Immediate effect of smoking on serum lipids and lipoproteins in patients with hypertension.
The association between smoking and coronary artery disease (CAD) is no longer in doubt. It has been suggested that smoking is one of the most readily correctable coronary risk factors. W.H.O. has launched a concerted public compaign against smoking. It is ironical, however, that the mechanism by which smoking promotes CAD still eludes us.
It has been suggested that smoking induced alterations in serum lipid and lipoprotein profile can make one susceptible to CAD. However, not all smokers develop hyperlipidaemia and CAD. It has been reported that patients of myocardial infarction. react abnormally to smoking and show a far greater in crease in serum free fatty acids (FFA) immediately after smoking as compared to healthy subjects.
To our knowledge, immediate effects of smoking on serum lipids and lipoproteins in patients of hypertension-another potent coronary risk factor-have not been investigated. Therefore, we decided to study the immediate effects of smoking on serum cholesterol, triglycerides, lipoproteins and free fatty acids in normal subjects and patients of hypertension to find out:
(i) whether smoking produces an immediate change in serum cholesterol, triglycerides and lipoproteins, and
(ii) whether serum FFA response to smoking is different in patients of hypertension as compared to normal subjects.
Fifty male subjects, 45-60 years old, belonging to middle and high income groups and engaged in sedentary occupations, constituted the material of the study. Twenty five of them were healthy controls and the remaining 25 were patients of primary hypertension. In the latter, the systolic blood pressure ranged from 150 to 220 mm of Hg and the diastolic blood pressure ranged from 100 to 130 mm of Hg. Blood pressure of each subject was recorded on at least two occasions in the resting state.
None of the subjects was obese or underweight. None was taking any medication known to affect the parameters studied. All the subjects had been smoking more than 5 cigarettes a day for over a year. 80% of the subjects in each group smoked upto 20 cigarettes a day and 20% smoked over 20 cigarettes a day. Thus, only 20% of the subjects were heavy smokers according to Billimoria et al. Heavy smokers were not grouped separately because of a small number. But their proportion was similar in both the groups.
The subjects were asked to fast overnight. In the morning, venous blood samples were collected from each subject in the sitting posture without using tourniquets. Each subject was then asked to smoke 2 filter-tipped "Wills Navy Cut" cigarettes consecutively. Most workers have studied the immediate effects of smoking after the subjects smoked 2 cigarettes consecutively., ,  Ten minutes after completion of smoking a second blood sample was collected from each subject.
Each blood sample was analysed for serum cholesterol, triglycerides, lipoproteins and free fatty acids. Haemolysed samples were discarded. The data were analysed statistically by Student's t-test for paired data.
There was no significant change in serum cholesterol, triglycerides and lipoproteins after smoking in healthy controls as well as in patients of hypertension [Table - 1].
Serum FFA rose significantly after smoking in healthy subjects as well as in patients of hypertension
[Table - 2]. The extent of rise in the two groups was comparable.
Smoking, hypertension and hyperlipidaemia are among the major coronary risk factors and, when present together, have a cumulative or synergistic effect. Smoking immediately raises serum FFA ,,, and long term smoking leads to hyperlipidaemia and a change in serum lipoprotein pattern towards that of the CAD patients., ,  It has been suggested that patients of CAD show an exaggerated rise in serum FFA after smoking and this could explain the smoking-hyperlipidaemia-CAD association. ,,
If hypertensive patients reacted to smoking similarly, the risk of developing CAD would be greater in smoker hypertensives than in non-smoker hypertensives. This could also explain, at least partially, the synergistic effects of hypertension and smoking as coronary risk factors. We have not come across any report on the immediate effects of smoking on serum lipids and lipoproteins in hypertensive patients. Hence the present study.
We have not observed a significant change in serum cholesterol, triglycerides and lipoproteins immediately after smoking in both normal subjects and hypertensive patients. Similar observations have been made earlier in healthy subjects, ,  and patients of CAD.
The immediate rise in serum FFA after smoking in normal subjects observed by us is also well documented.,,, We have observed an identical FFA response to smoking in normal subjects and hypertensive patients which cannot be compared due to lack of earlier reports. Our observations suggest that the synergistic actions of hypertension and smoking as coronary risk factors are not mediated by the immediate effects of smoking on serum lipids and lipoproteins. Other mechanisms to explain the synergism between hypertension and smoking need to be investigated.