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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 3  |  Issue : 2  |  Page : 38-44

Atherogenic indices and smoking habits in cigarette smokers


1 Department of Chemical Pathology, Federal Medical Centre, Makurdi, Nigeria
2 Department of Medical Laboratory, Medical Center Division, Akanu Ibiam Federal Polytechnic, Unwana, Nigeria

Date of Submission10-Mar-2018
Date of Acceptance24-May-2018
Date of Web Publication12-Jul-2018

Correspondence Address:
Dr. Ayu Agbecha
Department of Chemical Pathology, Federal Medical Centre, Makurdi
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ed.ed_5_18

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  Abstract 


Background and Objective: Dyslipidemia is a mechanistic factor between cigarette smoking and cardiovascular diseases (CVD). Normolipidemic smokers may still be at risk of CVD, hence the need to better characterize serum lipids with atherogenic indices. This study aimed at determining atherogenic indices in relation to smoking habits in cigarette smokers.
Materials and Methods: The case–control study compared lipid indices of sixty male smokers with six anthropometrically matched non-smokers. Three comparable subgroups of smoking habits were statistically tested. Associations of serum lipids, atherogenic indices, and smoking habits were also determined.
Results: Significant high (P < 0.001) atherogenic indices, proatherogenic lipids (total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-c), very LDL-c, non-high-density lipoprotein cholesterol [HDL-c]), and significant low (P < 0.001) HDL-c were observed in smokers compared to controls. Significant differences (P < 0.002) in serum lipids and atherogenic indices were observed within the subgroups of cigarette sticks smoked per day. Significant positive (P < 0.002) correlation of cigarette sticks smoked per day with proatherogenic lipids and atherogenic indices was observed in smokers, whereas significant inverse (P < 0.001) correlation was observed with HDL-c.
Conclusion: Atherogenic indices proved to be a better predictor of cardiovascular risk, especially in settings of seeming normal lipid profile.

Keywords: Atherogenic indices, lipids, smokers


How to cite this article:
Agbecha A, Ameh AE. Atherogenic indices and smoking habits in cigarette smokers. Environ Dis 2018;3:38-44

How to cite this URL:
Agbecha A, Ameh AE. Atherogenic indices and smoking habits in cigarette smokers. Environ Dis [serial online] 2018 [cited 2022 Nov 30];3:38-44. Available from: http://www.environmentmed.org/text.asp?2018/3/2/38/236533




  Introduction Top


Tobacco smoking is an environmental risk factor of cardiovascular diseases (CVD).[1],[2] The world health organization (WHO) estimates “direct tobacco use cause over 6 million deaths each year and approximately 80% of over 1 billion smokers in the world live in low and middle income countries.”[3]

Abnormal plasma lipids have been observed as the mechanistic major risk factors of atherosclerotic vascular diseases.[4] Two major categories of plasma lipoproteins are routinely measured in the fasting state to determine cardiovascular risk; cholesterol ester (low-density lipoprotein cholesterol [LDL-c], high-density lipoprotein cholesterol [HDL-c], and triglyceride-rich lipoproteins [very low-density lipoprotein cholesterol (VLDL-c)]).[5]

Previous studies have shown that smoking induces abnormal plasma lipids that follows the pattern of increased concentration of serum total cholesterol (TC), triglycerides (TGs), LDL-c, VLDL-c, and decreased levels of HDL-c.[1],[2] Despite reports of dyslipidemia in high-risk individuals such as smokers, a number of routine lipid profile results may appear normal leading to erroneous rulings. In an attempt to better characterize the atherogenic potential of lipid profile, its parameters have been integrated as mathematical ratios of cholesterol ester and triglyceride-rich lipoproteins. The Castelli's risk index I and 2 (CAS-1 and CAS-2), atherogenic coefficient (AC),[6] TG/HDL ratio, and atherogenic index of plasma (AIP)[7],[8] have been used in predicting the risk of CVD in various clinical settings. Proatherogenic non-HDL-c is determined as a valid surrogate to apolipoprotein B 100 (Apo-B) in the assessment of atherogenic cholesterol and lipoprotein burden.[9] It is established that the measurement of non-HDL-c is a better predictor of CVD than LDL-c.[9]

To the best of our knowledge, this is the first study that will determine a combination of atherogenic indices in the prediction of cardiovascular risk in relation to smoking habits in the smoker group. Our study aimed at determining atherogenic indices in relation to smoking habits in cigarette smokers.


