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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 33  |  Issue : 2  |  Page : 65-69

Assessment of apolipoproteinsA1, E, and Insulin Resistance in Iraqi male patients with acute myocardial infarction


Al-Mustansiriyah Diabetic Centre, Baghdad, Iraq

Date of Submission01-Oct-2020
Date of Decision30-Oct-2020
Date of Acceptance20-Nov-2020
Date of Web Publication6-Jul-2023

Correspondence Address:
Dr. Hind Sh Ahmed
Al-mustansiriyah Diabetic Centre, Baghdad
Iraq
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IRJCM.IRJCM_4_21

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  Abstract 


Background: Insulin resistance (IR) is a risk factor for ischemic heart disease and myocardial infarction. It often manifests in myocardial infarction and is regarded as an independent predictor of in-hospital mortality, which can provide early risk stratification for recurrent acute coronary events. Objective: The aim of this study was to assess the levels of apolipoproteinsA1, E with IR in Iraqi male patients with acute myocardial infarction (AMI). Patients and Methods: Forty-five male patients with AMI were enrolled in this study. Their age range was 40–55 years and they are compared with 45 healthy male as a control group. All patients with AMI were checked up by a cardiologist in Iraqi Centre for Cardiovascular Diseases/Al-Hariry Hospital/Baghdad. Fasting venous blood samples were collected from all the subjects. Laboratory evaluations consisted of fasting serum glucose (FSG), glycated hemoglobin (HbA1c), serum insulin, and lipid profile. Furthermore, apolipoproteinsA1 and E levels were determined in this study. Results: There was a significant increase in FSG and insulin levels in patients group as compared to the controls. In addition, there was an elevation in HbA1c and homeostasis model assessment for IR in those patients, but they were not significant. There was a significant increase (P = 0.001) in serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol, while there was a significant decrease in serum high-density lipoprotein cholesterol in patients group as compared to the controls. Moreover, there was a significant increase (P = 0.001) in apolipoprotein E, while a significant decrease (P = 0.001) in apolipoproteinsA1in patients group as compared to the controls. Conclusions: Dyslipidemia, along with insulinemia and glycemia, is one of the most significant IR risk factors in the acute and early recovery phases of myocardial infarction.

Keywords: Acute myocardial infarction, apolipoproteins, insulin resistance


How to cite this article:
Ahmed HS. Assessment of apolipoproteinsA1, E, and Insulin Resistance in Iraqi male patients with acute myocardial infarction. IRAQI J COMMUNITY MED 2020;33:65-9

How to cite this URL:
Ahmed HS. Assessment of apolipoproteinsA1, E, and Insulin Resistance in Iraqi male patients with acute myocardial infarction. IRAQI J COMMUNITY MED [serial online] 2020 [cited 2023 Dec 4];33:65-9. Available from: http://www.journalijcm.org/text.asp?2020/33/2/65/380713




  Introduction Top


Acute myocardial infarction (AMI) is well-known pathologically as myocardial cell death due to prolonged ischemia. Lessened cellular glycogen, undisturbed myofibrils, and sarcolemmal disruption, are the chief ultra-structural fluctuations and are seen as initial as 10–15 min after the onset of ischemia.[1]

Insulin resistance (IR) is a risk feature for cardiovascular disease (CVD).[2] The IR frequently exhibits in AMI and is considered a liberated predictor of mortality, which may deliver initial risk stratification for frequent acute coronary proceedings.[3]

IR is defined as decreased sensitivity or responsiveness to the metabolic actions of insulin; consequently, a variety of restrictions, comprising traditional hyperinsulinemia and hyperglycemia, are deliberated to be IR markers. Nevertheless, some lipid metabolism factors are also supposed to be capable IR markers, with their effect on CVD being well-known. It is identified that free fatty acids block glucose carrying by preventing insulin's cooperation with hepatocytes and monocytes, foremost to hyperglycemia and IR progress.[4]

There is robust evidence that lipid abnormalities such as high plasma triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and decreased high-density lipoprotein cholesterol (HDL-C) levels are associated with increased stroke risk.[5]

Cholesterol can be complexed with apolipoproteins (apos). Besides its beneficial aspects in human physiology, an excess of cholesterol can also be harmful.[6] Several observational studies consistently show an association between elevated LDL-C and high prevalence of CVD in adults, and, on the other hand, between high HDL-C and reduced prevalence of these diseases. Although this concept has been recently debated.[7],[8]

ApoA1 is a major apo of HDL-C and is involved in the regulation of reverse cholesterol transport and the metabolism of HDL particles. This transport process is regulated by a physical interaction of apoA1 with its molecular partner, the ATP-binding cassette transporter A1, located in the plasma membrane.[9]

Apolipoproteins E (ApoE), a major constituent of very low-density lipoprotein (VLDL), has been shown to be an essential ligand for the uptake and clearance of atherogenic lipoproteins. Moreover, it has been demonstrated that apoE plays an important role in atherosclerosis by modifying inflammatory responses and facilitating cholesterol efflux from cells.[10] Hence, the aim of this study was to assess the levels of apoA1, E with IR in Iraqi male patients with AMI.


