{"id":1889,"date":"2015-03-28T06:30:55","date_gmt":"2015-03-28T06:30:55","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=1889"},"modified":"2017-01-04T08:00:40","modified_gmt":"2017-01-04T08:00:40","slug":"study-of-cardiac-status-and-lipid-profile-in-young-asymptomatic-cigarette-smokers-and-tobacco-chewers","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol4no1\/study-of-cardiac-status-and-lipid-profile-in-young-asymptomatic-cigarette-smokers-and-tobacco-chewers\/","title":{"rendered":"Study of Cardiac Status and Lipid Profile in Young Asymptomatic Cigarette Smokers and Tobacco Chewers"},"content":{"rendered":"

Introduction<\/strong><\/p>\n

Smoking is an escalating public health problem, especially in a developing country like India. Cigarette smoke is a dominant risk factor for premature or accelerated peripheral, coronary and cerebral atherosclerotic vascular diseases. One to three fold increases in risk of myocardial infarction has generally been noted among current cigarette smokers.1<\/sup><\/p>\n

Tobacco chewing is also very common in our country with tobacco chewers numbering equivalent to cigarette smokers.2<\/sup><\/p>\n

Tobacco cigarette smoking and tobacco chewing are clearly toxic to vessels causing endothelial injury by inducing impairment in prostaglandin biosynthetic capability and enhanced platelet activation.3<\/sup><\/p>\n

Smoking is also found to be associated with increased levels of low density lipoprotein cholesterol, triglycerides and decreased level of high density lipoprotein cholesterol. This directly increases the risk of coronary artery diseases.2<\/sup><\/p>\n

Various cigarette smoke products such as cotinine, polyaromatic hydrocarbons, cadmium, benzopyrene, polonium-210 and so many others are proved to be mutagenic and carcinogenic.4<\/sup><\/p>\n

A combine study of cardiac status and lipid profile in chronic smokers and tobacco chewers is not done till now.<\/p>\n

Most of workers have studied the effect of cigarette smoking on lipid profile. But, in present study, we tried to evaluate correlation among cigarette smokers, tobacco chewers with altered lipid profile and controls. We also analyzed whether tobacco chewing causes same degree of alteration in lipid profile as cigarette smokers does.<\/p>\n

Methods<\/strong><\/p>\n

The present study is conducted in department of physiology SRTR medical college and hospital, Ambajogai. The subjects for study were the volunteers from the society. A total of 90 subjects divided in three Groups were studied. The Groups are as follows:<\/p>\n

Group A \u00e0 \u00a030 Current Smokers (> 10 years)
\nGroup B\u00a0 \u00e0 30 Current Tobacco chewers (>10 years)
\nControls \u00e0 \u00a030 Non smokers \u2013 Non tobacco chewers<\/p>\n

The subjects were normal healthy volunteers without any current clinical complains in age Group of 20 \u2013 40 years. A detailed history, clinical examination and routine lab investigation were done to exclude diseases. Alcoholics and patients on lipid lowering drugs, Beta blockers and thiazide diuretics were also excluded from the study. History of smoking, duration and number of cigarette smoked per day, and also history of tobacco chewing duration and number of tobacco packets per day were evaluated in each subject. Subjects smoking more than 10 cigarettes per day currently and for more than 10 years were labeled as smokers (Group A). Subjects chewing tobacco more than 5 tobacco packets per day currently for more than 10 years were labeled as tobacco chewers (Group B). Controls are non smokers and non tobacco chewers. Informed written consent was taken from all the subjects.<\/p>\n

Following parameters were selected for present study:<\/p>\n

Lipid Profile<\/p>\n

Low Density Lipoproteins<\/p>\n

Very Low Density Lipoproteins<\/p>\n

High Density Lipoproteins<\/p>\n

Triglycerides<\/p>\n

Total Cholesterol<\/p>\n

Blood pressure<\/p>\n

Systolic Blood Pressure<\/p>\n

Diastolic Blood Pressure<\/p>\n

Mean Blood Pressure<\/p>\n

For lipid profile blood samples were taken in morning after 14 hour fast and estimation was done by enzymatic method using Beacon Kits.<\/p>\n

Blood pressure was recorded by using sphygmomanometer by auscultatory method in supine position under basal conditions.<\/p>\n

The obtained data was analyzed using statistical software SPSS 10.<\/p>\n

Results<\/strong><\/p>\n

The Mean, Standard Deviation, t-test and statistical significance (P value) of lipid profile parameters in Group A, Group B and Controls is as shown in Table 1. The lipid profile parameters were significantly increased in Group A and Group B when compared with controls (P < 0.001) except for HDL which was decreased significantly (P < 0.001) as compared to controls.\u00a0 On comparing Group A with Group B, there was no difference in lipid profile parameters except for HDL which shows significant decrease in Group A as compared with Group B (P <0.05)<\/p>\n

