|Year : 2018 | Volume
| Issue : 2 | Page : 225-228
Biochemical changes in adiponectin and myeloperoxidase in acute myocardial infarction
Raafat R Mohammed, Hussein Abdel-Maksoud, Yasser M Abdel-Nabi
Biochemistry Department, Faculty of Veterinary Medicine, Benha University, Benha, Egypt
|Date of Submission||29-Jan-2018|
|Date of Acceptance||21-Mar-2018|
|Date of Web Publication||17-Aug-2018|
Dr. Raafat R Mohammed
Central Laboratory, Faculty of Medicine, Benha University, Benha, Qalubia, 13111
Source of Support: None, Conflict of Interest: None
Background Nitric oxide is a common mediator for the action of adiponectin and myeloperoxidase (MPO). Its importance is as a predictor of acute myocardial infarction (AMI) severity.
Aim The aim of the present study was to find a relationship between plasma adiponectin level, MPO activity, lipid profile, serum nitrite/nitrate, and severity of AMI disease.
Patients and methods To achieve this aim, 30 patients with AMI with age ranged from 35 to older than 70 years and 10 clinically healthy participants as control were subjected to this study.
Results The result of this study showed a significant association between the occurrence of AMI and low adiponectin level, high MPO activity, low nitrite level, high total cholesterol level, high triacylglycerol level, high low-density lipoprotein-cholesterol level, low high-density lipoprotein-cholesterol level, and high low-density lipoprotein-cholesterol/high-density lipoprotein-cholesterol ratio. These parameters may all be regarded as predictors or risk factors for AMI.
Conclusion The findings of the present study suggest that hyperlipidemia, vascular inflammation, and oxidative stress are primary interacting mediators in the pathogenesis of AMI.
Keywords: acute myocardial infarction, adiponectin, myeloperoxidase
|How to cite this article:|
Mohammed RR, Abdel-Maksoud H, Abdel-Nabi YM. Biochemical changes in adiponectin and myeloperoxidase in acute myocardial infarction. Benha Med J 2018;35:225-8
|How to cite this URL:|
Mohammed RR, Abdel-Maksoud H, Abdel-Nabi YM. Biochemical changes in adiponectin and myeloperoxidase in acute myocardial infarction. Benha Med J [serial online] 2018 [cited 2018 Oct 18];35:225-8. Available from: http://www.bmfj.eg.net/text.asp?2018/35/2/225/239186
| Introduction|| |
Adipose tissue secretes many proatherogenic and antiatherogenic adipokines such as leptin and adiponectin that play an important role in the pathogenesis of atherosclerosis and coronary artery disease . The adipokines, leptin and adiponectin, are considered as a potentially important link between systemic inflammatory processes and cardiovascular disease ,.
Myeloperoxidase (MPO) is a leukocyte-derived proinflammatory and proatherogenic enzyme that participates in the processes of development, progression, and complication of coronary artery disease through various mechanisms . MPO converts low-density lipoprotein (LDL) into an atherogenic form, oxidized LDL; provides oxidative stress condition; and decreases nitric oxide (NO) bioavailability, all leading to atherosclerosis ,,,. Thus, adiponectin was hypothesized to play a role in acute myocardial infarction (AMI) , and MPO also plays a pathophysiologic role in AMI .
NO has a role in both acute and chronic inflammation and was proposed to play a role in AMI atherogenesis .
This study was aimed to find a relationship among plasma adiponectin level, MPO activity, lipid profile, and serum NO metabolites (nitrite/nitrate) in patients with AMI.
| Patients and methods|| |
The study was done in the Emergency Center in Faculty of Medicine, Alexandria University Hospital, on 30 patients complaining of acute chest pain and 10 healthy individuals as control. Inclusion and exclusion criteria for the diagnosis of patients with AMI were applied . Then, they were classified into four groups according to ages, control, and three diseased groups:
- Group I consists of 10 healthy individuals from 35 to 70 years as a control group.
- Group II consists of 10 patients with AMI from 30 to 50 years.
- Group III consists of 10 patients with AMI from 51 to 70 years.
