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Serum lipoproteins during treatment with antihypertensive drugs
P Weidmann1, C Ferrier, H Saxenhofer
1Medizinische Poliklinik, University of Berne.
Insights
Certain antihypertensive drugs can negatively impact cholesterol levels, increasing coronary heart disease risk. However, some medications like ACE inhibitors, calcium channel blockers, and low-dose indapamide appear to have neutral or beneficial effects on lipoproteins.
Area of Science:
- Cardiology
- Pharmacology
- Metabolic Syndrome
Background:
- Hypertension and dyslipidemia are key coronary risk factors.
- Antihypertensive medications can influence lipoprotein metabolism.
- Understanding these interactions is crucial for cardiovascular risk management.
Purpose of the Study:
- To evaluate the effects of various antihypertensive drugs on serum lipoproteins.
- To identify antihypertensive therapies with neutral or beneficial effects on lipid profiles.
- To compare the lipoprotein-altering potential of different drug classes.
Main Methods:
- Review of studies examining antihypertensive drug effects on lipoproteins (HDL-C, LDL-C, triglycerides).
- Analysis of data from short-term (1-12 months) treatment periods.
- Comparison of effects across different drug classes including diuretics, beta-blockers, and others.
Main Results:
- Diuretics often increase LDL-C and triglycerides, though some like low-dose indapamide may not.
- Beta-blockers can increase triglycerides and decrease HDL-C, with variations based on selectivity and ISA.
- ACE inhibitors, calcium channel blockers, and prazosin generally show neutral or favorable effects on lipoproteins.
Conclusions:
- Antihypertensive drug choice significantly impacts lipoprotein profiles.
- ACE inhibitors, calcium channel blockers, and specific beta-blockers or diuretics may be preferred for patients with dyslipidemia.
- Further long-term studies are needed to confirm sustained effects.
Abstract:
Hypertension and certain alterations in serum lipoproteins such as a decrease in high density lipoprotein-cholesterol (HDL-C), an increase in low density lipoprotein-cholesterol (LDL-C) and perhaps also elevated triglycerides (Tg), are complementary coronary risk factors. Moreover, it has become evident that several of the drugs used for standard antihypertensive therapy may also interact with lipoprotein metabolism. The following has been observed after 1 to 12 months of treatment. Various diuretics can significantly increase LDL-C and/or very LDL-C and total C/HDL-C ratio, while HDL-C is often largely unchanged; Tg also are often elevated. LDL-C increased in diuretic-treated men and in chlorthalidone-treated postmenopausal women but not in chlorthalidone-treated premenopausal women. The latter may be protected from this side effect. Drug dosages were usually high in these studies. Indapamide, given at a dose of 2.5 mg/day, seems to exert no relevant effect on the lipoproteins. It is not established whether this difference is related to the nature of the drugs or the doses used. There is little doubt that the dose of chlorthalidone used was greater than that required for a full antihypertensive effect of this drug. Several beta-blockers given as monotherapy induce significant increases in Tg and a tendency for decreases in HDL-C. These changes are most prominent on non-selective beta 1+2-blockers without partial intrinsic sympathomimetic activity (ISA), less pronounced on highly selective beta 1-blockers without ISA, and even more discrete or absent on beta-blockers with distinct ISA. Other sympatholytics such as reserpine, methyldopa, debrisoquine, urapidil, clonidine, labetalol, or postsynaptic alpha-blockers (prazosin, trimazosin, doxazosin etc.) did not affect or, postsynaptic alpha-blockers in particular, sometimes even slightly decreased Tg or LDL-C and very LDL-C values. During combination therapy, diuretic-induced increases in LDL-C were at short term prevented or reversed by the concomitant administration of certain beta-blockers, but not by sympatholytics such as reserpine, methyldopa or clonidine. With combined diuretic-prazosin treatment, a tendency for slightly higher HDL-C was reported. Angiotensin converting enzyme inhibitors (captopril, enalapril) and calcium channel blockers (verapamil, nifedipine, nitrendipine, diltiazem) seem to be largely devoid of undesirable effects on serum lipoproteins. Monotherapy with the potent direct vasodilator carprazidil improved blood pressure and significantly increased HDL-C. Whether and to what extent the observed variations in lipoproteins may persist beyond 1 year of treatment is as yet unclear.(ABSTRACT TRUNCATED AT 400 WORDS)