Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 645 Clinicl Study Of Some Physiologicl Prmeters in Ptients With Acute Coronry Syndrome (ACS) in Thi-Qr Governorte / Irq Aly Mjid, Hdeel Rsheed Frj, Sjd. S. Afft Deprtment of Chemistry, College of Science,University of Thi-Qr,Irq Corresponding uthor:ali_83@yhoo.com Astrct Ojective: The cute coronry syndromes [unstle ngin (UA) nd cute myocrdil infrction (AMI)] re more dngerous thn others ischemic hert diseses (IHD) due to cute morphologicl chnges in therosclerotic plques which cuse (cute ischemi) severe imlnce etween myocrdium demnd nd oxygen supply. The present study ws designed to determine nd compre the levels of (GOT, GPT, Totl protein, Alumin,Gloulin nd Uric cid) in ptients with (ACS) nd helthy individuls. Mteril nd Methods: serum glutmte oxlocette trnsminse (S.GOT), serum glutmte pyruvte trnsminse (S.GPT), serum totl protein, serum lumin, serum gloulin nd serum uric cid levels were mesured in 75 sujects which were divided into three groups : (25) ptients of UA nd (25) ptients of AMI, were compred with (25) helthy sujects (control).results:the levels of serum glutmte oxloctte trnsminse(s.got), serum glutmte pyruvte trnsminse(s.gpt), serum lumin nd serum uric cid were significnt increse in ptients of (UA) nd (AMI) when compred with control. Wheres the levels of serum lumin showed significnt decrese in ptients of (UA) in comprison with control group, wheres its levels ws not ffected in lood serum of (AMI) ptients in comprison with control. While the levels of serum gloulin showed significnt increse in ptients of AMI in comprison with control group, wheres its levels ws not ffected in lood serum of (UA) ptients in comprison with control (p 0.01).Conclusion: High levels of GOT, GPT, gloulin nd low levels of totl protein nd lumin could e custive for ACS. Key word : Acute coronry syndrome, ischemic hert diseses, GOT, GPT, totl protein, lumin, uric cid, coronry hert diseses. 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 646 Introduction Acute Coronry Syndromes (ACS) is term used to descrie group of conditions resulting from cute myocrdil ischemi (insufficient lood flow to hert muscle) nd rnging from unstle ngin (incresing, unpredictle chest pin) to non STelevtion myocrdil infrction (NSTEMI) nd ST-elevtion myocrdil infrction (STEMI). The conditions re relted to vrying degrees of nrrowing or lockge of single or multiple coronry rteries tht provide lood, oxygen nd nutrients to the hert. This life-thretening disorder is mjor cuse of emergency medicl cre nd hospitliztion.(1) Coronry hert disese (CHD) is the leding cuse of deth in the whole world.(2) Ptients with ACS re divided into two groups: Ptients with nd without ST segment elevtion. ACS without ST segment elevtion (NSTEACS) lso includes unstle ngin pectoris (UA) nd non-st elevtion myocrdil infrction (NSTEMI). It is importnt to note tht UA is defined s ischemic chest pin t rest without rise in serum crdic iomrkers, while the estlishment of NSTEMI dignosis requires rise in serum crdic iomrkers. ACS with ST segment elevtion (STEMI) includes oth ST segment elevtion nd rise in serum crdic iomrkers.(3) Connection of UA, NSTEMI nd STEMI is sed on the fct tht these re closely connected conditions with similr pthogenesis nd clinicl presenttion, ut they do differ y the level of severity.(4) The World Helth Orgniztion estimtes tht ir pollution is responsile for 800,000 premture deth worldwide ech yer.(5) Numerous nonspecific mnifesttions my e recognized in ptients with cute MI. Although they re not generlly employed in estlishing the dignosis, wreness of their coexistence with infrction is importnt to void misinterprettion or erroneous dignosis of other disorders.