- Group IV consists of 10 patients with AMI with age more than 70 years.
A cardiologist in the coronary care unit finally established the diagnosis of AMI guided by the WHO criteria.
During coronary angiography, using a cardiac catheter, 10 ml of blood was withdrawn and collected from every patient and control healthy participant after overnight fasting. The blood samples were divided into two parts.
The first one was evacuated into tubes with 5% EDTA. Plasma samples were collected after centrifugation and used freshly for determination of adiponectin concentration . The remaining granulocyte/erythrocyte pellets were further processed for separation of neutrophils to assess MPO activity ,.
The remaining 5 ml of blood is evacuated in tubes without an anticoagulant and then allowed to clot and centrifuged for isolation of serum, which was used freshly for determination of NO metabolites (nitrate/nitrite) , total cholesterol , triacylglycerol (TG) , high-density lipoprotein-cholesterol (HDL-C), LDL-C, and very low-density lipoprotein-cholesterol (VLDL-C) concentrations .
| Results|| |
The data presented revealed that AMI is accompanied by significant decrease (P<0.05) in the mean values of plasma adiponectin level, serum nitrite, serum nitrate, and serum HDL-C and a significant increase (P<0.05) in the activity of MPO, serum total cholesterol, TG, LDL-C, and VLDL-C in comparison with the mean values recorded in the control healthy individual group ([Table 1] and [Table 2]).
|Table 1 Mean values±SE of plasma adiponectin (ng/ml), myeloperoxidase activity (unit/mg protein), serum nitrite (µmol/l), and serum nitrate (µmol/l) in control healthy and individuals with AMI|
Click here to view
|Table 2 Mean values±SE of serum total cholesterol (mg/dl), triacylglycerol (mg/dl), HDL-cholesterol (mg/dl), LDL-cholesterol (mg/dl), and VLDL-cholesterol (mg/dl) in healthy control and individuals with acute myocardial infarction|
Click here to view
| Discussion|| |
Myocardial infarction is exhibited in 10–15% of patients presented to the hospitals with chest pain annually .
Cardiovascular biomarkers including MPO, adiponectin, interleukins, and chemokines are under intensive validation and research .
The present study showed that plasma adiponectin level was significantly lower in patients with AMI (groups II, III, and IV) compared with the control group, which was in agreement with previous studies ,,, and this might be owing to a strong inflammatory activity in the atheromatous plaque .
The reported significant negative correlation between adiponectin level and age in patients with AMI could be owing to a possible disturbed adipokines synthesis or secretion in old-age individuals, an explanation that might support the concept of old age being a risk factor .
Moreover, the reported significant positive correlation between adiponectin and NO metabolites (nitrite/nitrate) levels could be explained by the assumption that adiponectin increases NO production by promoting the activity of endothelial nitric oxide synthase or by ameliorating the suppression of endothelial nitric oxide synthase activity by oxidized LDL .
It was found that MPO activities serve as a strong and independent predictor of endothelial dysfunction in humans, giving a mechanistic link between oxidation, inflammation, and cardiovascular disease . Moreover, MPO causes modification of HDL in AMI and generates dysfunctional HDL . Studies have shown that MPO levels are a predictor of death after chest pain and AMI. MPO has recently been shown to contribute to microvascular obstruction in patients with AMI. During myocardial ischemia-reperfusion sequences, microvascular function is associated with recruitment of polymorphonuclear neutrophils and has been attributed to decreased bioavailability of NO. Endothelium-dependent microvascular function is a multifactorial process involving endothelial injury or dysfunction, neutrophil accumulation, overproduction of reactive oxygen species, thrombus embolization, and activation of the coagulation cascade .
The present study showed a significant increase in MPO activity in patients with AMI (groups I, II, and III) compared with the controls. This might be related to its secretion from activated leukocytes under inflammatory conditions .
Similarly, MPO has been shown to activate metalloproteinases and to promote destabilization and rupture of atherosclerotic plaque surface, thus MPO could be related to the future risk of AMI events .
