|Year : 2016 | Volume
| Issue : 1 | Page : 36-42
Association of smoking with blood lipids in coronary heart disease patients admitted in Taiping Hospital, Perak, Malaysia
A.T.M. Emdadul Haque1, Shah Reza Bin Kamaruzzaman1, Mainul Haque2
1 Faculty of Medicine, Universiti Kuala Lumpur Royal College of Medicine Perak, 30450 Ipoh, Perak, Malaysia
2 Unit of Pharmacology, Faculty of Medicine, Universiti Sultan Zainal Abidin, Medical Campus, Jalan Sultan Mahmud, 20400 Kuala Terengganu, Malaysia
|Date of Web Publication||22-Dec-2015|
A.T.M. Emdadul Haque
Associate Professor, Faculty of Medicine, Universiti Kuala Lumpur Royal College of Medicine Perak, 30450 Ipoh, Perak
Source of Support: None, Conflict of Interest: None
Introduction: Cigarette smoking is one of the predisposing factors for cardiovascular diseases as it may increase low-density lipoproteins (LDLs) levels and decrease high-density lipoproteins (HDLs). Objective: To measure the blood level of LDL and HDL and compare the result between smokers and nonsmokers who suffered from coronary heart diseases (CHDs). Materials and Methods: This is a cross-sectional study. The information was collected by using a checklist from the records of CHD patients, admitted to Taiping General Hospital, Perak, Malaysia. Data collected were interpreted to find any significant association between smoking, level of total cholesterol, triglycerides, HDL, and LDL. Results: Among the 196 patients included in this study, 85 were active smokers (43.4%), 54 ex-smokers (27.6%), and 57 nonsmokers (29%). Out of 171 patients with decreased level of HDL, 90.6% were smokers, 88.9% ex-smokers, and 80.7% of nonsmokers. It was found that significant changes occurred among the groups with decreased level of HDL (P < 0.05). Conclusion: HDL level is more reduced among the smokers compared to the ex-smokers and nonsmokers especially in the female.
Keywords: Coronary heart diseases, lipid profile, Malaysia, smoking
|How to cite this article:|
Haque AE, Kamaruzzaman SB, Haque M. Association of smoking with blood lipids in coronary heart disease patients admitted in Taiping Hospital, Perak, Malaysia. Med J DY Patil Univ 2016;9:36-42
|How to cite this URL:|
Haque AE, Kamaruzzaman SB, Haque M. Association of smoking with blood lipids in coronary heart disease patients admitted in Taiping Hospital, Perak, Malaysia. Med J DY Patil Univ [serial online] 2016 [cited 2022 Aug 17];9:36-42. Available from: https://www.mjdrdypu.org/text.asp?2016/9/1/36/172426
| Introduction|| |
Coronary heart disease (CHD) has been an important public health problem in Malaysia, causing a lot of morbidity and mortality for a long time as like many other countries in both developing and developed the world. ,,,, "Coronary artery disease develops when the coronary arteries - the major blood vessels that supply them with blood, oxygen, and nutrients - become damaged or diseased."  The narrowing of the cardiac vasculature can be due to a number of factors. One of the most important is cigarette smoking. Tobacco can predispose to plaque formation through inflicting injury to the blood vessels by decreasing high-density lipoprotein-cholesterol (HDL-C) and increasing low-density lipoprotein-cholesterol (LDL-C).  Plaque formation is one of the major predisposing factors of CHD and it can cause thickening of the arterial wall (atherosclerosis).  Thickened and narrowed blood vessels lead to depletion of blood supply to the heart. The oxygen demanding heart will infarct as the oxygen supply cannot meet the oxygen requirement.  Some studies were done to identify the risk factors for the development of CHD that was a leading cause of death and disability in both developed and developing countries. ,,,,,, Risk factors that are related to the development of CHD are cigarette smoking, increased fat consumption, increased serum cholesterol level, glucose intolerance, high blood pressure (BP), and obesity. ,,,, Some reputed journals mentioned that the risk factors for CHD are increased LDL, decreased HDL, and increase in total cholesterol and cigarette smoking. ,,, In some studies, it was also cited that abnormalities in blood lipids, smoking, and high BP were the major risk factors for the development of CHD. ,,,,, Studies revealed that established risk factors for the development of CHD are dyslipidemia: Specifically the increase in LDL and fasting triglycerides (TGs) and a decrease in HDL, cigarette smoking, diabetes, obesity, and physical inactivity. ,,, Any form of tobacco use can influence the levels of LDL and HDL and play a significant role in the development of CHD. Furthermore, there are many studies associating smoking with decreased levels of HDL. ,,
- To obtain the sociodemographic data, and the serum LDL-C and HDL-C concentrations of the CHD patients
- To compare the results between smokers and nonsmokers suffered from CHD
- To find an association of cigarette smoking with HDL-C and LDL-C levels
- To correlate between sociodemographic factors and the serum level of LDL-C and HDL-C.