(6) Asprtte minotrnsferse (AST, lso sometimes termed S.GOT) nd lnine minotrnsferse (ALT, lso sometimes termed S.GPT) re widely distriuted in cells throughout the ody. AST is found primrily in hert, liver, skeletl muscle, nd kidney, while ALT is found primrily in liver nd kidney, with lesser mounts in hert nd skeletl muscle. AST nd ALT ctivity in liver re out 7,000 nd 3,000 times serum ctivities, respectively.(7) ALT is exclusively cytoplsmic; oth mitochondril nd cytoplsmic forms of AST re found in ll cells.(8) The hlf-life of totl AST is 17 ± 5 hours, while tht of ALT is 47 ± 10 hours.(9) The hlf-life of mitochondril AST verges 87 hours.(10) In dults, 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 647 AST nd ALT ctivities re significntly higher in mles thn in femles, nd reference intervls vry with ge. Exmintion of the proteins in plsm cn provide informtion reflecting disese sttes in mny different orgn systems. Although the totl protein determintion gives some informtion out the ptient's generl sttus regrding nutrition, or severs orgn disese, further frctiontions yield fr more cliniclly useful informtion.(11) The clculted difference etween the totl protein nd lumin represents the vlue of ll gloulins, composite of the other frctions tht individully my rise severl folds in severe disorders.(12) Alumin is the mjor protein of humn plsm, usully consisting up to two thirds of the totl plsm protein.(13) Aout 40% of the lumin is present in the plsm, nd the other 60% is present in the extrcellulr spce.(14) However, the concentrtion of lumin in the smller intrvsculr comprtment is much higher ecuse of the reltive impermeility of the lood vessel wll. This concentrtion grdient cross the cpillry memrne is importnt in mintining plsm volume. (15) Uric cid is nturlly occurring product of purine metolism(y xnthine oxidse from xnthine nd hypoxnthine), which plys different roles in humn ody. (16) Uric cid is present in plsm in reltively high concentrtions: in men 302±60 µmol/l; in women, 234±52µmol/L. (16) Humns hve no enzyme to further oxidse uric cid, so n ccess of uric cid is excreted y kidney.(17) Uric cid is wek cid (pk 5.8) nd distriuted throughout the extrcellulr fluid comprtment s sodium urte. (18) We iming to mesure some physiologicl prmeters including (GOT, GPT, totl protein, lumin, gloulin nd uric cid in serum of ACS ptients. Mterils nd Methods This study ws conducted t AL-Hussein Teching Hospitl in Thi-Qr/Irq, especilly coronry cre unit (CCU). It included (75) sujects, control(25) nd ptients(50) dignosed with(acute Myocrdil Infrction nd unstle Angin/ Non STEMI). Aout(5mL)of lood smples of the ptients with unstle ngin (UA) NSTEMI, cute myocrdil infrction(ami) ptients nd controls were tken nd llowed to clot t room temperture in empty disposle tues centrifuge to seprte it in the centrifuge t 3000 rotor per minute (rpm)for 10min,the serum smples were seprted nd stored t (-20ºC) until nlyzed for serum glutmte oxlocette trnsminse 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 648 (S.GOT), glutmte pyruvte trnsminse(s.gpt),serum totl protein,serum lumin(al), gloulin, serum uric cid. Kits of glutmte oxlocette trnsminse(got) nd glutmte pyruvte trnsminse(gpt), totl protein,alumin(al), uric cid were purchsed from Biolo (Frnce) Sttisticl Anlysis : Dt were sttisticlly nlyzed using Pckge Socil Sciences (SPSS) for Windows version 12.0 softwre. All experimentl dt were expressed s men ± stndrd devition(sd). Results In this study we mesured the level of glutmte oxlocette trnsminse (GOT), glutmte pyruvte trnsminse (GPT),totl protein, lumin(al),gloulin,uric cid mong ptients with different ACS (UA/Non STEMI, AMI nd helthy individuls. Tle (1) shows significnt increse in concentrtions of serum glutmte oxlocette trnsminse (GOT) in group AMI in comprison with group UA/NSTEMI (p<0.01). Also there is