Study of the Arginase Activity and Other Biochemical Parameters in Patients with Coronary Artery Disease in Baghdad Governorate-Iraq
Keywords:KEYWORDS: Coronary Artery Disease , Arginase , Troponin I , dyslipidemia , hs-CRP
The most prevalent form of heart disease and the main cause of death in both developed and developing nations is CAD. It happens when "plaque," or cholesterol or other fatty deposits that accumulate on the inner wall of the artery, narrows or blocks the arteries that deliver blood to the heart. Over time, chest pain might develop as a result of the reduction in blood flow to the heart caused by this plaque accumulation. The study was designed to find if Arginase acts as a biomarker for diagnosing Coronary Artery Disease (CAD). A total of 90 individual samples were included in the present study, the control group consist of 40 healthy individual samples, while the CAD patients were 50 individual samples. Some biochemical parameters such as fasting blood glucose (FBG), troponin I(TnI), high sensitivity C-reactive protein (hs-CRP), lipid profile, lactate dehydrogenase (LDH), and Arginase activity were analyzed. The results of the current study showed no significant differences in the average age of patients (67.00±6.78) when compared with the control group (61.10±6.46), P>0.05. A significant increase Was found in the FBI level, cholesterol, triglycerides, very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), TnI, hs-CRP, LDH, and Arginase activity in the patient's group when compared with the control group. While significant decrease (P<0.05) was revealed in the high-density lipoprotein (HDL) level in CAD patients in comparison to the control group. Also, there was a positive significant correlation between Arginase activity with each age and FBG. As for the ROC operator curve for Arginase, it was found that the area under the curve (AUC) was 0.953 with a sensitivity of 90%, and specificity of 95%. The results in the present study indicate a possible use of Arginase as a diagnostic marker for CAD.
Chaudhary P., Kumar R., Verma A. K., Singh D., Yadav V., Chhillar A. K., and Chandra R. (2006). "Synthesis and antimicrobial activity of N-alkyl and N-aryl piperazine derivatives". Bioorganic & medicinal chemistry, 14(6), 1819-1826.
Rathish I. G., Javed K., Ahmad S., Bano S., Alam M. S., Pillai K. K., and Bagchi V. (2009). "Synthesis and antiinflammatory activity of some new 1, 3, 5-trisubstituted pyrazolines bearing benzene sulfonamide". Bioorganic & medicinal chemistry letters, 19(1), 255-258.
Bansilal B., Ali N., Afzal N., Khan T. S., and Shahjahan S. (2007). "Antioxidant status in coronary heart disease (CHD) patients with type 2 diabetes mellitus". Journal of Ayub Medical College Abbottabad.
Mamolo M. G., Zampieri D., Falagiani V., Vio L., and Banfi E. (2001). "Synthesis and antimycobacterial activity of 5-aryl-1-isonicotinoyl-3-(pyridin-2-yl)-4, 5-dihydro-1H-pyrazole derivatives". Il Farmaco.
Negi A. S., Kumar J. K., Luqman S., Shanker K., Gupta M. M., Kand hanuja S. P. S. (2008). "Recent advances in plant hepatoprotectives: a chemical and biological profile of some important leads". Medicinal Research Reviews.
Clemente G., van Waarde A. F. ,Antunes I., Dömling A.,and H. Elsinga P. (2020)." Arginase as a potential biomarker of disease progression: a molecular imaging perspective". International Journal of Molecular Sciences.
Caldwell R. W., Rodriguez P. C., Toque H. A., Narayanan S. P., and Caldwell R. B. (2018)."Arginase: a multifaceted enzyme important in health and disease". Physiological reviews.
Yu H., Yoo P. K., Aguirre C. C., Tsoa R. W., Kern R. M., Grody W. W.,and Iyer R. K. (2003). "Widespread expression of arginase I in mouse tissues: biochemical and physiological implications". Journal of Histochemistry & Cytochemistry.
Suman M., and Rajnikant M. (2017). "Mitochondrial membrane-bound activity of arginase is independent of nitrogen excretion pattern in ureogenic and non-ureogenic vertebrates".
Shah S. F. A., Khan M. J., Iqbal T., Akram S., Waheed F., Satti H. S., and Hussain S. (2019). "Arginase-1 variants and the risk of familial coronary artery disease in subjects originating from Pakistan". Genetic Testing and Molecular Biomarkers.
Shemyakin A. (2012)."Arginase Inhibition Improves Endothelial Function in Patients with Coronary Artery Disease and Type 2 Diabetes". Circulation.
Wernly B., Pernow J., Kelm M., and Jung C. (2020). "The role of arginase in the microcirculation in cardiovascular disease". Clinical Hemorheology and Microcirculation.
Bekpinar S., Gurdol F., Unlucerci Y., Develi S., and Yilmaz A. (2011). "Serum levels of arginase I are associated with left ventricular function after myocardial infarction". Clinical biochemistry.
Porembska Z.,and Kedra M. (1975). "Early diagnosis of myocardial infarction by arginase activity determination". Clinica Chimica Acta.
Porembska, Z., & Kedra, M. (1975). "Early diagnosis of myocardial infarction by Arginase activity determination".Clinica Chimica Acta.
