Am J Obstet Gynecol 1996;174:288-91.
Kato M, Hisatome I, Tomikura Y, Kotani K, Kinugawa T, Ogino K, et al. Status of endothelial dependent vasodilation in patients with hyperuricemia. Am J Cardiol 2005;96:1576-8.
Erdoğan D, Güllü H, Çalışkan M, Yıldırım E, Bilgi M, Ulus T, et al. Relationship of serum uric acid to measures of endothelial function and atherosclerosis in healthy adults. Int J Clin Pract 2005;59:1276-82.
Tavil Y, Kaya MG, Oktar SO, Şen N, Okyay K, Yazıcı HU, et al. Uric acid level and its association with carotid intima-media thickness in patients with hypertension. Atherosclerosis 2008;197:159-63.
Tillett WS, Francis T Jr. Serological reactions in pneumonia with a non- protein somatic fraction of pneumococcus. J Exp Med 1930;52:561-71.
Calabró P, Willerson JT, Yeh ET. Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation 2003;108:1930-2.
Yasojima K, Schwab C, McGeer EG, McGeer PL. Generation of C-reactive protein and complement components in atherosclerotic plaques. Am J Pathol 2001;158:1039-51.
Venugopal SK, Devaraj S, Jialal I. Macrophage conditioned medium induces the expression of C-reactive protein in human aortic endothelial cells: potential for paracrine/autocrine effects. Am J Pathol 2005;166:1265-71.
Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987;316:1371-5.
Newburger JW, Takahashi M, Gerber MA, Gewitz MH, Tani LY, Burns JC, et al. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation 2004;110:2747-71.
Ross R. Atherosclerosis-an inflammatory disease. N Engl J Med 1999;340:115-26.
Demopoulos VP, Olympios CD, Fakiolas CN, Pissimissis EG, Economides NM, Adamopoulou E, et al. The natural history of aneurysmal coronary artery disease. Heart 1997;78:136-41.
Farquharson CA, Butler R, Hill A, Belch JJ, Struthers AD. Allopurinol improves endothelial dysfunction in chronic heart failure. Circulation 2002;106:221-6.
Jaramillo M, Naccache PH, Olivier M. Monosodium urate crystals synergize with IFN-gamma to generate macrophage nitric oxide: involvement of extracellular signal-regulated kinase 1/2 and NF-kappa B. J Immunol 2004;172:5734-42.
Turhan H, Erbay AR, Yasar AS, Balci M, Bicer A, Yetkin E. Comparison of c-reactive protein levels in patients with coronary artery ectasia versus patients with obstructive coronary artery disease. Am J Cardiol 2004;94:1303-6.
Aydin M, Tekin IO, Dogan SM, Yildirim N, Arasli M, Sayin MR, Aktop Z. The levels of tumor necrosis factor-alpha and interleukin-6 in patients with isolated coronary artery ectasia. Mediators Inflamm 2009;2009:106145.
Dogan A, Tuzun N, Turker Y, Akcay S, Kaya S, Ozaydin M. Matrix metalloproteinases and inflammatory markers in coronary artery ectasia: Their relationship to severity of coronary artery ectasia. Coron Artery Dis 2008;19:559-63.
Koşar F, Sincer İ, Aksoy Y, Topal E, Çehreli S. Increased aortic stiffness in patients with coronary artery ectasia. Coron Artery Dis 2005;16:499-504.
Torzewski J, Torzewski M, Bowyer DE, Fröhlich M, Koenig W, Waltenberger J, et al. C-reactive protein frequently co-localizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arterioscler Thromb Vasc Biol 1998;18:1386-92.
Torzewski M, Rist C, Mortensen RF, Zwaka TP, Bienek M, Waltenberger J, et al. C-reactive protein in the arterial intima: role of C-reactive protein receptor-dependent monocyte recruitment in atherogenesis. Arterioscler Thromb Vasc Biol 2000;20:2094-9.
Cao JJ, Thach C, Manolio TA, Psaty BM, Kuller LH, Chaves PH, et al. C-reactive protein, carotid intima-media thickness, and incidence of ischemic stroke in the elderly: the Cardiovascular Health Study. Circulation 2003;108:166-70.
Curb JD, Abbott RD, Rodriguez BL, Sakkinen P, Popper JS, Yano K, et al. C-reactive protein and the future risk of thromboembolic stroke in healthy men. Circulation 2003;107:2016-20.
James SK, Armstrong P, Barnathan E, Califf R, Lindahl B, Siegbahn A, et al. Troponin and C-reactive protein have different relations to subsequent mortality and myocardial infarction after acute coronary syndrome: a GUSTO-IV substudy. J Am Coll Cardiol 2003;41:916-24.
Ockene IS, Matthews CE, Rifai N, Ridker PM, Reed G, Stanek E. Variability and classification accuracy of serial high-sensitivity C-reactive protein measurements in healthy adults. Clin Chem 2001;47:444-50.

ISSN: 2149-2972
Yayın Aralığı: Yılda 3 Sayı
Başlangıç: 1990
Yayıncı: Sağlık Bilimleri Üniversitesi, Kartal Koşuyolu Yüksek İhtisas Eğitim ve Araştırma Hastanesi