significnt increse in concentrtions of serum glutmte oxlocette trnsminse (GOT) in ll ptients groups in comprison with CTR group (p<0.01). Also there is significnt increse in concentrtions of serum glutmte pyruvte trnsminse (GPT) in ll ptients groups in comprison with CTR group (p<0.01). Tle(2) shows significnt decrese (p<0.01) in concentrtions of serum totl protein in ll ptients groups in comprison with control group CTR, nd there is no significnt differences in concentrtion of serum totl protein etween AMI nd UA group cn e oserved. While there is significnt decrese(p<0.01) in concentrtions of serum lumin in group UA in comprison with CTR group nd there is no significnt differences in concentrtions of serum lumin in group AMI in comprison with groups (CTR nd UA).Wheres significnt increse (p<0.01) in concentrtion of serum gloulin in group AMI in comprison with group CTR, nd there is no significnt differences in concentrtions of serum gloulin in group UA in comprison with groups (CTR nd AMI).While, there is significnt increse(p<0.01)in concentrtions of serum uric cid in ll ptients groups in 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 649 comprison with control group CTR, nd there is no significnt differences in concentrtions of serum uric cid etween AMI nd UA groups cn e oserved. Tle (1) Serum GOT nd GPT concentrtions of CTR, UA nd AMI groups. Groups n GOT(U/L) GPT(U/L) CTR 25 c 29.54±6.57P 21.33±5.43P UA 25 77.60±6.98P 48.80±7.17P AMI 25 94.80±7.35P 52.66±11.00P * Ech vlue represents men ± SD vlues with non-identicl superscript (, or c etc.) were considered significntly differences ( P 0.01 ). CTR : Control group. UA: unstle ngin group. AMI: Acute myocrdil infrction group. Tle (2) Serum Ttl protein, Alumin, Gloulin nd Uric cid of CTR, UA nd AMI groups. Groups n Totl protein(mg/dl) Alumin(mg/dL) Gloulin(mg/dL) Uric cid(µmol/l) CTR 25 6.59±0.49 P 5.32±0.05P 1.27±0.23 P 210.30±65.90 P UA 25 5.31±0.58 P AMI 25 5.90±0.47 P 3.79±0.64P 1.51±0.46P 308.65±96.37P 4.07±0.49 P 1.82±0.48 P 290.50±70.80P Legend s in tle (1). 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 650 100 90 80 70 S.GOT (U / L) 60 50 40 30 20 10 0 CTR UA AMI Groups Figure (1) : Serum GOT levels of (CTR),(UA/NSTEMI) nd (AMI) groups. 60 50 S.GPT ( U / L) 40 30 20 10 0 CTR UA AMI Groups Figure (2) : Serum GPT levels of (CTR),(UA/NSTEMI) nd (AMI) groups. 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 651 7 6 S.Totl protein (mg/dl) 5 4 3 2 1 0 CTR UA AMI Groups Figure (3) : Serum Totl protein levels of (CTR),(UA/NSTEMI) nd (AMI) groups. S.Alumin (mg/dl) 6 5 4 3 2 1 0 CTR UA AMI Groups Figure (4) : Serum Alumin levels of (CTR),(UA/NSTEMI) nd (AMI) groups. 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 652 S.Gloulin (mg/dl) 2 1.8 1.6 1.4 1.2 1 0.8 0.6 0.4 0.2 0 CTR UA AMI Groups Figure (5) : Serum Gloulin levels of (CTR),(UA/NSTEMI) nd (AMI) groups. 350 300 S.Uric cid ( umol / L ) 250 200 150 100 50 0 CTR UA AMI Groups Figure (6) : Serum Uric cid levels of (CTR),(UA/NSTEMI) nd (AMI) groups. Discussion Ischemic hert disese (IHD) is condition in which there is n indequte supply of lood nd oxygen to portion of the myocrdium; it typiclly occurs when there is n imlnce etween myocrdil oxygen supply nd demnd. The most common cuse of myocrdil ischemi is therosclerotic disese of n coronry rtery (or rteries) sufficient to cuse regionl reduction in myocrdil lood flow nd indequte perfusion of the myocrdium supplied y the involved coronry rtery,(19) nd hence IHD re often termed coronry hert disese or coronry rtery 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 653 diseses (CAD).