Table 1: Comparison Of Lipid Profile Amongst Cigarette Smokers, Tobacco Chewers And Control<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
LIPID<\/td>\nSTATS<\/td>\nGROUP-A<\/td>\nCONTROL<\/td>\nGROUP-B<\/td>\nCONTROL<\/td>\nGROUP-A<\/td>\nGROUP-B<\/td>\n<\/tr>\n
PROFILE<\/td>\n<\/td>\n <\/p>\n

N=30<\/td>\n

 <\/p>\n

N=30<\/td>\n

 <\/p>\n

N=30<\/td>\n

 <\/p>\n

N=30<\/td>\n

 <\/p>\n

N=30<\/td>\n

 <\/p>\n

N=30<\/td>\n<\/tr>\n

TOTAL<\/strong><\/p>\n

CHOL.<\/strong><\/td>\n

MEAN<\/p>\n

(mg\/dl)<\/td>\n

224.8<\/td>\n175.4<\/td>\n224.1<\/td>\n175.4<\/td>\n224.8<\/td>\n224.1<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n49.6<\/td>\n23.6<\/td>\n61.1<\/td>\n23.6<\/td>\n49.6<\/td>\n61.1<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 4.920<\/td>\nt = 4.07<\/td>\nt = 0.046<\/td>\n<\/tr>\n
p-value<\/td>\np < 0.001<\/td>\np < 0.001<\/td>\np > 0.05<\/td>\n<\/tr>\n
TG<\/strong><\/td>\nMEAN<\/p>\n

(mg\/dl)<\/td>\n

167.8<\/td>\n107.9<\/td>\n167.6<\/td>\n107.9<\/td>\n167.8<\/td>\n167.6<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n54.2<\/td>\n46.1<\/td>\n75.1<\/td>\n46.1<\/td>\n54.2<\/td>\n75.1<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 4.612<\/td>\nt = 3.712<\/td>\nt = 0.0073<\/td>\n<\/tr>\n
p-value<\/td>\np < 0.001<\/td>\np < 0.001<\/td>\np > 0.05<\/td>\n<\/tr>\n
HDL-C<\/strong><\/td>\nMEAN<\/p>\n

(mg\/dl)<\/td>\n

29.4<\/td>\n41.2<\/td>\n31.7<\/td>\n41.2<\/td>\n29.4<\/td>\n31.7<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n1.1<\/td>\n7.5<\/td>\n5.5<\/td>\n7.5<\/td>\n1.1<\/td>\n5.5<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 8.536<\/td>\nt = 5.602<\/td>\nt = 2.202<\/td>\n<\/tr>\n
p-value<\/td>\np < 0.001<\/td>\np < 0.001<\/td>\np < 0.05<\/td>\n<\/tr>\n
LDL-C<\/strong><\/td>\nMEAN<\/p>\n

(mg\/dl)<\/td>\n

161.8<\/td>\n112.6<\/td>\n158.9<\/td>\n112.6<\/td>\n161.8<\/td>\n158.9<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n44.5<\/td>\n20.6<\/td>\n59.3<\/td>\n20.6<\/td>\n44.5<\/td>\n59.3<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 5.493<\/td>\nt = 4.041<\/td>\nt = 0.2149<\/td>\n<\/tr>\n
p-value<\/td>\np < 0.001<\/td>\np < 0.001<\/td>\np > 0.05<\/td>\n<\/tr>\n
VLDL-C<\/strong><\/td>\nMEAN<\/p>\n

(mg\/dl)<\/td>\n

33.6<\/td>\n21.6<\/td>\n33.5<\/td>\n21.6<\/td>\n33.6<\/td>\n33.5<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n10.8<\/td>\n9.2<\/td>\n15.0<\/td>\n9.2<\/td>\n10.8<\/td>\n15.0<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 4.612<\/td>\nt = 3.712<\/td>\nt = 0.0073<\/td>\n<\/tr>\n
p-value<\/td>\np < 0.001<\/td>\np < 0.001<\/td>\np > 0.05<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

The mean of blood pressure parameters, t-test and statistical significance in Group A, Group B and Controls is as shown in Table 2. There is significant increase in systolic blood pressure of Group A and Group B when compared with controls (P < 0.001). Diastolic blood pressure is increase but not significantly in Group A and Group B when compared with controls. The mean blood pressure is increased significantly in Group A compared with controls but not significantly in Group B compared with controls. There is no difference in blood pressure parameters\u00a0\u00a0 in Group A when compared with Group B.<\/p>\n

