Koroner Arter Hastalarında Hipertansiyonun İnflamatuar Reaksiyona Additif Etkisi

Year 2013, Volume: 14 Issue: 3, 129 - 134, 01.12.2013

Ali Taner

Abstract

Objective: Investigation about an additional contribution of hypertension (HT) to inflammatory process in stable coronary artery disease (CAD). Material and Methods: Patients were divided into three groups . Group I only with CAD, Group II generated with patients with HT in addition to the CAD. The control group was created with healthy volunteers of similar age group. hs-CRP, IL-1β, IL-6, IL-10 and TNF-α levels were measured. Results: When hs-CRP levels are compared the value of hsCRP in patients with CAD was found to be significantly increased (HR: 1.4 ± 0.8 mg / L , control: 0.7 ± 0.6 mg / L , p <0.01). When the patients with HT in addition to the CAD and the patients in control group are compared , the value of hs-CRP were significantly increased in the group of CAD+HT (CAD+HT: 1.9 ± 1.2 mg / L, Control: 0.7 ± 0.6 mg /L, p <0.001 ). When the TNF-α and IL-1β levels between the CAD group and the control group are compared TNF-α and IL-1β levels in patients with CAD was found to have significantly increased TNF-α value. However, IL-10 levels were not different between groups. Conclusion: Even if it is stable, the inflammatory response in patients with CAD was significantly higher than that in the control group. HT demonstrated an additive effect on the inflammatory process

Keywords

Coronary artery disease; stabil angina; inflammatory markers

Koroner Arter Hastalarında Hipertansiyonun İnflamatuar Reaksiyona Additif Etkisi

Abstract

Amaç: Stabil koroner arter hastalığında (KAH) hipertansiyonun (HT) inflamatuar sürece ilave katkısının olup olmadığını araştırmaktır. Gereç ve Yöntem: Hastalar üç gruba ayrıldı; Grup I sadece KAH olan, Grup II ise KAH’a ilaveten HT’si olan hastalardan oluşturuldu. Kontrol grubu benzer yaş grubunda sağlıklı gönüllülerden oluşturuldu. hs-CRP, IL-1β, IL-6, IL-10 ve TNFα’nın düzeyleri ölçüldü. Bulgular: hs-CRP değerleri karşılaştırıldığında, KAH grubunda hs-CRP değerinin anlamlı derecede artmış olduğu bulundu (KAH: 1.4±0.8 mg/L, Kontrol: 0.7±0.6 mg/L, p <0.01). KAH’a HT’nin eşlik ettiği grup ile kontrol grubu karşılaştırıldığında KAH+HT grubunda hs-CRP değerinin anlamlı derecede artmış olduğu saptandı (KAH+HT:1.9±1.2 mg/L, Kontrol: 0.7±0.6 mg/L, p <0.001). KAH grubu ile kontrol grubu arasındaki TNF-α ve IL-1β değerleri karşılaştırıldığında KAH grubunda TNF-α değerinin anlamlı derecede artmış olduğu bulundu. Bununla birlikte, IL-10 değerleri karşılaştırıldığında gruplar arasında fark olmadığı belirlendi. Sonuç: Stabil dahi olsa, KAH hastalarında kontrol grubuna göre artmış inflamatuar yanıt saptandı. HT’nin inflamatuar süreç üzerine additif etkisi gösterilemedi