  Materials and Methods Top


Selection of participants

Participants involved in this case–control study comprised of a total of 120 patients undergoing health checkup at a tertiary health-care institution in North Central Nigeria. The study was carried out from September 2014 to January 2015 after an approval from Institutional Ethical Committee and a written informed consent obtained from study participants. A structured questionnaire containing information about anthropometric parameters, lifestyle, smoking habit, and medical history was used in collecting preliminary data for the selection criteria. Inclusion criteria males aged between 20 and 44 years, who were either nonsmokers or active smokers of at least 1-year duration. Exclusion criteria: (i) individuals with a history of medical disorders such as diabetes, hypertension, hepatic, and renal and cardiac diseases, (ii) Ex-smokers, alcoholics, obese, and family history of dyslipidemia, (iii) individuals on medications such as beta blockers, steroids, vitamin supplementation, herbal medications, and lipid-lowering drugs.

Study design

The participants were divided into two comparable groups; smoker and control group comprising anthropometrically matched 60 apparently healthy male cigarette smokers and nonsmokers, respectively. The smoker group was further divided into three subgroups according to the average number of cigarette sticks smoked per day; Group A = 1–5, Group B = 6–10, and Group C = >10 cigarette sticks smoked per day. The smoker group was also divided into three subgroups based on the duration of smoking; 1–5, 6–10, and >10 years.

Blood sample collection

After an overnight 12 h fast, 5 ml of venous blood was aseptically drawn with a Vacutainer set at the antecubital vein of each participant into a plain tube. After clot was allowed to retract, the blood was centrifuged at 3000 rpm for 15 min and serum separated into another plain container for laboratory analysis of lipids.

Laboratory testing

Fresh serum was used in determining TC, HDL-c, and TGs. TC was determined by the cholesterol esterase method. The HDL-c was determined by the cholesterol esterase method after fractional separation from other lipids. TGs were determined using the lipase method. Friedewald's equation was used in estimating VLDL-c and LDL-c.[10] Non-HDL-c was calculated as the difference between TC and HDL-c.[9] Plasma lipid abnormality was based on the expert panel of the National Cholesterol Education Programme (NCEP) cutoff values.[5] Therefore, TC, TGs, LDL-c VLDL-c, and non-HDL-c levels, respectively, exceeding 5.17 (200.0), 1.71 (150.0), 2.59 (100.0), 0.78 (30.0), and 3.36 (130.0) mmol/L (mg/dl) and HDL levels below 1.03 (45.0) mmol/L (mg/dl) were considered abnormal. The atherogenic indices were calculated as follows: Castelli's risk index (CAS-1) = TC/HDL, CAS-2 = LDL/HDL, AC = (TC–HDL)/HDL, TG/HDL ratio and AIP = log (TG/HDL),[6],[7],[8] CAS-1, CAS-2, AC, TG/HDL, and AIP mean values exceeding 3.5, 3.0, 3.0, 2.60, and 0.1,[6],[8],[11],[12],[13] respectively, were used as predictor values of cardiovascular risk in smoker groups.

Statistical analysis

The IBM Armonk, New York, United States, statistical package for the social sciences version 21 was used in analyzing the data generated. Descriptive statistics were used in determining the means and standard deviations of the parameters measured. Student's t-test was used in comparing the means of parameters in smoker and control groups. Analysis of variance was used in analyzing mean values of lipid indices according to smoking habits. Pearson's correlation analyses were used to determine the association between parameters measured in smokers. A two-tailed P < 0.05 was indicative of statistical significance.


  Results Top


The mean values of age and body mass index (BMI) presented in [Table 1] were the anthropometric parameters matched in comparing the smoker and control groups. The mean values of age and BMI of the smoker group were not significantly different from the control group. The mean values of serum lipids and atherogenic indices of smokers compared with nonsmokers are presented in [Table 2]. Mean values of proatherogenic lipids (TC, TGs, LDL-c, VLDL-c, and non-HDL-c) and atherogenic indices (CAS-1, CAS-2, AC, TG/HDL, and AIP) were significantly higher (P< 0.001) in the smoker group than control. However, a significant decrease (P< 0.001) in the mean level of HDL-c was observed in smokers compared to nonsmokers.
Table 1: Anthropometric parameters of nonsmokers with smokers