Table 2: Comparison Of Blood Pressure Amongst Cigarette Smokers, Tobacco Chewers And Control<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
BLOOD<\/p>\n

PRESSURE<\/td>\n

STATS<\/td>\nGROUP-A<\/p>\n

N=30<\/td>\n

CONTROL<\/p>\n

N=30<\/td>\n

GROUP-B<\/p>\n

N=30<\/td>\n

CONTROL<\/p>\n

N=30<\/td>\n

GROUP-A<\/p>\n

N=30<\/td>\n

GROUP-B<\/p>\n

N=30<\/td>\n<\/tr>\n

SYSTOLIC<\/strong><\/p>\n

B P <\/strong><\/td>\n

MEAN<\/p>\n

(mmHg)<\/td>\n

135.4<\/td>\n127.1<\/td>\n135.7<\/td>\n127.1<\/td>\n135.4<\/td>\n127.1<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n13.3<\/td>\n6.2<\/td>\n12.7<\/td>\n6.2<\/td>\n13.3<\/td>\n6.2<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 3.107<\/td>\nt = 3.315<\/td>\nt = 0.079<\/td>\n<\/tr>\n
p-value<\/td>\np < 0.01<\/td>\np < 0.01<\/td>\np > 0.05<\/td>\n<\/tr>\n
DIASTOLIC<\/strong><\/p>\n

B P<\/strong><\/td>\n

MEAN<\/p>\n

(mmHg)<\/td>\n

85.3<\/td>\n81.9<\/td>\n83.1<\/td>\n81.9<\/td>\n85.3<\/td>\n83.1<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n9.3<\/td>\n5.3<\/td>\n8.83<\/td>\n5.3<\/td>\n9.3<\/td>\n8.83<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 1.738<\/td>\nt = 0.6029<\/td>\nt = 0.9673<\/td>\n<\/tr>\n
p-value<\/td>\np > 0.05<\/td>\np > 0.05<\/td>\np > 0.05<\/td>\n<\/tr>\n
MEAN<\/strong><\/p>\n

BLOOD<\/strong><\/p>\n

PRESSURE<\/strong><\/td>\n

MEAN<\/p>\n

(mmHg)<\/td>\n

102.0<\/td>\n97<\/td>\n100.6<\/td>\n97<\/td>\n102.0<\/td>\n100.6<\/td>\n<\/tr>\n
\u00b1 SD<\/td>\n10.4<\/td>\n4.5<\/td>\n9.6<\/td>\n4.5<\/td>\n10.4<\/td>\n9.6<\/td>\n<\/tr>\n
t \u2013 test<\/td>\nt = 2.446<\/td>\nt = 1.878<\/td>\nt = 0.5524<\/td>\n<\/tr>\n
p-value<\/td>\np < 0.05<\/td>\np > 0.05<\/td>\np > 0.05<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

Discussion<\/strong><\/p>\n

Our present study showed significantly increase in all lipid profile parameters except HDL-C which decreased significantly in cigarette smokers and tobacco chewers when compared with controls.<\/p>\n

Similar findings were reported by N S Neki et.\u00a0 al (2001)5<\/sup>, A Venkatesan et\u00a0 al (2006)1<\/sup>, S B Sharma et al (2005)6<\/sup>, K V Pugalendi et al (1990)7<\/sup>, J Whig et al (1992)8<\/sup>, M Khurana et al (2000)2<\/sup>, Micheal H et al (1980)9<\/sup><\/p>\n

One of the major reason for above changes is nicotine stimulates sympathetic adrenal system leading to increase secretion of catecholamines resulting in increased lipolysis, increased concentration of plasma free fatty acid which further result in increased secretion of hepatic free fatty acid and triglycerides along with VLDL-C in blood stream.5<\/sup><\/p>\n

Furthermore on comparing the lipid profile between cigarette smokers and tobacco chewers it was seen that there was no statistically significant difference in lipid profile of smokers and tobacco chewers suggesting that though cigarette smoking and tobacco chewing through there gaseous and chemical contents might be having different action at different sites of different organ, but as far as lipid metabolism is concerned both have equal and comparable adverse effect, probably the common culprit is nicotine. This point is worth attention as tobacco chewing is very popular in India and recent studies are showing that coronary heart disease is emerging as major killer in Indians.<\/p>\n

Also in our study of blood pressure parameters, we observed significant increase in systolic blood pressure in cigarette smokers and tobacco chewers when compared with controls. Diastolic blood pressure was higher but statistically not significant in cigarette smokers and tobacco chewers when compared with controls. Also mean blood pressure is increased in both smokers and tobacco chewers when compared with controls but the increase is significant in cigarette smokers but statistically not significant in tobacco chewers.<\/p>\n

