|Year : 1987 | Volume
| Issue : 2 | Page : 65-8
Effect of calcium channel blockers on serum lipid profile.
RB Verma, VK Chaudhary, VK Jain
R B Verma
|How to cite this article:|
Verma R B, Chaudhary V K, Jain V K. Effect of calcium channel blockers on serum lipid profile. J Postgrad Med 1987;33:65-8
|How to cite this URL:|
Verma R B, Chaudhary V K, Jain V K. Effect of calcium channel blockers on serum lipid profile. J Postgrad Med [serial online] 1987 [cited 2020 Nov 29 ];33:65-8
Available from: https://www.jpgmonline.com/text.asp?1987/33/2/65/5291
Beta blockers and some other antihypertensive drugs such as, thiazides and prazosin when used for long periods are known to affect the lipid profile and consequently increase the risk for coronary atherosclerosis,, It has been suggested that in cases of hypertension and agina, this effect may outweigh the beneficial effects of the drug., Although the effect of propranolol on lipid profile is well documented,,, little information is available about the effect of calcium channel blockers. Hence, the present study was undertaken to evaluate the effect of some commonly used calcium channel blockers such as verapamil, nifedipine and prenylamine lactate on the serum lipid profile.
MATERIAL AND METHODS
Patients of stable angina, attending the outpatient department of the heart clinic, S. N. Medical College, Agra were selected for the study. Patients with history of pre infarction syndrome, severe congestive heart failure, myocardial infarction, diabetes, hypertension as well as the obese and the smokers were excluded from the study. Those who had marked or familial hyper-lipidemia and requiring drug therapy were not included in the study. A total of 20 patients received verapamil in a dose of 240 mg per day, 14 patients receive nifedipine in the dose of 30 mg per day and 18 patients received prenylamine lactate in the dose of 180 mg per day, for a period of six months. Patients were instructed to continue the same diet which they were taking in the past 3 months prior to commencement of study. During the period of study, these patients also received oral isosorbide dinitrate 5-10 mg four to six times a day and sublingual nitroglycerine to control the acute symptoms.
The lipid profile was done before starting the treatment and at the end of 3 and 6 months. The patients who developed pie-infarction syndrome, acute myocardial infarction, heart failure or severe hypertension during the period of study were eliminated from the study. The patients were asked to abstain from alcohol at least 24 hours prior to the investigations. The serum was collected in the morning after 12 hours' fasting. They were not administered the morning dose of the trial drug on the day of investigation. From the serum samples of the patients, serum cholesterol, serum triglyceride, and high density lipoprotein cholesterol (HDLC), were estimated. The very low density lipoprotein cholesterol (VLDLC) and low density lipoprotein cholesterol (LDLC) values were calculated by difference. The cholesterol ratio was calculated from the following formula.
Cholesterol ratio = HDL cone x 100
VLDLC + LDLC
Paired 't' test was used to compare the difference between pretreatment and post treatment values.
A total of 42 patients successfully completed the study. Out of these, 32 patients were males and 20 were females. The mean age of patients was 54.6 years with the range 47 years to 60 years.
The effects of verapamil, nifedipin and prenylamine lactate on the lipid profile of the patients have been shown in [Tables 1], [Tables 2], and [Tables 3] respectively. In all the groups, no significant difference could be found between the pre- and post-treatment levels.
The present study was designed to evaluate the effect of verapamil, nifedipin and prenylamine lactate on serum lipids in patients of stable angina. These 3 drugs belong to a new class of drugs, the calcium channel blockers. Their effect on serum cholesterol, triglyceride, HDLC and cholesterol ratio was estimated in the above group of patients. It is known that serum cholesterol and triglycerides are directly related to the development of atherosclerosis.,, On the other hand HDLC concentrations are inversely related to atherosclerosis and risk of ischaemic heart disease.,
In the present study, we kept the patients on verapamil (n = 20), nifedipin (n =14) and prenylamine lactate (n = 18) for a period of 6 months, eliminating all factors which might alter the lipid profile. The study reveals no statistically significant alteration on either serum cholesterol, serum triglyceride, HDL level and cholesterol ratio, after 3 months and 6 months.
Increase in the levels of serum cholesterol, serum-triglycerides and lowered values of HDLC adversely affect the process of atherosclerosis, increasing the risk of coronary artery disease. This particular fact that calcium channel blockers do not produce deleterious effect on lipid profile seems to be advantageous over beta blockers which are known to affect the lipid profile adversely.
|1||Abell, L. L., Levy, B. L., Brodie, B. B. and Kendall, F. E.: A simplified method for estimation of total cholesterol in serum and demonstration of its specificity. J. Biol. Chem., 195: 357-366, 1952.|
|2||Bachorik, P. S., Wood, P. D. S., Alber's, J. J.: Plasma high density lipoprotein cholesterol concentrations determined after removal of other lipoproteins by heparin/ manganese precipitation or by ultracentrifugation. Clin. Chem., 22: 1828-1834, 1976.|
|3||3.Bauer, J. H., Brooks, C. S., Weinstein, I., Wilcox, H. H., Heimberg, M., Burch, R. N. and Barkley, R.: Effects of diuretics and propranolol on plasma lipoprotein lipids. Clin. Pharmacol. & Therap., 30: 35-43, 1981.|
|4||Burstein, M., Scholnick, H. R. and Morfin, R.: Rapid method for the isolation of lipoproteins from human serum by precipitation by polyanions. J. Lipid Res., 11: 583-585, 1970.|
|5||Gordon, T., Castelli, W. P., Hjortland M. C., Kannel, W. B. and Dawber, T. R.: High density lipoproteins as a protective factor against coronary artery disease; The Framingham study. Amer. J. Med., 62: 707-714, 1977.|
|6||Helgeland, A., Hjermann, I. and Leren, P.: High density lipoprotein cholesterol and antihypertensive drugs; The Oslo study. Brit. Med. J., ii: 403, 1978.|
|7||Helley, I. B., Rosenman, R. H., Bawol, R. D. and Brand, R. J.: Epidemiology as a guide to clinical decision. The association between triglycerides and coronary heart disease. New Engl. J. Med., 302: 1383-1389, 1980.|
|8||Kannel, W. B., Castelli, W. P. and Gordon, T.: Cholesterol in the prediction of atherosclerotic disease. New perspectives based on the Framingham study. Ann. Int. Med., 90: 85-91, 1979.|
|9||Leren, P., Helgoland, A., Holeme, I., Foss, P. O., Hjermann, I. and Lund-Larsen, P. G.: Effect of propranolol and prazocin on blood lipids, The Oslo study, Lancet, ii: 4-6, 1980.|
|10||Shekelle, R. B., Shryock, A. M., Paul, O., Lepper, M., Stamler, J., Liu, S. and Rayner, W. J.: Diet, serum cholesterol and death from coronary heart disease, the Western electric study. New Engl. J. Med., 304: 65-70, 1981.|
|11||Tan, M. H.: H.D.L. cholesterol: the negative risk factor for coronary heart disease. Ann. Acad. Med. Singapore, 9: 491-495, 1980.|
|12||U.S. Department of Health and Human Science: Lipid Research Clinic Programme. Mannual and Laboratory Operations. Lipid and Lipoprotein Analysis. N.I.H. Publication No. 75, Revised September 1982. |