| Materials and Methods|| |
It is a retrospective cross-sectional study. The records of all the CHD patients admitted to Taiping Hospital between May 2011 and July 2011 were collected to gather necessary information. A Data Collection Sheet was designed to collect the patients' demographic data and risk factors-related information. "The diagnosis of hypertension is made when the average of 2 or more diastolic BP measurements on at least 2 subsequent visits is ≥90 mmHg or when the average of multiple systolic BP readings on 2 or more subsequent visits is consistently ≥140 mmHg. Isolated systolic hypertension is defined as systolic BP ≥140 mmHg and diastolic BP <90 mmHg. Individuals with high normal BP tend to maintain pressures that are above average for the general population and are at greater risk for development of definite hypertension and cardiovascular events than the general population."  Highly qualified consultant cardiologist confirmed CHD. Physical examination and necessary diagnostic blood test and electrocardiography (ECG) was done immediately. Later, when the patient was stable and improved computer tomography scan, stress testing, and angiography done. Inclusion criteria: All the CHD patients admitted to Taiping Hospital from May 2011 to July 2011. Exclusion criteria: Patients are having no CHD and the patients whose lipids profile was not done. IBM SPSS Statistics Version 20 was used to analyse the data. Variables were tested using Pearson test, simple individual t-test, and Chi-square test.
| Results|| |
Of the 280 CHD patients admitted to the hospital, 196 cases were selected according to research criteria, and the data were extracted from the records. The age range of the patients was from 36 to 87 years, and the mean age ± standard deviation was 60.32 ± 11.67 for 116 males and 65.25 ± 11.42 for 80 females [Figure 1]. Smoking status between genders was divided into the smoker, nonsmoker, and ex-smoker. 25% (50) and 18% (35) of males and females of total study population, respectively, were smokers [Table 1]. The study subjects consist of Malay, Chinese, Indian, and others with the number of subjects 125, 37, 30, and 4, respectively [Figure 2]. Among them, 25% (48), 11% (22), and 6% (13) of Malay, Chinese, and Indian origin, respectively, were smokers [Table 2].
A statistically significant (Chi-square test, P = 0.0492) correlation was found between smoking habit and high BP of the patients admitted to Taiping Hospital for CHD. Eight percent (15) and 3% (7) of males and females of total population, respectively, had high total blood cholesterol level, and a significant (Chi-square test, P < 0.05) correlation between smoking habit and high total cholesterol level in blood was found [Table 3]. Fourteen percent (27) and 6% (11) of males and females, respectively, had increased LDL level [Table 4], and there was a significant (Chi-square test, P < 0.005) correlation observed between smoking habit and high level of LDL. Fifty-three percent (104) and 34% (67) of males and females, respectively, had decreased HDL level [Table 5], and there was a significant (P < 0.005) correlation observed between smoking habit and low level of HDL. Among 85 smoker study population, 23% (45) and 16% (32) of males and females have decreased level of HDL cholesterol, respectively [Table 5]. Ten percent (20) and 5% (10) of males and females, respectively, had increased TG level [Table 6], and there was also a significant (Chi-square test, P < 0.005) correlation observed between smoking habit and high level of TG in the blood.
