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Serum Lipoproteins During Treatment with Antihypertensive Drugs

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Summary

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 anti-hypertensive 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-treatedpostmenopausal 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 β-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 β1+2− blockers without partial intrinsic sympathomimetic activity (ISA), less pronounced on highly selective β1blockers without ISA, and even more discrete or absent on β-blockers with distinct ISA.

Other sympatholytics such as reserpine, methyldopa, debrisoquine, urapidil, clonidine, labetalol, or postsynaptic α-blockers (prazosin, trimazosin, doxazosin etc.) did not affect or, postsynaptic α-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 β-blockers, but not by sympatholytics such as reserpine, methyldopa or clonidine. With combined diureticpra-zosin treatment, a tendency for slightly higher HDL-C was reported.

Angiotensin converting enzmye 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. Therefore, at present these lipoprotein effects should be categorised as associated biochemical effects and no more. Long term studies are needed to clarify the pathogenic and prognostic relevance oflipoprotein changes induced by certain diuretics and/or β-blockers. In the meantime, it is of clinical interest that several of the generally available antihypertensive drugs seem to be ‘neutral’ or sometimes perhaps even potentially beneficial with regard to lipoprotein metabolism.

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  1. Medizinische Poliklinik, University of Berne, Freiburgstrasse 3, CH-3010, Berne, Switzerland

    Peter Weidmann (Professor of Medicine), Claudia Ferrier, Hermann Saxenhofer, Dominik E. Uehlinger & Bernhard N. Trost (Professor of Medicine)

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  1. Peter Weidmann
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  2. Claudia Ferrier
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  3. Hermann Saxenhofer
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  4. Dominik E. Uehlinger
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  5. Bernhard N. Trost
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Weidmann, P., Ferrier, C., Saxenhofer, H. et al. Serum Lipoproteins During Treatment with Antihypertensive Drugs. Drugs 35 (Suppl 6), 118–134 (1988). https://doi.org/10.2165/00003495-198800356-00017

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  • DOI: https://doi.org/10.2165/00003495-198800356-00017

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