Kövamees O., Shemyakin A., and Pernow J. (2016). "Amino acid metabolism reflecting arginase activity is increased in patients with type 2 diabetes and associated with endothelial dysfunction". Diabetes and vascular disease research.
Ryoo S., Bhunia A., Chang F., Shoukas A., Berkowitz D. E., and Romer L. H. (2011). "OxLDL-dependent activation of arginase II is dependent on the LOX-1 receptor and downstream RhoA signaling". Atherosclerosis.
Zhang R., Ji, Z., Qu Y., Yang M., Su Y., Zuo W., and Li Y. (2020)." Clinical value of ARG1 in acute myocardial infarction patients: Bioinformatics-based approach". Biomedicine & Pharmacotherapy.
Sharma S. B., Garg S., Veerwal A.,and Dwivedi S. (2008)."hs-CRP and oxidative stress in young CAD patients: a pilot study". Indian journal of clinical biochemistry.
Khaki K. F., Yaghoubi A. R., Zarghami N., and Rahbani M. (2011). "Evaluation of hs-CRP, antioxidant markers and MDA in patients of Coronary Artery Disease (CAD) containing Non-Smokers and Non-Diabetics". Clinical Biochemistry.
Arroyo-Espliguero R., Avanzas P., Cosín-Sales J., Aldama G., Pizzi C., and Kaski J. C. (2004). "C-reactive protein elevation and disease activity in patients with coronary artery disease". European heart journal.
Khatibi F. K., Yaghoubi A., Zarghami N., Rahbani M., and Babaie H. (2013). "Evaluation of hs-CRP, Antioxidant Markers andMDA in Patients of Coronary Artery Disease (CAD) Containing Non-Smokers and Non-Diabetics". Journal of Cardiovascular and Thoracic Research.
Jia Y., Wen W., Yang Y., Huang M., Ning Y., Jiao X., and Zhang M. (2021). "The clinical role of combined serum C1q and hsCRP in predicting coronary artery disease". Clinical Biochemistry.
Romero M. J., Platt D. H., Tawfik H. E., Labazi M., El-Remessy A. B., Bartoli M., and Caldwell R. W. (2008)."Diabetes-induced coronary vascular dysfunction involves increased arginase activity". Circulation research.
Zhou Z., Mahdi A., Tratsiakovich Y., Zahorán S., Kövamees O., Nordin F., and Pernow J. (2018). "Erythrocytes from patients with type 2 diabetes induce endothelial dysfunction via arginase I". Journal of the American College of Cardiology.
Kim J. H., Bugaj L. J., Oh Y. J., Bivalacqua T. J., Ryoo S., Soucy K. G., and Berkowitz D. E. (2009)."Arginase inhibition restores NOS coupling and reverses endothelial dysfunction and vascular stiffness in old rats". Journal of applied physiology.
Jung C., Grün K., Betge S., Pernow J., Kelm M., Muessig J.,and Franz M. (2017)."Arginase inhibition reverses monocrotaline-induced pulmonary hypertension". International Journal of Molecular Sciences.
Ren B., Van Kampen E., Van Berkel T. J., Cruickshank S. M., and Van Eck M. (2017). "Hematopoietic arginase 1 deficiency results in decreased leukocytosis and increased foam cell formation but does not affect atherosclerosis". Atherosclerosis, 256, 35-46.
Pourcet B., and Pineda-Torra I. (2013). "Transcriptional regulation of macrophage arginase 1 expression and its role in atherosclerosis". Trends in cardiovascular medicine, 23(5), 143-152.
Malakar A. K., Choudhury D., Halder B., Paul P., Uddin A., and Chakraborty S. (2019)." A review on coronary artery disease, its risk factors, and therapeutics". Journal of cellular physiology.
Quitter F., Figulla H. R., Ferrari M., Pernow J., and Jung C. (2013). "Increased arginase levels in heart failure represent a therapeutic target to rescue microvascular perfusion". Clinical hemorheology and microcirculation.
Shah S. F. A., Iqbal T., Qamar R., Rafiq M. A., and Hussain S. (2018). "ARG1 gene polymorphisms and their association in individuals with essential hypertension: a case-control study". DNA and Cell Biology.
Zhao X., Wang D., and Qin L. (2021). "Lipid profile and prognosis in patients with coronary heart disease: a meta-analysis of prospective cohort studies". BMC cardiovascular disorders. Disord.
Ramirez A., and Hu P. P. (2015)."Low high-density lipoprotein and risk of myocardial infarction". Clinical Medicine Insights: Cardiology.
Arora S., Qamar A., Gupta P., Vaduganathan M., Chauhan I., Tripathi A. K., and Gupta M. D. (2019). "Design and rationale of the North Indian ST‐Segment Elevation Myocardial Infarction Registry: A prospective cohort study". Clinical cardiology.
Venkateshwarlu M.,and Gayathri C. (2015)."Study of significance of estimation of lipid profile in patient with acute myocardial infarction". Int J Inf Res Rev.
Kopel E., Kivity S., Morag-Koren N., Segev S., and Sidi Y. (2012)."Relation of serum lactate dehydrogenase to coronary artery disease". The American journal of cardiology.
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