A significant negative correlation was shown in this study between MPO activity and NO metabolites (nitrite/nitrate) levels, due to the uptake of MPO by endothelial cells through transcytotic process to accumulate within the subendothelial space, and to consume NO, thus interfering with the atheroprotective effect of NO .
Estimated serum levels of both NO metabolites (nitrite and nitrate) were significantly lower in patients with AMI compared with controls.Increasing number of cardiovascular risk factors was correlated with the degree of decrease in nitrite level. There were high levels of NO metabolites in both acute and chronic inflammatory conditions including atherosclerosis .
The levels of lipid profile were significantly changed in patients with AMI, which is in agreement with a study that had significantly higher levels of total cholesterol, LDL-C, VLDL-C, triglycerides, LDL-C/HDL-C, total cholesterol/HDL-C, and lower levels of HDL-C as compared with the controls .
In the present study, a significant correlation between lipid profile and adiponectin and MPO was shown. In addition, a significant correlation was found between lipid profile and NO metabolites as mentioned before .
| Conclusion|| |
In conclusion, AMI occurs accompanied by low levels of adiponectin, nitrite, nitrate, and HDL-C and high levels of MPO activity, total cholesterol, TG, and LDL-C ratio. These may all be regarded as risk factors and could be used as diagnostic tools for AMI.
The present study findings show the importance of NO as a predictor of AMI severity, a common mediator for the action of adiponectin and MPO, besides its possible interaction with dyslipidemia and hypertension. These findings point to the importance of NO in diagnosis and treatment of AMI.
Financial statement and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Calabro P, Maddaloni V, Malvezzi M et al.
Adipose tissue − mediated inflammation: the missing link between obesity and cardiovascular disease? Intern Emerg Med 2009; 4:25–34.
Guzik TJ, Korbut R. Adipocytokines − a novel link between inflammation and vascular function? J Physiol Pharmacol 2006; 57:505–528.
Berg AH, Scherer PE. Adipose tissue, inflammation and cardiovascular disease. Circ Res 2005; 96:939–949.
Nicholls SJ, Hazen SL. Myeloperoxidase and cardiovascular disease. Arterioscler Thromb Vasc Biol 2005; 25:1102–1111.
Stocker R, Keaney JF. Role of antioxidant modifications in atherosclerosis. Physiol Rev 2004; 84:1381–1478.
Carr AC, McCall MR, Frei B. Oxidation of LDL by myeloperoxidase and reactive nitrogen species. Reaction pathways and antioxidant protection. Arterioscler Thromb Vasc Biol 2000; 20:1716–1723.
Abu-Soud HM, Hazen SL. Nitric oxide is a physiological substrate for mammalian peroxidases. J Biol Chem 2000; 275:37524–37532.
Xu J, Xie Z, Reece R et al.
Uncoupling of endothelial nitric oxidase synthase by hypochlorous acid: role of NAD(P)H oxidase-derived superoxide and peroxynitrite. Arterioscler Thromb Vasc Biol 2006; 26:2688–2695.
Kershaw EE. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004; 89:2548–2556.
Abu-Soud HM, Hazen SL. Nitric oxide modulates the catalytic activity of myeloperoxidase. J Biol Chem 2000; 275:5425–5430.
Channon KM, Qian HS, George SE. Nitric oxide synthase in atherosclerosis and vascular injury. Artherioscl Thromb Vas Biol 2010; 20:1873.
Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial information redefined a consensus document of the joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial information. J Am Coll Cardiol 2010; 36:959–969.
Faraj M, Havel PJ, Phelis S, Blanke D. Plasma acylation stimulating protein, adiponectin, leptin and ghrelin before and after weight loss induced by gastric bypass surgery in morbidly obese subjects. J Clin Endocrinol Metab 2003; 88:1594–1602.
Hjorth R, Jonsson AK, Vretblad P. A rapid method for purification of human granulocytes using Percoll. A comparison with dextran sedimentation. J Immunol Methods 1981; 43:95–106.
Gross GJ, Auchampach JA. Blockage of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs. Cir Res 1992; 70:223–233.
Bories PN, Bories C. Nitrate determination in biological fluids by enzymatic one step assay with nitrate reductase. J Clin Chem 1995; 41:904–907.