| Discussion|| |
The records of the 196 patients admitted for CHD in Taiping Hospital, Perak, Malaysia, were considered in this study. The main finding was that smoking play a key role in decreasing the level of HDL. In this study, 91% of smokers have the low level of HDL compared to only 81% of nonsmokers who suffered from CHD. The percentage of ex-smokers with decreased level of HDL was 89% (Chi-square test, P < 0.05). Female patients were seemed to be more sensitive to smoking in terms of reduced level of HDL. This study showed that 91% of women smokers had reduced level of HDL when compared to 86% of female ex-smokers and only 76% of female nonsmokers (Chi-square test, P < 0.05). This result is in agreement with the previous studies. ,,, HDL was absolutely and relatively more reduced in female smokers than in male smokers compared to nonsmokers of the same sex. , A reduced HDL concentration in smokers may be related to sex hormone metabolism ,, but so far, the apparently greater reduction in women has been only little explored.  A possible cause of the sex difference is an interaction of some hormonal factors with the component of the inhaled smoke.  HDL has been claimed as a more important risk factor for CHD than total cholesterol, especially in women,.  while epidemiological studies disagree regarding the role of TGs.  TGs were a significant predictor univariate and in models that include total cholesterol but became nonsignificant in both sexes as soon as HDL were included.  There are studies that reported similar result ,,,, but there are exceptions too. 
In this study, there was no association observed in the level of TGs, LDL, and total cholesterol among smokers, ex-smokers, and nonsmokers. These might be because there are a lot of other factors that influence serum lipid profile that could not be assessed in this study.
| Conclusion|| |
Among the CHD patients admitted to Taiping Hospital, Perak, Malaysia, the HDL level is more reduced in smokers compared to ex-smokers and nonsmokers. The study findings regarding female smokers were more prominent than female nonsmokers. It was also observed that the changes in the serum lipids tend to be high with the increase in duration and intensity of smoking.
The risk of the rise in serum cholesterol with an increase in LDL-C and decrease HDL-C assume a great significance since this has been the pattern associated with CHD. The squat level of HDL-C in cigarette smokers increases exposure of the vascular endothelium to impaired clearance of TG-rich lipoproteins perhaps provide a mechanism, and smoking itself predisposes to greater risk of developing atherosclerotic plaques and CHD. It is a retrospective cross-sectional hospital data-based study with its own limitation. Therefore, these findings need to be validated by conducting a well-designed prospective study to obtain better data and serve common people of Malaysia.
The authors are much grateful to the hospital staff who helped to extract the data. Moreover, researchers are heavily indebted to the Dean, Faculty of Medicine, Universiti Kuala Lumpur, and other academic and nonacademic staff for their kind cooperation.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
American Heart Association (Fighting Heart Disease and Stroke). A Public Health Action Plan to Prevent Heart Disease and Stroke. Centre for Disease Control and Prevention. U.S. Department of Health and Human Services; 2013. Available from: http://www.cdc.gov/dhdsp/action_plan/pdfs/action_plan_1of7.pdf
[Last Access on 2015 Jun 1].
Weatherall D, Greenwood B, Chee HL, Wasi P. Science and technology for disease control: Past, present, and future. In: Jamison DT, Breman JG, Measham AR, Alleyne G, Claeson M, Evans DB, et al
., editors. Disease Control Priorities in Developing Countries. 2 nd
ed., Ch. 5. Washington, (DC): World Bank; 2006. Available from: http://www.ncbi.nlm.nih.gov/books/NBK11740/
. [Last Access on 2015 Jun 1].
Tong SF, Low WY, Ng CJ. Profile of men′s health in Malaysia: Problems and challenges. Asian J Androl 2011;13:526-33.