Keywords

Koroner arter hastalığı; stabil angina; inflamatuar markerler

References

• Gordon T, Kannel WB. Premature mortality from coronary heart disease. The framingham study. JAMA 1971;215(10):1617-25.
• Choi H, Cho DH, Shin HH, Park JB. Association of high sensitivity C reactive protein with coronary heart disease prediction, but not with carotid atherosclerosis, in patients with hypertension. Circ J 2004;68(4):297-303.
• Gensini GF, Comeglio OM, Colella A. Classical risk factors and emerging elements in the risk profile for coronary artery disease. Eur Heart Journal 1998;19(Suppl A):53-61.
• Pietri P, Vyssoulis G, Vlachopoulos C, et al. Relationship between low-grade inflammation and arterial stiffness in patients with essential hypertension. J Hypertens 2006;24(11):2231-8.
• Frohlich ED. Potential mechanisms explaining the risk of left ventricular hypertrophy. Am J Cardiol 1987;59(2):91-7.
• Novo S, Abringnani MG, Corda M, Strano A. Cardiovascular structural changes in hypertension: possible regression during long-term antihypertensive treatment. Eur Heart J 1991;12(Suppl G):47-52.
• Farkas K, Kolossvary E, Jarai Z, Nemcsik J, Farsang C. Noninvasive assessment of microvascular endothelial function by laser doppler flowmetry in patients with essential hypertension. Atherosclerosis 2004;173(1):97- 102.
• Lekakis JP, Papathanassiou S, Papaioannou TG, et al. Oral L-arginine improves endothelial dysfunction in patients with essential hypertension. Int J Cardiol 2002;86(2-3):317-23.
• Burnett JC Jr. Coronary endothelial dysfunction in the hypertensive patient: from myocardial ischemia to heart failure. J Hum Hypertens 1997;11(1):45-9.
• Pagano PJ, Clark JK, Cifuentes-Pagano ME, Clark SM, Callis GM, Quinn MT. Localization of a constitutively active phagocyte-like NADPH oxidase in rabbit aortic adventitia: enhancement by angiotensin II. Proc Natl Acad Sci USA 1997;94(26):14483-8.
• Mervaala EM, Müller DN, Park JK, et al. Monocyte infiltration and adhesion molecules in a rat model of high human renin hypertension. Hypertension 1999;33(1 Pt 2):389-95.
• Dörffel Y, Lätsch C, Stuhlmüller B, et al. Preactivated peripheral blood monocytes in patients with essential hypertension. Hypertension 1999;34(1):113-7.
• Puddu P, Puddu GM, Zaca F, Muscari A. Endothelial dysfunction in hypertension. Acta Cardiol 2000;55(4):221- 32.
• Lemarie CA, Esposito B, Tedgui A, Lehoux S. Pressure
• induced vascular activation of nuclear factor-kappa B: role in cell survival. Circ Res 2003;93(3):207-12.
• Renaudin C, Bataillard A, Sassard J. Partial transfer of genetic hypertension by lymphoid cells in Lyon rats. J Hypertens 1995;13(12 Pt 2):1589-92.
• Martinez Amenós A, Buendia E, Carreras L, et al. Humoral and cellular immunological abnormalities in hypertensive patients. J Clin Hypertens 1985;1(2):153-60.
• Fu ML. Abnormal immune system and hypertension: where arewe? Ann Med 1995;27(6):671-4.
• Verma S, Wang CH, Li SH, et al. A self-fulfilling prophecy: C reactive protein attenuates nitric oxide production and inhibits angiogenesis. Circulation 2002;106(8):913-9.
• Maat MP, Haverkate F, Kluft C. Relationship between CRP and clinical course of unstable angina depends on assay method. Vascul Pharmacol 2002;39(3):113-5.
• Hingorani AD, Cross J, Kharbanda RK, et al. Acute systemic inflammation impairs endothelium dependent dilatation in humans. Circulation 2000;102(9):994-9.
• Bhagat K, Moss R, Collier J, Vallance P. Endothelial "stunning" following a brief exposure to endotoxin: a mechanism to link infection and infarction? Cardiovasc Res 1996;32(5):822-9.
• Chung NA, Beevers DG, Lip G. Effects of losartan versus hydrochlorothiazide
• damage/dysfunction, angiogenesis and tissue factor in essential hypertension. Blood Pres 2004;13(3):183-9.
• Felmeden DC, Blann AD, Spencer CG, Beevers DG, Lip GY. A comparison of flow-mediated dilatation and von Willebrand factoras markers of endothelial cell function in health and in hypertension: relationship to cardiovascular risk and effects of treatment: a substudy of the Anglo- Scandinavian Cardiac Outcomes Trial. Coagul Fibrinolysis 2003;14(5):425-31.
• Sieg-Dobrescu D, Burnier M, Hayoz D, Brunner HR, Waeber B. The return of increased blood pressure after discontinuation of antihypertensive treatment is associated with an impaired postischemic skin blood flow response. J Hypertens 2001;19(8):1387-92.
• Nagano M, Nakamura M, Sato K, Tanaka F, Segawa T, Hiramori K. Association between serum C-reactive protein levels and pulse wave velocity: a population-based cross- sectional study in a general population. Atherosclerosis 2005;180(1):189-95.
• Mattace-Raso FU, van der Cammen TJ, van der Meer
• IM, et al. C-reactive protein and arterial stiffness in older adults: 2004;176(1):111-6. Study.
• Atherosclerosis 27. Mc Eniery CM, Wilkinson IB. Large artery stiffness and inflammation. J Hum Hypertens 2005;19(7)507-9.
• Mc Carron RM, Wang L, Siren AL, Spatz M, Hallenbeck JM. endothelial
• normotensive rats. Am J Physiol 1994;267(6 Pt 2):2491-7. from cells hypertensive
• and Okamura T, Moriyama Y, Kadowaki T, Kanda H, Ueshima H. Non-invasive measurement of brachial-ankle pulse wave velocity is associated with serum C-reactive protein but not with alphatocopherolin Japanese middle-aged male workers. Hypertens Res 2004;27(3):173-80.
• Nurnberger J, Keflioglu-Scheiber A, Opazo Saez AM, Wenzel RR, Philipp T, Schafers RF. Augmentation index is associated 2002;20(12):2407-14. J
• Hypertens 31. Higashi Y, Sasaki S, Nakagawa K, Matsuura H, Oshima T, Chayama K. Endothelial function and oxidative stress in renovascular 2002;346(25):1954-62. N Engl J
• Med Chrysohoou C, Pitsavos C, Panagiotakos DB, Skoumas J, Stefanadis C. Association between prehypertension status and inflammatory markers related to atherosclerotic disease: The ATTICA Study. Am J Hypertens 2004;17(7):568- 73.
• Gage JE, Hess OM, Murakami T, Ritter M, Grimm J, Krayenbuehl HP. Vasoconstriction of stenotic coronary arteries during dynamic exercise in patients with classic angina pectoris: reversibility by nitroglycerin. Circulation 1986;73(5):865-76.
• Chang JA, Froelicher VF. Clinical and exercise test markers of prognosis in patients with stable coronary artery disease. Curr Probl Cardiol 1994;8(3):533-87.
• Fox KM. European trial on reduction of cardiac events with Perindopril in stable coronary artery disease investigators. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo- controlled, multicentre trial (the EUROPA study). Lancet 2003;362(9386)782-8.