  Patients and Methods Top


Forty-five male patients with AMI were enrolled in this study. Their age range was (40–55) years and they are compared with 45 healthy male as the control group. Privacy and confidentiality were considered after verbal consent. Patients were given the right to withdraw from the study at any time. The questionnaire included duration of AMI, family history, height, weight, heart disease, and hypertension for patients and control groups. All patients with AMI were checked up by a cardiologist in Iraqi Centre for CVDs/Al-Hariry Hospital/Baghdad. The diagnosis of AMI was dependent on the following criteria: (1) typical history of acute chest pain and (2) unequivocal changes of MI in the electrocardiogram to confirm the diagnosis.

Patients with liver, renal, thyroid function disease, and hormonal abnormalities were excluded from this study.

Anthropometric parameters involved body mass index (BMI), systolic- and diastolic-blood pressure (SBP, DBP) are estimated. BMI is calculated according to the following equation:[11]



Laboratory evaluations consisted of fasting serum glucose (FSG), glycated hemoglobin (HbA1c), serum lipid profile including: (Serum total cholesterol [TC], TG, HDL-C, VLDL, LDL-C), and serum insulin. IR was estimated using the homeostasis model assessment for IR (HOMA-IR) index according to the following equation:[12]

HOMA-IR = G0 × I0/405

Furthermore, serum apoA1 and E levels were determined by (Cusabio, China) kit.

Statistical analysis

Statistical package of social science (SPSS) version 17.0 international software for statistical analysis, USA was used for the analysis of data. Results are expressed as means ± standard deviation Student's t-test was used to compare between the groups. The P ≤ 0.05 was considered statistically significant.


  Results Top


Anthropometric and clinical characteristics of patients and control are shown in [Table 1]. There was a significant increase (P ≤ 0.05) in BMI, SBP, and DBP in AMI patients as compared to the controls. There was no significant difference in age between the two groups.
Table 1: Anthropometric and clinical characteristics of patients and control

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There was a significant increase (P = 0.01) in FSG and insulin levels in AMI patients as compared to the controls [Table 2]. In addition, there was an elevation in HbA1c and HOMA-IR in AMI patients, but they were not significant.
Table 2: Glycemic parameters of patients and control

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Lipid profile parameters are presented in [Table 3]. There was a significant increase (P = 0.001) in serum TC, TG, LDL-C, and VLDL in AMI group as compared to the controls. Furthermore, there was an elevation in lipid ratios, but they were not significant. A significant increase in apoE, while a significant decrease (P = 0.001) in apoA1was found in AMI patients as compared to the controls [Table 4].
Table 3: Lipid profile parameters of patients and control

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Table 4: Apolipoproteins A-1 and E among patients and control

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There was a significant negative correlation between apoA1and BMI, FSG, serum insulin, TC, TG, LDL-C, and apoE in AMI patients. While, there was a significant positive correlation between apoA1 and serum HDL-C in AMI patients as compared to the controls [Table 5].
Table 5: The correlation coefficient of apolipoproteins A-1 with other parameters in acute myocardial infarction patients

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  Discussion Top


In this study, it has been shown that an association existed between increased lipid-testing intervals of and elevated risk of AMI among Iraqi male patients, which is in agreement with the study of Jellinger et al., in 2017.[13]

There was a significant increase in BMI between the patients and the controls. Furthermore, there was an increase in FSG, HbA1c, insulin, and HOMA-IR in AMI patients. Thus, any method to predict insulin sensitivity in normoglycemic individuals should first be compared with fasting insulin.

Mahato et al., in 2011 reported that estimated risk of CVD has shown to be increased by 18% for each 1% increase in absolute HbA1c value. A positive relationship between HbA1c and CVD has been demonstrated in nondiabetic cases even within normal range of HbA1c. It has been estimated that reducing the HbA1c level by 0.2% could lower the mortality by 10% according to that study.[14]

In addition, it has been reported that a number of clinical and metabolic abnormalities have been associated with IR. The metabolic disorders classified included hyperglycemia, dyslipidemia, and hypertension. However, they did confirm that the best method was dependent on glucose status.[15]

Levels of fasting insulin in AMI patients were above 25 μIU/ml, which is the upper limit of the normal insulin reference range. Thus, all patients in this study were hyperinsulinemic.