(20) Ptients with ischemic hert disese fll into two lrge groups: ptients with chronic CAD who most commonly present with stle ngin nd ptients with cute coronry syndrome (ACS). The ltter group, in turn, is composed of ptients with cute myocrdil infrction (AMI) with ST-segment elevtion on their presenting electrocrdiogrm (STEMI) nd those with unstle ngin (UA) nd non-st-segment elevtion MI (UA/NSTEMI). (19) In the present study, mrkers of myocrdil injury including GOT, GPT were significntly higher in AMI nd UA groups compred with control group. These results were greed with those stted y Bergovec et l.(2009) (3) who oserved tht mrkers of myocrdil injury cn e detected in the lood strem fter the onset of ischemic chest pin, which then llows the differentition etween UA(i.e., no iomrkers in circultion ; usully trnsient, if ny) nd NSTEMI (i.e., elevted iomrkers). The decrement in totl serum proteins concentrtion in ptients with UA nd AMI cn e explined y the fct tht myocrdil infrction is one of the condition tht initites the cute phse response, nd tht cn ffect the levels of specific heptic proteins (e.g: cute phse protein). (11) The depression, which hppened in serum lumin levels in cse of UA, is ccording to some cuses: (1) Incresing of the lumin excretion y kidney. (21) (2) Diffusing of the lumin into dmged tissues y mens of incresed permeility of lood vessels. (22) (3) Inflmmtion is considered the principle cuse of decrese in the serum lumin, however, IL-6 directly decreses the expression of lumin messenger RNA nd finlly. (23) (4) Its ntioxidnt function. According to the points (3) nd (4): (stopping for the lumin production nd consumption of the lumin to scvenge free rdicls with continuously. On the other hnd, n elevtion in serum gloulins tht is oserved in serum of AMI ptients cn e explined y the fct tht tissue dmge triggers the sequence of iochemicl nd cellulr events ssocited with inflmmtion, which include stimultion of synthesis of the cute phse proteins, with rise in the α1- nd α2- gloulin frctions.(15) The chnges of gloulins ina MI ptients cn e confirmed y the significnt differences in the PAGE pttrens of serum ptients when compred with control group. The different or dditionl nds tht pper in glycoprotein profile of the AMI ptients, prticulrly, in the gloulins region, cn e ttriuted to the fct, tht mny proteins of 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 654 cellulr memrns re glycoproteins, therefore when the myocyte cells ecme necrotic or ded (cell dmge), these proteins re relesed into the lood nd cuse ltrtion in serum glycoprotein profile.(24,25) This difference etween the men level of serum uric cid for ptients in ACS group nd control sujects cn e relted to denosine synthesis nd relese which re up regulted under conditions of hypoxi nd tissue ischemi.(26,27) Ischemi lso promotes the conversion of xnthine dehydrogense (XDH) to xnthineoxidse (XO), s the likely result of incresed intrcellulr clcium, nd ctivtion of proteses.wheres XDHctivity does not produce ctive oxygen species, the XOrection is mjor source of free rdicls during ischemi/reperfusion injury. So rised serum uric cid concentrtions re powerful predictor of crdiovsculr risk nd poor outcome. (28) References 1.Gururjn,P.; Gurumurthy,P. nd Nyr,P. Lipid profile nd non-enzymic ntioxidnt sttus in ptients with cute coronry syndrome in South Indi.Hert Lung nd Circultion.,19(2):75-80;2010. 2. World Helth Orgniztion. Chronic Ostructive Pulmonry Disese (COPD).,315;2009. 3. Bergovec,M.; Vrzic,H. nd Rjcn Spoljric,I. Fetures nd pthophysiology of cute coronry syndrome [ Olici ptofiziolgij kutnog koronrnog sindrom].acute Medic Crotic : Csopis Hrvtske Akdemije Medcinskih Znnosti.,63(1):3-7;2009. 4. Flconnet,C.; Crllo,S. nd Roffi,M. Acute coronry syndrome : Guidelines nd geritrics specificity (syndrome coronrien igu : Guidelines et specificite geritrique). Revue Medicle Suisse.,5(204):1137-1147;2009. 