Health Care

Supervisor And Principal Investigator

Dr. Maher Abdel-Latife Rashed, Ph.D.

Health Care Services

 Dr. Maher Rashed

Smoking As A major Risk Factor For Coronary Artery Disease

In Mahalla Cardiac Center

"By Maher Rashed et al., 2001"^#

Rashed MA*, El-Shourbagy OA** and Aziz SS***

*Cardiology specialist, Mahalla cardiac center, ministry of health and population.

**Professor of preventive medicine and public health, institute of postgraduate childhood studies, Ain Shams university.

*** Lecturer of medical childhood studies, institute of postgraduate childhood studies, Ain Shams university.

Abstract

Smoking is known as one of the changeable risk factors that were known to promote atherosclerosis and consequent CHD. The present study is designed to review the independence of smoking as a risk factor for CHD in our community. A total of 280 persons attending Mahalla Cardiac Center were studied at the period from first of June 2000 to last of December 2000. Subjects with major risk factors rather than smoking were excluded. The present study approved that is an increased incidence of ischemic heart and altered lipid profile with smoking. So, control of IHD is mandatory with cessation of smoking habit.

Background. -Smoking is known as one of the major risk factors for atherosclerosis and ischemic heart disease patients. Cardiovascular diseases were described to be changeable in mortality and morbidity coinciding with changes in dietary and smoking habits, body weight, blood pressure, and physical activity.

Objective. -To review drawbacks of smoking on coronary heart disease and to compare the effects of smoking on plasma lipids in patients with ischemic heart disease versus normal subjects.

Design. -A case control study.

Participants. -A total of 280 persons attending Mahalla Cardiac Center (outpatient clinic departments) were studied. Subjects with major risk factors rather than smoking were excluded. Our studied subjects were classified into two groups smokers (no.=156) and non-smokers (no.=124) groups.

Method. - Complete medical history and examination. Total cholesterol, triglycerides, LDL-C and HDL-C, evidence of ischemia and/or infarction assessed by ECG and/or echocardiography.

Results. -There is an increased incidence of ischemic heart disease in smokers versus non-smokers especially those of middle aged group. Also, significant percentage increase in total cholesterol by 9%, triglycerides by 8.9%, LDL-C by 13.4% but decreased HDL-C by 5.8% in smokers group as compared with the control non-smokers.

Conclusions. - Smoking habit -as a pollution- constitutes one the major risk factors for ischemic heart disease in our community like others. Regression and control of IHD epidemics is mandatory with cessation of smoking habit.  

Key words: Smoking - ischemic heart disease - Lipids - Ischemic heart disease - Lipoprotein disorders.

Introduction:

Coronary heart disease is a leading cause of death in developed countries (Courti et al., 1996). Mortality rates attributed to IHD vary between countries. It has been falling in many western countries in over the past 20-30 years. During the same period, there have been striking in creases in the IHD mortality rate in men and women in the less affluent industrialized countries (Gerald Shaper, 1997). However, Kennon et al., (1998) in his study of the acute coronary syndromes has reported that myocardial infarction is favored by cigarette smoking. Ian MacFarlane, (1991) has reported that tobacco accounts for 20% of all coronary heart disease.

Atherosclerosis is described to be multifactorial. Environmental as well as genetic factors play important roles in the pathophysiology of this process. Environmental factors include cigarette smoking, saturated fat and dietary cholesterol consumption and overnutrition which are associated with the development of symptomatic cardiovascular diseases (Hoeg, 1996).

Aim of the study:

It is important to study drawbacks of smoking on coronary heart disease and to compare the effects of smoking on plasma lipids. Also, this study aims to study the independence of smoking as a risk factor for ischemic heart disease. needs more study in our community.

Patients:

A total of 280 persons attending Mahalla Cardiac Center (outpatient clinic departments) were studied at the period from first of June 2000 to last of December 2000.

 Criteria of exclusion:

Patients with major known risk factors other than dyslipoproteinemia (like hypertension, diabetes mellitus) were excluded. Hereditary dyslipidemic cases were also excluded.

Criteria of inclusion:

Our subjects were attended to Mahalla Cardiac center outpatient clinic either for routine medical chick-up or for medical examination. There was no age and/or sex limited.

Methods:

All subjects were instructed to fast for 14 hours, and 3 ml venous blood sample were obtained by venipuncture. Sera were separated and immediately used for biochemical study. Enzymatic colorimetric determination of total cholesterol, triglycerides, high-density lipoproteins were done according to Stein (1987), McGrown et al., (1983) and Warnick et al., (1979) respectively. Low-density lipoproteins were calculated from the Friedwald formula (1972).