This study reveals increased levels of TC, TG, LDL-C, and decreased levels of HDL-C. The main disorders of lipid metabolism in this study are hypercholesterolemia and hypertriglyceridemia. This finding is in concord with a previous study on hypertriglyceridemia.[16]

Dyslipidemia characterized by elevated TC, LDL-C, and lowered HDL-C, is a conventional risk factor observed in AMI patients, and is the major cause of atherosclerosis are suggested to act synergistically with non-lipid risk factors to increase atherogenesis. On the other hand, a characteristic dyslipidemia is also associated with IR. Insulin affects the liver apos production. It regulates the enzymatic activity of lipoprotein lipase (LPL) and cholesterol ester transport protein. All these factors are likely cause of dyslipidemia in CVD. Moreover, insulin deficiency reduces the activity of hepatic lipase, and several steps in the production of biologically active LPL may be altered in AMI.[17]

Kimm et al., in 2010, demonstrated that the lipid ratios of TC/HDL-C, TG/HDL-C, and LDL-C/HDL-C as well as TG and HDL-C, were each consistently associated with the number of metabolic syndrome components, IR based on homeostatic model assessment. The lipids ratios that include information on at least two measures might have a more integrated explanation than single lipid measures such as TG or LDL-C with HDL-C. They were useful makers for both men and women, especially TG/HDL-C ratio in men. Based on the present results, this ratio considers as a simple means to estimate atherogenic dyslipidemia.[18]

Serum HDL-C has been used to predict a person's risk of developing atherosclerosis. Like high LDL-C and low HDL-C <40 mg/dl are associated with a higher risk of developing CVD. Increased TG and decreased HDL-C are considered to be a major risk factor for the development of IR and MS. The TG/HDL-C ratio is also widely used to assess the lipid atherogenesis.[19]

Abnormalities in lipoprotein metabolism are important in atherogenesis, obesity, IR, and diabetes; all being major areas of concern for public health, individual wellbeing, and research.

Holmes et al., in 2018, recently confirmed these results in a nested case–control study showing that apoA1 was strongly associated with the risk of MI. Serum apoA1 of, 120 mg/dl for men and, 140 mg/dl for women approximately correspond to what is considered as low for HDL-C,[20] which is in agreement with the present data.

Total number of apoE is increased in metabolic abnormalities are better reflected by TG/HDL-C ratio than LDL-C alone. Once these lipid complexes begin to circulate through the blood, LPL bound to the capillary endothelium of muscles and adipose tissue converts their TG to FA and glycerol. These molecules are then used for energy by most cells or reassembled into TG for storage in adipose tissue.[21]

In general, patients in this study had low levels of HDL-C and apoA1 while high levels of LDL-C, apoE, and TG levels, which typically coexist in people with IR.[22]

Low HDL-C concentrations among people with DM may indicate a specific reduction in large HDL particles as well as a possible increase in small HDL particles, which may not necessarily significantly reduce apoA1 levels. Moreover, the multiplex apo test can be performed in the nonfasting state.[23]


  Conclusions Top


Dyslipidemia, along with insulinemia and glycemia, is one of the most significant IR risk factors in the acute and early recovery phases of MI. Dyslipidemia is characterized by a high lipid level; an imbalance in apos metabolism; and a deficiency of apoA1 in the acute and early recovery periods of MI. ApoA1 and E can be used as promising molecular markers to stratify the risk of recurrent acute coronary events in MI patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Kallol S, Huang X, Muller S, Ontsouka C, Albrecht C. Novel insights into concepts and directionality of maternal-fetal cholesterol transfer across the human placenta. Int J Mol Sci 2018;19:2334.  Back to cited text no. 8
    
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Nishio K, Shigemitsu M, Kusuyama T, Fukui T, Kawamura K, Itoh S, et al. Insulin resistance in nondiabetic patients with acute myocardial infarction. Cardiovasc Revasc Med 2006;7:54-60.  Back to cited text no. 10
    
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Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ, et al. American association of clinical endocrinologists and American college of endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract 2017;23:1-87.  Back to cited text no. 13
    
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Mahato RV, Gyawali P, Raut P, Regmi P, Singh K, Pandeya DR, et al. Association between glycemic control and serum lipid profile in type 2 diabetic patients: Glycated hemoglobin as a dual biomarker. Biomed Res 2011;22:375-80.  Back to cited text no. 14
    
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McAuley KA, Williams SM, Mann JI, Walker RJ, Lewis-Barned NJ, Temple LA, et al. Diagnosing insulin resistance in the general population. Diabetes Care 2001;24:460-4.  Back to cited text no. 15
    
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Regmi P, Gyawali P, Shrestha R, Sigdel M, Mehta KD, Majhi S. Pattern of dyslipidemia in type 2 diabetic subjects in Eastern Nepal. JNAMLS 2009;10:11-3.  Back to cited text no. 16
    
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Mendivil CO, Zheng C, Furtado J, Lel J, Sacks FM. Metabolism of very-low-density lipoprotein and low-density lipoprotein containing apolipoprotein C-III and not other small apolipoproteins. Arterioscler Thromb Vasc Biol 2010;30:239-45.  Back to cited text no. 17
    
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Holmes MV, Millwood IY, Kartsonaki C, Hill MR, Bennett DA, Boxall R, et al. Lipids, lipoproteins, and metabolites and risk of myocardial infarction and stroke. J Am Coll Cardiol 2018;71:620-32.  Back to cited text no. 20
    
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Nordestgaard BG, Langsted A, Mora S, Kolovou G, Baum H, Bruckert E, et al. Fasting is not routinely required for determination of a lipid profile: Clinical and laboratory implications including flagging at desirable concentration cutpoints – A joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. Clin Chem 2016;62:930-46.  Back to cited text no. 23
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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