Ministry of Health Malaysia. Clinical Practice Guidelines. [MOH/P/PAK/171.08 (GU)]. Prevention of Cardiovascular Disease in Women. 1 st
ed. Malaysia: Ministry of Health; 2008. http://www.moh.gov.my/attachments/3892.pdf
[Last Access on 2015 Jun 1].
Centers for Disease Control and Prevention (US), National Center for Chronic Disease Prevention and Health Promotion (US); Office on Smoking and Health (US). How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Cardiovascular Diseases. Atlanta (GA): Centers for Disease Control and Prevention (US); 2010. p. 6. Available from: http://www.ncbi.nlm.nih.gov/books/NBK53012/
[Last Access on 2015 Jun 1].
Alexander RW. Theodore Cooper Memorial Lecture. Hypertension and the pathogenesis of atherosclerosis. Oxidative stress and the mediation of arterial inflammatory response: A new perspective. Hypertension 1995;25:155-61.
Fox J, Pandit-Taskar N, Strauss HW. Cardiac anatomy and pathophysiology of coronary circulation as a basis for imaging. In: Paolo M, Giuliano M, editors. Basic Cardiac Imaging to Image Fusion. Milan: Springer; 2013. p. 1-14. Available from: http://www.dx.doi.org/10.1007/978-88-470-2760-2_1
[Last Access on 2015 Jun 1].
Pallister RA. Cardiac infarction in Malaya. Br Med J 1957;1:27-30.
Khoo KL, Tan H, Khoo TH. Cardiovascular mortality in Peninsular Malaysia: 1950-1989. Med J Malaysia 1991;46:7-20.
Khor GL. Ethnic characteristics of coronary heart disease risk factors and mortality in peninsular Malaysia. Asia Pac J Clin Nutr 1994;3:93-8.
Gaziano T, Reddy KS, Paccaud F, Horton S, Chaturvedi V. Cardiovascular disease. In: Jamison DT, Breman JG, Measham AR, Alleyne G, Claeson M, Evans DB, et al
., editors. Disease Control Priorities in Developing Countries. 2 nd
ed., Ch. 33. Washington (DC): World Bank; 2006. Available from: http://www.ncbi.nlm.nih.gov/books/NBK11767/pdf/Bookshelf_NBK11767.pdf
[Last Access on 2015 Jun 1].
Institute of Medicine (US) Committee on Preventing the Global Epidemic of Cardiovascular Disease: Meeting the Challenges in Developing Countries; Fuster V, Kelly BB, editors. Promoting Cardiovascular Health in the Developing World: A Critical Challenge to Achieve Global Health. Epidemiology of Cardiovascular Disease. Washington (DC): National Academies Press (US); 2010. p. 2. Available from: http://www.ncbi.nlm.nih.gov/books/NBK45693/pdf/Bookshelf_NBK45693.pdf
[Last Access on 2015 Jun 1].
Gaziano TA, Bitton A, Anand S, Abrahams-Gessel S, Murphy A. Growing epidemic of coronary heart disease in low- and middle-income countries. Curr Probl Cardiol 2010;35:72-115.
Buttar HS, Li T, Ravi N. Prevention of cardiovascular diseases: Role of exercise, dietary interventions, obesity and smoking cessation. Exp Clin Cardiol 2005;10:229-49.
Ockene IS, Miller NH. Cigarette smoking, cardiovascular disease, and stroke: A statement for healthcare professionals from the American Heart Association. American Heart Association Task Force on Risk Reduction. Circulation 1997;96:3243-7.
Rigotti NA, Pasternak RC. Cigarette smoking and coronary heart disease: Risks and management. Cardiol Clin 1996;14:51-68.
Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an independent risk factor for cardiovascular disease: A 26-year follow-up of participants in the Framingham Heart Study. Circulation 1983;67:968-77.