5. The World Helth Report 2002. Reducing risks, promoting helthy life. in World Helth Orgniztion (WHO) (dtse online);2002. Aville from Http://www.who.int/whr/2002/en/whr02 _en.pdf. 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 655 6. Brunwld,E.; Zipes,D.P. nd Lippy,P. "Hert Disese: textook of Crdiovsculr Medicine ",6 th edn.eds.w.b.sunders compny. Phildelphi., p.1131-1136;2001. 7.Lott,J.A. nd Wolf,P.L. Alnine nd sprtte minotrnsferse (ALT nd AST). Clinicl enzymology : cseoriented pproch. Chicgo, Yer Book Medicl Pulishers., 111-138;1986. 8. Rej,R. Mesurement of minotrnsferses : Prt 1. Asprtte minotrnsferse. CRC Crit Rev Clin L Sci.,21:99-106 ; 1984. 9. Price,P.C. nd Alerti,K.G.M.M. Biochemicl Assessment of Liver Function. in Wright R, Alerti KGMM, Krrn S, Millwrd Sdler GH(eds): Liver nd Bilir Disese Pthophysiology, Dignosis, Mngement. London : W.B. Sunders., 381-416;1979. 10. Pnteghini,M. Asprtte minotrnsferse isoenzymes. Clin Biochem., 23:311-319; 1990. 11. Kpln,L.A.; Pesce,A.J. nd Kzmierczk,S.C. "Clinicl Chemistry : Theory, Anlysis Correltion ", 4 th edn. Eds. Mosy. London., p. 570-575,627; 2003. 12. Burtis,C.A. nd AshwoodE.R. " Tetiz Fundmentls of Clinicl Chemistry ", 4 th edn. Eds. W.B. Sunders compny. Phldelphi., p. 272,274,275,376,727; 1996. 13. Peters,T. Serum lumin : Recent progress in the understnding of its structure nd iosynthesis. Clin. Chem., 23:5; 1977. 14. Murry,R.K.; Grnner,D.K.; Mys,P.A. nd Rodwell,V.W. " Hrper, s Illustrted Biochemistry ", 26 th edn. Eds. McGrw-Hill. USA., p. 205-583;2003. 15. Myne,P.D. " Clinicl Chemistry in dignosis nd Tretment ", 6 th edn. Eds.. Arnold., p.224,225,317,322; 2002. 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 656 16. Simic,M.G. nd Jovnovic,S.V. Antioxidnt Mechnisms of Uric Acid. J. AM Chem Soc., 111:15;1989. 17. Rodionov,R.N. " Urtes n endogenous ntioxidnt ". Free rdicls in Biology nd Medicine. Iow City.,IA 52242:77-222 ; 2003. 18. Clerg,M.J. nd Kjoller,E. Uric cid s mrker of pthophysiologicl mechnism in ptient with crdiovsculr disese. UgeskrLeger., 167(40): 3771-3774; 2005. 19. Dennis,L.; Ksper,E.B.; Anthony,S. nd Fuci. Hrrison, s Principles of Internl Medicine.17 th ed. McGrw-Hill., 1434-1436 ; 2008. 20. Michel,R.N. nd Cotrn,R.S. Cell injury, dpttion, nd deth. Roins Bsic Pthology. 7 th ed. Philddelphi: W.B. Sunders Compny.,p. 3-31; 2003. 21. Berton,G.; Citro,T. nd Plmieri,R. Alumin excretion rte increses during cute myocrdil infrction nd strongly predicts erly mortlity. Circultion., 96:3338-3345; 1997. 22. Weijenerg,M.P.; Feskens,E.J.M.; Souverijn,J.H.M. nd Kromhout,D. Serum lumin, coronry hert disese risk, nd mortlity in n elderly cohort. Epidemiology., 8(1): 87-92; 1997. 23. Kysen,G.A.; Duin,J.A.; Muller,H.G. nd Rosles,L. Inflmmtion nd reduced lumin synthesis ssocited with stle decline in serum lumin hemodilysis ptients. Kidney Interntionl., 65(4):1408-1415 ; 2004. 24. Bishop,M.L.; Fody,E.P. nd Schoeff,L. "Clinicl Chemistry : Principles, Procedures, Correltions " 5 th Edn. eds. Lippincott. Willims nd Wilkins. Phildelphi., p. 200-202,290-,370,372,503-508; 2005. 25. Gokmen,S.S.; Kilicli,G.; Ozcelik,F. nd Gulen,S. Serum totl nd lipid- ound silic cid levels following cute MI. Clin. Chem. L. Med., 38(12):1249-55;2000. 2014
Interntionl Journl of Scientific & Engineering Reserch, Volume 5, Issue 1, Jnury-2014 657 26. Rtikinen,M.J.; Peuhkurinen,K.J. nd Hssinen, I.E. Contriution of endothelium nd crdiomyocytes to hypoxi-induced denosine relese. J Mol Cell Crdiol., 26: 1069 1080; 1994. 27. Fredholm,B.B. nd Sollevi,A. Crdiovsculr effects of denosine.clin Physio., 6:1-21;1986. 28. Angel Chmorro.; Victor Och.; Alvro Cervero.; Mrin Revill.; Rmon Deutofeu. nd John, H. Aponte: Prognostic significnce of uric cid serum concentrtion in ptients with Acute Ischemic Stroke. Stroke., 33: 1048-1052; 2002. 2014