All cases were subjected to electrocardiogaphic assessment (Goldberger, 1992) and echocardiographic study (Harvey Feingenbaum, 1994) for evaluation of ischemia and/or myocardial infarction.

Our studied subjects were classified into two main groups, smokers group (no.=156) and non-smokers group (no.=124). Subgroups were classified according to age (0-15, 16-30, 31-45, 46-60, and 61-75 years) and also according to sex (male and female). Statistical analysis was performed by the Microsoft Excel version (Soft Art. Inc., 1997) on IBM computer.

Results:

Table (1): Main values of age in total subjects and classified subgroups (Both non-smokers and smokers).

Table (1) show mean, standard deviation and percentage differences of total age groups and also classified subgroups in both non-smokers and smokers groups.

Table (2): Lipid profile in total subjects (Both non-smokers and smokers).

Table (2) shows mean and standard deviation of the lipid profile of our studied cases (controlled non-smoking group and smoking group). It also shows student’s test and the percentage difference between smokers group and control group i.e. non-smokers.

Table (3): Ischemic heart disease in total subjects in non-smokers (i.e. control) group versus smokers group.

Table (3) shows mean and standard deviation of ischemic heart disease recorded in both controls non-smokers and smokers groups. It also shows students’ t test and the percentage differences between these groups.

Table (4): Ischemic heart disease according to age groups in smokers group versus non-smokers (i.e. control) group.

Table (4) shows mean and standard deviation of the ischemic events of both controlled non-smoking and smoking groups according to age groups (31-45 years), (46-60 years), (61-75 years). Table (4) also shows student’s test, p value and the percentage difference.

Table (5): Ischemic heart disease according to male sex in non-smokers (i.e. control) group versus smokers group.

Table (5) shows mean and standard deviation of the ischemic events of both controlled non smoking and smoking groups regarding to male gender (sex) in recorded cases in our study. Table (5) also shows student’s t test and the percentage difference between these groups.

Discussion:

Ischemic heart disease is reported as the most common cause of premature morbidity and mortality among men in the developed world, and represents the most common cause of emergency admission to hospital (Wright and Fox, 1993).

Several studies showed that smoking is a major risk factor for coronary heart disease and that a positive relationship occurs between smoking and coronary atherosclerosis (Zieke et al., 1999). Smoking and risk of developing CAD and its progression was also approved by Manfroi et al., (1994) and Waters et al., (1996). Other studies have also documented that patients with diffuse atherosclerosis were more frequently former smokers than those with isolated CAD (47% vs. 35.7%, P<0.01 respectively) (Meco JF and others, 1998).

Worldwide tobacco consumption shows wide variations. The prevalence of smoking shows increasing rapidly in the last decades all over the world. In UK, it has steadily declined. In 1972, 51% of males smoked, which has been fallen to 31% by 1990 (Crofton 1990).

The present study is designated to evaluate smoking effects as a major risk factor for CAD and its effects on plasma lipids in Mahalla Cardiac Center.

Our study shows relatively high mean percentage of smoking (Table 1) [51%, 49%, 51% and 51% in total age group (31-75 years) and in subgroups (31-45, 46-60 and 61-75 years) respectively] as compared with other published reports. Crofton (1990) reported that smoking prevalence in Egypt in 1988 was 35% of males smoked and 3% of females smoked. However, he has described that differences may occur due to low-income populations in studied area and also due to lack of health knowledge.

Smoking was proved to increases LDL-C and triglyceride levels but decreases HDL-C (Brischetto et al., 1983). Craig and his colleagues (1989) have analyzed 54 published studies on cigarette smoking.  They found that smokers had about 3% higher total cholesterol, 9.1% higher triglyceride, 1.7% higher LDL-C but 5.7% lower HDL-C in serum.

In agreement with previous studies, the present study showed that smoking increases TC, TG and LDL-C by 9%, 8.9% and 13.4% respectively. But, HDL-C showed to be decreased by 5.8% (Table 2).

However, some differences between rural and urban areas were reported by Singh RB, (1998). He reported the average serum cholesterol concentrations were 4.91 mmol/l in urban and 4.22 mmol/l in rural subjects without any sex differences.

Cigarette smoking is considered a predicting factor for CAD development (Brouwer DA 1997). Smoking is causally related to CHD and is an independent risk factor for development of myocardial infarction (Burley, 1997). Smoking was approved to be significantly associated with any coronary disease (Guerci 1998). These agree with our study as ischemic events show significant difference (p<0.001) in smokers versus non-smokers (Table 3).