McGee DL, Reed DM, Yano K, Kagan A, Tillotson J. Ten-year incidence of coronary heart disease in the Honolulu Heart Program. Relationship to nutrient intake. Am J Epidemiol 1984;119:667-76.
Vergeer M, Holleboom AG, Kastelein JJ, Kuivenhoven JA. The HDL hypothesis: Does high-density lipoprotein protect from atherosclerosis? J Lipid Res 2010;51:2058-73.
Kapur NK, Ashen D, Blumenthal RS. High density lipoprotein cholesterol: An evolving target of therapy in the management of cardiovascular disease. Vasc Health Risk Manag 2008;4:39-57.
Natarajan P, Ray KK, Cannon CP. High-density lipoprotein and coronary heart disease: Current and future therapies. J Am Coll Cardiol 2010;55:1283-99.
Gordon T, Castelli WP, Hjortland MC, Kannel WB, Dawber TR. Diabetes, blood lipids, and the role of obesity in coronary heart disease risk for women. The Framingham study. Ann Intern Med 1977;87:393-7.
Grundy SM, Balady GJ, Criqui MH, Fletcher G, Greenland P, Hiratzka LF, et al.
Primary prevention of coronary heart disease: Guidance from Framingham: A statement for healthcare professionals from the AHA Task Force on Risk Reduction. American Heart Association. Circulation 1998;97:1876-87.
O′Donnell CJ, Elosua R. Cardiovascular risk factors. Insights from Framingham Heart Study. Rev Esp Cardiol 2008;61: 299-310.
Kones R. Primary prevention of coronary heart disease: Integration of new data, evolving views, revised goals, and role of rosuvastatin in management. A comprehensive survey. Drug Des Devel Ther 2011;5:325-80.
Zhang X, Patel A, Horibe H, Wu Z, Barzi F, Rodgers A, et al.
Cholesterol, coronary heart disease, and stroke in the Asia Pacific region. Int J Epidemiol 2003;32:563-72.
Emberson JR, Whincup PH, Morris RW, Walker M. Re-assessing the contribution of serum total cholesterol, blood pressure and cigarette smoking to the aetiology of coronary heart disease: Impact of regression dilution bias. Eur Heart J 2003;24:1719-26.
Asiki G, Murphy GA, Baisley K, Nsubuga RN, Karabarinde A, Newton R, et al.
Prevalence of dyslipidaemia and associated risk factors in a rural population in South-Western Uganda: A community based survey. PLoS One 2015;10:e0126166.
Perk J, De Backer G, Gohlke H, Graham I, Reiner Z, Verschuren M, et al.
European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts). Eur Heart J 2012;33:1635-701.
Warburton DE, Nicol CW, Bredin SS. Health benefits of physical activity: The evidence. CMAJ 2006;174:801-9.
Wong ND. Epidemiological studies of CHD and the evolution of preventive cardiology. Nat Rev Cardiol 2014;11:276-89.
He BM, Zhao SP, Peng ZY. Effects of cigarette smoking on HDL quantity and function: Implications for atherosclerosis. J Cell Biochem 2013;114:2431-6.
Ogawa K, Tanaka T, Nagoshi T, Sekiyama H, Arase S, Minai K, et al.
Increase in the oxidised low-density lipoprotein level by smoking and the possible inhibitory effect of statin therapy in patients with cardiovascular disease: A retrospective study. BMJ Open 2015;5:e005455.
Carretero OA, Oparil S. Essential hypertension. Part I: Definition and etiology. Circulation 2000;101:329-35.
Garrison RJ, Kannel WB, Feinleib M, Castelli WP, McNamara PM, Padgett SJ. Cigarette smoking and HDL cholesterol: The Framingham offspring study. Atherosclerosis 1978;30:17-25.
Criqui MH, Wallace RB, Heiss G, Mishkel M, Schonfeld G, Jones GT. Cigarette smoking and plasma high-density lipoprotein cholesterol. The Lipid Research Clinics Program Prevalence Study. Circulation 1980;62(4 Pt 2):IV70-6.