When comparison was done between cigarette smokers and tobacco chewers we found increase in systolic blood pressure in tobacco chewers than smokers though the difference is not significant. There is no significant increase in diastolic blood pressure in cigarette smokers compared with tobacco chewers. Also there is slightly increase in mean blood pressure in cigarette smokers than tobacco chewers but the difference is statistically not significant.<\/p>\n

Our findings are in line with findings of S B Sharma et al (2005)6<\/sup>, Fennessy F et al (2003)10<\/sup>, Singh K et al (2004)11<\/sup>, Wolk R et al (2005)12<\/sup>.<\/p>\n

Both cigarette smoking and tobacco chewing are forms of physiological stress which stimulates hypothalamo-pituitary-adrenal system which results in increased secretion of catecholamines which increases myocardial activity resulting in increased cardiac output and thus increased systolic blood pressure.<\/p>\n

Diastolic blood pressure is a measure of peripheral resistance which does not undergo much fluctuation under slight physiological stressfull condition. If stress is for prolonged time diastolic blood pressure may increase but our study is in young subjects. This may be the reason why there is no statistically significant difference among cigarette smokers, tobacco chewers and controls. Although diastolic blood pressure is more in cigarette smokers and tobacco chewers compared with controls.13<\/sup><\/p>\n

Mean blood pressure is more towards diastolic blood pressure. As diastolic blood pressure is not significantly different in cigarette smokers, tobacco chewers and controls, the mean blood pressure is also not significant statistically although we found only statistical significant difference between cigarette smokers and controls.<\/p>\n

Conclusion<\/strong><\/p>\n

Our present study emphasizes the role of cigarette smoking and tobacco chewing in adverse changes on lipid profile and blood pressure. Also our study showed that tobacco chewing has comparable effect to cigarette smoking on lipid profile and blood pressures. For further evaluation we recommend a detailed study with a large size sample.<\/p>\n

References<\/strong><\/p>\n

    \n
  1. Venkatesan et al. Effects of smoking on lipid profile and lipid peroxidation in normal subjects. Indian Journal of Physiology and Pharmacology. 2006: 50(3), 273 \u2013 278.<\/li>\n
  2. Khurana, D Sharma, P.D Khandelwal. Lipid profile in smokers and tobacco chewers- a comparative study. JAPI. 2000 ; 48(9).<\/li>\n
  3. Casey R. G et al. Young male smokers have alyered platelets and endothelium that precedes atherosclerosis. Platelets; 2001 Nov. 12(7) 415- 418.<\/li>\n
  4. Potts R. J et al. Sperm chromatin damage associated with male smoking. Mutat \u2013 Res. 1999 Jan 25; 423 (1-2), 103 \u2013 11.<\/li>\n
  5. S Neki. Lipid profile in chronic smokers \u2013 A clinical study. Journal of Indian academy of clinical medicine. Mar 2001. Vol 3(1); 51 \u2013 54<\/li>\n
  6. B Sharma et al. Coronary risk variable in young asymptomatic smokers. Indian journal of Med Res. 122, 2005; 205 \u2013 210.<\/li>\n
  7. V Pugalendi, S Ramakrishnan. Blood cholesterol and HDL-C in cigarette smokers. IJPP. 1991; 35(2); 138 \u2013 140.<\/li>\n
  8. J Whig et al. Serum lipids and lipoprotein profiles of cigarette smokers and passive smokers. Indian journal Med Res (B) 96, 1992; 282 \u2013 287.<\/li>\n
  9. Micheal H. et al. Cigarette smoking and plasma HDL-C . Circulation 62 (4) 1980.<\/li>\n
  10. Fennesssy F, Casey R. G, Bouchier Hayes D. Peripheral and central arterial hemodynamics interactions are early abnormality in young male cigarette smokers. Eur J. Vasc. Endovase. Surg. 2003; 25(2); 152 \u2013 158.<\/li>\n
  11. Singh K. Effect of smoking on QT interval, QT dispersion and rate pressure product. Indian heart journal. 2004; 56(2); 140 \u2013 142.<\/li>\n
  12. Wolk R et al. Hemodynamic and autonomic effects of smokeless tobacco in healthy young men. J. Am. Coll. Cardiol.2005; 15; 45(6); 910 \u2013 914.<\/li>\n
  13. Ganong F. W. Review of medical physiology. 22nd<\/sup> edition 2005; 677 \u2013 678.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Introduction Smoking is an escalating public health problem, especially in […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[10],"tags":[],"class_list":["post-1889","post","type-post","status-publish","format-standard","hentry","category-vol4no1"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/1889","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=1889"}],"version-history":[{"count":5,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/1889\/revisions"}],"predecessor-version":[{"id":12987,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/1889\/revisions\/12987"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=1889"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=1889"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=1889"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}