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Table 2: Comparison of mean values of serum lipids and atherogenic indices in smokers and nonsmokers

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Mean age, BMI, lipid levels, and atherogenic indices of smokers according to the average number of cigarette sticks smoked per day are presented in [Table 3]. There was no significant difference (P > 0.05) in age, BMI within Groups A (1–5 cigarette sticks), B (6–10 cigarette sticks), and C (>10 cigarette sticks), whereas a significant difference (P< 0.002) in serum lipids and atherogenic indices was observed within the groups compared. A post hoc analysis comparing Group A with Group B and C showed a significant higher (P< 0.05) TC, LDL-c, non-HDL-c, TG/HDL, and AIP in Group A than Groups B and C, whereas HDL-c levels significantly reduced (P< 0.03) in Group A compared to each of the other groups. The increment of TGs, VLDL-c, CAS-1, CAS-2, and AC in Group A was significant (P< 0.05) when compared to Group C. However, no significant difference (P< 0.05) in TGs, VLDL-c, CAS-1, CAS-2, and AC was observed between Group A and B. A post hoc test to compare Group B and C revealed a significant higher (P< 0.05) TC, TGs, VLDL-c, non-HDL-c, CAS-1, AC, AIP, and TG/HDL in Group B than Group C, whereas a significant low (P< 0.03) HDL-c and a nonsignificant (P > 0.05) difference in CAS-2 was observed in Group B compared to C.
Table 3: Comparison of mean values of lipids and atherogenic indices in various groups of cigarette sticks smoked per day in smokers

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Mean age, BMI, lipid levels, and atherogenic indices of smokers based on the duration of smoking are presented in [Table 4]. No significant difference (P > 0.05) in BMI, lipids, and atherogenic indices was observed within the groups compared. Although a significant difference (P< 0.001) in age was observed within the comparable groups, age had no confounding impact on lipids and atherogenic indices.
Table 4: Comparison of mean values of lipids and atherogenic indices in various groups of years of duration of smoking in smokers

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Pearson's correlation of smoking habits with lipids and atherogenic indices in smokers is presented in [Table 5]. A significant positive (P< 0.002) correlation of average cigarette sticks smoked per day with proatherogenic lipids and atherogenic indices was observed in smokers, whereas a significant inverse (P< 0.001) correlation was observed between average cigarette sticks smoked per day and HDL-c. No significant (P > 0.05) correlation in the duration of smoking with proatherogenic lipids and atherogenic indices was observed in smokers. Pearson's correlation coefficients of anthropometry (age and BMI), lipids, and atherogenic indices in smokers are presented in [Table 6]. Relevant to our study, no significant correlation (P > 0.050) in anthropometry with lipids and atherogenic indices were observed in smokers. A significant positive (P< 0.005) correlation of proatherogenic lipids with atherogenic indices was observed in smokers. Furthermore, in the smokers, a significant inverse (P< 0.005) correlation of HDL-c with proatherogenic lipids and a significant inverse (P< 0.005) correlation of HDL-c with atherogenic indices were observed.
Table 5: Pearson's correlation of smoking habits with lipids and atherogenic indices in smokers

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Table 6: Pearson correlation coefficients of anthropometry, serum lipids, and atherogenic indices in smokers

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  Discussion Top


Cigarette smoking has been demonstrated to be an important factor in the development of CVD (atherosclerosis, coronary artery disease, and peripheral vascular disorders) by alteration of plasma lipoprotein levels.[14] Other previous studies have established the role of deranged lipid profile in the progression of coronary artery disease.[5] We determined newer proatherogenic parameters in addition to previously established lipids in smokers. Confounding factors of dyslipidemia such as sex, age, and obesity were taken into consideration by selecting nonobese and younger male participants. The smoker and control group were anthropometrically matched to obtain results strictly based on the effect of cigarette smoke and not confounding factors. Results obtained in smokers by comparing lipid parameters within groups of average cigarette sticks smoked per day were not influenced by the anthropometric effect. Despite the unavoidable significant difference in age existing within groups of duration of smoking, anthropometry was not impactful on lipids compared in smokers. Our results, thus, were free from anthropometric interferences.