Taylor KG, Carter TJ, Valente AJ, Wright AD, Smith JH, Matthews KA. Sex differences in the relationships between obesity, alcohol consumption and cigarette smoking and serum lipid and apolipoprotein concentrations in a normal population. Atherosclerosis 1981;38:11-8.
Forey BA, Fry JS, Lee PN, Thornton AJ, Coombs KJ. The effect of quitting smoking on HDL-cholesterol - A review based on within-subject changes. Biomark Res 2013;1:26.
Njølstad I, Arnesen E, Lund-Larsen PG. Smoking, serum lipids, blood pressure, and sex differences in myocardial infarction. A 12-year follow-up of the Finnmark Study. Circulation 1996;93:450-6.
Bolego C, Poli A, Paoletti R. Smoking and gender. Cardiovasc Res 2002;53:568-76.
Semmens J, Rouse I, Beilin LJ, Masarei JR. Relationship of plasma HDL-cholesterol to testosterone, estradiol, and sex-hormone-binding globulin levels in men and women. Metabolism 1983;32:428-32.
Michnovicz JJ, Hershcopf RJ, Naganuma H, Bradlow HL, Fishman J. Increased 2-hydroxylation of estradiol as a possible mechanism for the anti-estrogenic effect of cigarette smoking. N Engl J Med 1986;315:1305-9.
Michnovicz JJ, Hershcopf RJ, Haley NJ, Bradlow HL, Fishman J. Cigarette smoking alters hepatic estrogen metabolism in men: Implications for atherosclerosis. Metabolism 1989;38:537-41.
Prescott E, Hippe M, Schnohr P, Hein HO, Vestbo J. Smoking and risk of myocardial infarction in women and men: Longitudinal population study. BMJ 1998;316:1043-7.
Bush TL, Fried LP, Barrett-Connor E. Cholesterol, lipoproteins, and coronary heart disease in women. Clin Chem 1988;34: B60-70.
Austin MA. Plasma triglyceride as a risk factor for coronary heart disease. The epidemiologic evidence and beyond. Am J Epidemiol 1989;129:249-59.
Pocock SJ, Shaper AG, Phillips AN. Concentrations of high density lipoprotein cholesterol, triglycerides, and total cholesterol in ischaemic heart disease. BMJ 1989;298: 998-1002.
Criqui MH, Heiss G, Cohn R, Cowan LD, Suchindran CM, Bangdiwala S, et al.
Plasma triglyceride level and mortality from coronary heart disease. N Engl J Med 1993;328:1220-5.
Sharrett AR, Ballantyne CM, Coady SA, Heiss G, Sorlie PD, Catellier D, et al.
Coronary heart disease prediction from lipoprotein cholesterol levels, triglycerides, lipoprotein(a), apolipoproteins A-I and B, and HDL density subfractions: The Atherosclerosis Risk in Communities (ARIC) Study. Circulation 2001;104:1108-13.
Bittner V, Johnson BD, Zineh I, Rogers WJ, Vido D, Marroquin OC, et al.
The triglyceride/high-density lipoprotein cholesterol ratio predicts all-cause mortality in women with suspected myocardial ischemia: A report from the Women′s Ischemia Syndrome Evaluation (WISE). Am Heart J 2009;157:548-55.
Frohlich J, Dobiásová M. Fractional esterification rate of cholesterol and ratio of triglycerides to HDL-cholesterol are powerful predictors of positive findings on coronary angiography. Clin Chem 2003;49:1873-80.
Bainton D, Miller NE, Bolton CH, Yarnell JW, Sweetnam PM, Baker IA, et al.
Plasma triglyceride and high density lipoprotein cholesterol as predictors of ischaemic heart disease in British men. The Caerphilly and Speedwell Collaborative Heart Disease Studies. Br Heart J 1992;68:60-6.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]