Allian CC, Poon LS, Chan CGS, Richmond W, Fu PC. Enzymatic determination of total serum cholesterol. J Clin Chem 1974; 20:470–475.
Carr TP, Andresen CJ, Rudel LL. Enzymatic determination of triglyceride, free cholesterol and total cholesterol in tissue lipid extracts. Clin Chem 1993; 26:39–42.
Baldo G. Cholesterol determination in HDL, HDL2 and HDL3 fractions after polyanion precipitation: a comparison between chemical extractive and totally enzymatic procedure. Clin Chem Acta 1985; 146:81–86.
Bauer JD. Clinical laboratory methods. 9th ed. Missorri: CV company waistline industry; 1982. 555.
Ross R. Atherosclerosis an inflammatory disease. N Engl J Med 2009; 340:115–126.
Mangge H. Beyond cholesterol − new cardiovascular biomarkers. Nestle Nutr Inst Workshop Ser 2016; 84:81–88.
Ebersole JL, Kryscio RJ, Campbell C, Kinane DF, McDevitt J, Christodoulides N et al.
Salivary and serum adiponectin and C-reactive protein levels in acute myocardial infarction related to body mass index and oral health. J Periodontal Res 2017; 52:408–418.
Tsukinoki R, Morimoto K, Nakayama K. Association between lifestyle factors and plasma adiponectic level in Japanese men. Lipids Health Dis 2005; 4:27.
Lim HS, Tayebjee MH, Tan KT, Patel JV, Macfadyen RJ, Lip GYH. Serum adiponectin in coronary heart disease: ethnic differences and relation to coronary artery disease severity. Heart 2005; 91:1605–1606.
Krosnodebski P, Opolski G, Karnafel W. Plasma adiponectin levels in acute myocardial infarction and during the postinfarction recovery period in patients with type 2 diabetes mellitus. Pubmed 2011; 69:924–930.
Shoji T, Koyama H, Fukumoto S, Maeno T, Yokoyama H, Shinohara K. Platelet activation is associated with hypoadiponectinemia and carotid atherosclerosis. Atherosclerosis 2005; 188:190–195.
Motoshima H, Wu X, Mahadev K, Goldstein BJ. Adiponectin suppresses proliferation and superoxide generation and enhances NOS activity in endothelial cells treated with oxidized LDL. Bioch Biophys Res Comm 2004; 315:267–271.
Baldus S, Heeschen C, Meinertz T, Zeither AM, Eiserich JP, Munzel T. Myeloperoxidase serum levels predict risk in patients with acute coronary syndromes. Circulation 2003; 108:1440.
Tietge UJF. The impact of myeloperoxidase on HDL function in myocardial infarction. Curr Opin Endocrinol Diabetes Obes 2018; 10:1097.
Stamboul K, Zeller M, Rochette L, Cottin Y, Cochet A, Leclereq T et al.
Relation between high levels of myeloperoxidase in the culpritartery and microvascular obstruction, infarct size and reverse remodeling in ST-elevation myocardial infarction. PLoS One 2017; 12:179929.
Yokoyama M. Oxidant stress and atherosclerosis. Curr Opin Pharmacol 2004; 4:110–115.
Baldus S, Eiserich JP, Mani A. Endothelial transcytosis of myeloperoxidase confers specificity to vascular ECM proteins as targets of tyrosine nitration. J Clin Invest 2001; 108:1759–1770.
Whiteman M, Rose P, Halliwell B. Inhibition of hypochlorous acid-induced oxidative reactions by nitrite: is nitrite and antioxidant? Biophys Res Comm 2003; 303:1217–1224.
Shirafkan A, Marjani A, Zaker F. Serum lipid profiles in acute myocardial infarction patients in Gorgan. Biomed Res 2012; 23:119–124.
Leitner JM, Pernerstofer-Schoen H, Weiss A, Schindler K, Reiger A, Jilma B. Age and sex modulate metabolic and cardiovascular risk markers of patients after 1 year of highly active antiretroviral therapy (HAART). Atherosclerosis 2006; 187:177–185.
[Table 1], [Table 2]