Results of our study showed higher levels of TC, TGs, VLDL-c, LDL-c, and lower level of HDL-c in smokers compared to nonsmokers. This present finding is in consonance with that of Gepner et al.[1] and Gamit et al.,[2] who observed higher levels of TC, TGs, VLDL-c, and LDL-c and lower level of HDL-c in smokers. Despite the significant difference observed in lipid levels of this study, the mean values of TC (4.71 mmol/L), HDL-c (1.10 mmol/L), LDL-c (2.63 mmol/L), and VLDL-c (0.44 mmol/L) in smokers were not abnormally enough to predict cardiovascular risk when compared to NCEP cutoffs. Only the mean value of TGs (2.19 mmol/L) was above the normal cutoff (1.71 mmol/L). The present study found elevated non-HDL-c in smokers compared to nonsmokers. The mean value of non-HDL-c (3.61 mmol) was abnormally above the NCEP normal cutoff (3.36 mmol/L). Our study further observed a positive correlation of non-HDL-c with TC, TGs, VLDL-c, and LDL-c and negative correlation of non-HDL-c with HDL-c. This positive association of non-HDL-c with proatherogenic lipids and negative correlation with antiatherogenic HDL-c in the smoker group affirms the atherogenic potential of non-HDL-c. Studies have proved the determination of non-HDL-c (a surrogate of apo B) to be a better predictor of CVD than LDL-c and estimate the level of all apo B-carrying lipoproteins.[9] Measurement of apo B provides direct information on the number of atherogenic particles (LDL and non-LDL) collectively known as non-HDL lipoproteins.[9]

Previous studies prove and support the use of atherogenic indices in predicting cardiovascular risk in various clinical settings. In the prediction of cardiovascular risk, the normal range of CAS-1 is reported as ≤3.5[6] and ≤3.0 for CAS-2.[11] In another study, it was observed that individuals with CAS-2 value >5 pose a greater risk of coronary events.[15] The ratio TG/HDL, initially proposed by Gaziano et al., proved to be stronger than CAS-1 and CAS-2 in predicting myocardial infarction.[16] The authors explained that the strong association between TG/HDL and coronary heart disease risk suggests a metabolic link between the TG- and cholesterol ester-rich lipoproteins in increasing myocardial infarction risk. da Luz et al.[7] explained that TGs/HDL-c ratio was found to be a powerful independent marker of extensive coronary disease. Bampi et al.[17] reported TG/HDL ratio as a determinant of coronary artery disease by noninvasive methods. The TG/HDL ratio was later improved by logarithmic transformation into AIP in the significant prediction of atherosclerosis.[18] AIP represents the relationship between protective and atherogenic lipoprotein and is associated with the size of pro- and anti-atherogenic lipoprotein particle.[18] Reports show that AIP increases significantly with increasing atherogenic risk, with reference ranges of –0.24 in healthy individuals to 0.51 in advanced atherosclerotic cases.[18] AIP values of –0.3–0.1 have been associated with low cardiovascular risk, whereas medium risk is linked with a range of 0.1–0.24 and >0.24 associated with high-risk group.[13] Based on this, the AIP has been used in predicting CVD in various clinical settings.[19],[20],[21],[22] Bhardwaj et al.[8] explained that AC reflects the atherogenic potential of the entire spectrum of lipoprotein fractions. This is because it measures cholesterol in LDL, VLDL, and IDL fractions in relation to antiatherogenic HDL-c, and hence an indicator of CVD risks.

This study found elevated values of atherogenic indices in smokers compared to nonsmokers. Mean values of CAS-1 (4.56), AC (3.56), and AIP (0.31) in smoker group were abnormally higher than the cutoff values, whereas CAS-2 (2.61) and TG/HDL-c (2.13) values were normal. The present study further observed a positive correlation between TC, LDL-c, TGs, VLDL-c, non-HDL-c, and atherogenic indices. However, antiatherogenic HDL-c was inversely correlated with atherogenic indices. Our result is in conformity with that of Niroumand et al.,[20] who in a cross-sectional study of noncommunicable disease risk factors' surveillance, observed a significant positive correlation of AIP with TC, TGs, and LDL-c and inverse correlation with HDL-c. Pusapati et al.[12] also found a negative association between HDL-c and atherogenic indices in coronary artery disease patients. Ugwuja et al.[21] in a cross-sectional study of overweight and obese civil servants showed that plasma lipids were positively correlated with atherogenic indices, except for HDL-c, which was negatively correlated with atherogenic indices and LDL-c. Nansseu et al.[22] in a cardiovascular risk prediction study in postmenopausal women showed that AIP was positively and significantly correlated with TC. The abnormally high non-HDL-c and atherogenic indices coupled with their correlation with serum lipids observed in our study suggest an increased risk of CVD development in the seemingly normolipidemic smokers.