Waters et al. (1996) explained developing CAD as its progression to be increased by smoking. Also, Wilson et al., (1999), found that smoking is significantly associated with severity and extent of CAD. From the other point of view, smoking cessation for 1 year results in statistically significant atherosclerosis regression (Ornish, Brown, Schertez, 1990).

Cigarette smoking is a risk factor for coronary artery disease in both sexes and is present at higher levels in middle-aged men than women (Price and Fowkes, 1997).

Also, Von Eyben et al., (1996) found that the age at acute myocardial infarction is related significantly to the extent of smoking (p<0.001). Smoking was associated with a 3-fold increase in raised lesions of the abdominal aorta. This was explained as the risk factors for adult coronary artery disease accelerate atherogenesis in the teenage years and their effects are amplified in young adulthood, 20-30 years before coronary artery disease becomes clinically manifest (McGill and McMahan, 1998). Also, major manifestation of clinical coronary artery disease were described by Kannel and colleagues (1990) to be doubled in incidence with each decade of life after age 45.

In agreement with these studies, the present study showed a significant increased incidence of ischemic heart disease in smokers versus non smokers with decreased grade of significance (Quai square= 22, p<0.001, Quai square= 11.25, p<0.001 and Quai square= 6.5, p<0.05) in age groups 46-60, 31-46 and 61-75 years respectively (Table 4).

In general, non-fatal myocardial myocardial infarction rates are five times as great among cigarette smokers at age 30-49, three times great at ages 50-59 and twice as great at ages 60-79. In smokers in the last age range, half of the myocardial infarctions can be attributed to the effects of tobacco. The increased risk of CHD among smokers declines with age probably because of the selective loss of smokers due to premature deaths (Task Force of the European Society of Cardiology, 1997).

Male gender was reported by Guerci et al.,  (1998) to be significantly associated with any coronary disease and obstructive coronary disease. The results of the Oslo Study Group in 1981 demonstrated a 47% decrease in the incidence of myocardial infarction and sudden death in high risk, middle aged men randomized to dietary means and smoking cessation. Also, a 50% decrease in CHD incidence in the same study as a response to avoidance of high-fat foods and smoking (Hjermann et al., 1981).

Also, Price and Fowkes (1997) have evaluated the incidence of coronary artery disease in industrialized countries to be three to four times higher in men than in women. This may be explained by increased prevalence of smoking in males.

The present study showed significant increased incidence of ischemic heart disease in males smokers versus non-smokers (p<0.001), while non-significant incidence was recorded in smoker female versus non-smokers (Table 5).

Differences in the incidence of ischemic heart disease between males and females were largely evaluated. Major manifestation of clinical coronary artery disease showed women lagging behind men in incidence by 20 years (Kannel and colleagues, 1990). Also, women showed to be lagged after men in the extent of atherosclerosis in the right coronary artery by about 5 years (McGill and McMahan, 1998).

As regards to urbanization, IHD prevalence was significantly higher in men compared to women in both urban (11.0 vs. 6.9%) and rural subjects (Singh RB, 1998). This may explain some recorded differences.

Cigarette smoke is loaded with free radicals of many different kinds (Pryor, 1987), which initiate the propagation of a  'chain reaction' (Freeman and Carpo, 1982). This may also explain the recorded differences in IHD in males versus females, which contributed with the same variations in smoking prevalence.

Also, cigarette smoke also activates phagocytes within the lung. Hence people who smoke are under oxidative stress (Halliwell, 1987). Such oxidative stress can produce damage to many different systems. Quinn and colleagues, (1987) have demonstrated that endothelial cells, macrophages and smooth muscle cells can all oxidize LDL. Then the oxidized LDL will be phagocytosed by monocytes/macrophages and thus many vacuolated foam cells are produced. In addition, cigarette smoke can damage the protein ceroluplasmin, a major antioxidant in plasma (Halliwell, 1987).

In general, Todd Miller and colleagues (1997) summarized effects of smoking as to enhance atheromata formation in different arterial beds, stimulate sympathetic nervous system activity, increase coronary artery tone, lower HDL cholesterol, and enhance oxidation of LDL cholesterol.

Conclusion:

It could be concluded that smoking has deleterious effect on cardiovascular system. It concludes that smoking may affect the myocardium either through direct toxic and destructive effect or through atherogenesis and consequent coronary artery disease. So prevention of smoking or at least put antioxidants into considerations may play a major role in halting atherosclerosis and/or coronary heart disease.

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^{# The Annual Scientific Meeting Of Institute Of Postgraduate Childhood Studies and Childhood Studies Centre, Ain Shams University, Mars 2001.}