The present study observed dyslipidemia and statistically raised atherogenic indices according to average cigarette sticks smoked per day. Our finding was further supported by the observation of a positive correlation of proatherogenic lipids and atherogenic indices with average cigarette sticks smoked per day. There was increased TC, LDL-c, TGs, VLDL-c, and non-HDL-c but decreased HDL-c along with increased number of sticks of cigarettes smoked. The mean levels of TC and VLDL-c in all the groups compared remained normal despite the increase in a number of cigarettes sticks smoked per day, whereas abnormally high TGs were observed in all the groups. Proatherogenic LDL-c and non HDL-c levels were abnormally high in individuals that smoked >5 sticks of cigarettes per day, whereas antiatherogenic HDL-c mean values were normal in smokers who smoked <10 sticks of cigarettes per day. Among the atherogenic indices measured in this study, CAS-1 and AIP mean values were abnormally high in all the groups as the number of sticks of cigarettes smoked per day increased. The AC mean value was normal in individuals who smoked <6 sticks of cigarettes per day and high for individuals that smoked >5 sticks. Mean values of CAS-2 and TG/HDL were high only in smokers that smoked >10 sticks of cigarette per day. This study, however, observed no statistical change in plasma lipids and atherogenic indices according to duration of smoking. The pattern of dyslipidemia in relation to smoking habits observed by our finding is in consonance with that of Bišanović et al.,[23] who reported higher mean values of TC, TGs, and LDL-c and lower value of HDL-c in smokers according to the number of sticks of cigarettes smoked daily. Their study further reported that a number of cigarette sticks smoked per day impacted more on status of lipids and cardiovascular effects than duration of smoking. We suggest the determination of cardiovascular risk in smokers is assessed with a combination of lipid profiling and atherogenic indices in clinical and research setting.

The proposed mechanism by which smoking promotes atherosclerosis is unknown. Evidence exist that atherosclerosis is an inflammatory disease [24] initiated by the injurious effects of oxidized LDL-c on the vascular endothelium.[25] Nicotine has been observed to cause increase in circulating TGs, LDL-c, TC, and VLDL-c levels and decrease in HDL-c.[26] Mechanisms leading to altered plasma lipids by nicotine include: (a) stimulation of the sympathetic-adrenal system resulting to raised catecholamines production and (b) stimulation of cholinergic receptors in the brain and autonomic ganglia. The binding of nicotine to these receptors stimulates the opening sodium-calcium channel, followed by entry of sodium and calcium, with the subsequent release of neurotransmitters.[27] Catecholamine and other neurotransmitters upregulate lipolysis and free fatty acids transport to the liver. Hepatic re-esterification of these acids occurs with a further increase in secretion of liver free fatty acids, TGs, and VLDL-c into the bloodstream.[28] Plasma lipoprotein lipase enhances the release of TGs from VLDL to become LDL particles and small dense LDL. LDL particles and their associated contents lodged in the endothelium are frequently oxidized by free radicals. Inflammatory responses are triggered in the endothelium in response to oxidized LDL particles, resulting in the recruitment of monocytic white blood cells into arterial wall which transform into macrophages.[26] The ingestion of oxidized LDL particles by tissue macrophages triggers a cascade of immunological events leading to the formation of foam cells and the subsequent production of an atheroma in the absence of HDL removal of fats from these specialized cells.[26],[28] HDL is termed good cholesterol because of its role in removing fats from artery walls. It transports cholesterol and TGs out of artery walls, reduces macrophage accumulation, prevents, and regresses atherosclerosis overtime, thus preventing cardiovascular disease.


  Conclusion Top


Atherogenic indices seem to be better predictors of cardiovascular risk, especially in settings where the absolute values of lipid profile seem normal or not markedly deranged. Proatherogenic non-HDL-c also proved to be an excellent cardiovascular risk predictor, whose measurement could replace apo B in centers with insufficient resources. As per our knowledge, this is the first report to predict cardiovascular risk in smokers using multiple atherogenic indices.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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[PUBMED]  [Full text]  
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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]


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