The effects of antihypertensive agents on serum lipids and lipoproteins

Optimizing cardiovascular risk reduction during antihypertensive therapy.

“…68 - 72 While informative, these studies have not always provided insight into the mechanisms of these effects. It is not the intent of this review to provide an encyclopedic reference to all reported studies but rather to summarize the consensus of the observations.…”

“…Not only have the benzodiathiazide agents been implicated, but also chlorthalidone and loop diuretics such as furosemide, particularly when given at antihypertensive doses. 72 Indapamide at a dose of 25 mg/ day has been reported to have no adverse lipid effects, 54 -55 although one study reported an elevation in serum cholesterol with this agent. 73 The reformulation of metolazone with increased bioavailability (Mykrox) was found to raise cholesterol, triglycerides, and LDL when 0.5 mg was given, as was hydrochlorothiazide plus triamterene.…”

“…0-Blockers decrease hepatic and lipoprotein lipase activity, thus accounting for the increases in plasma trigryceride levels. 77 Although less extensively studied, /3-blockers with intrinsic sympathomimetic activity and those with combined a-adrenergic and 0-adrenergic receptor blocking properties do not appear to exhibit these adverse 72 Despite an adverse effect on the lipid profile, propranolol treatment was shown to decrease plaque formation in cholesterol-fed rabbits. 16 The relevance of this observation to human atherogenesis remains to be defined.…”

The effect of moxonidine on plasma lipid profile and on LDL subclass distribution

“…In subjects who display any lipid abnormalities, thiazide diuretics and beta-blockers may not be an appropriate first-step treatment, since they appear to alter the lipid profile unfavourably, at least in short-term studies. [1][2][3][4] Additionally, beta-blocker use is associated with a predominance of smaller, denser LDL particles and less HDL mass, 5,6,18 lipoprotein changes that might be expected to increase coronary artery disease risk 19 and offset the beneficial effects of antihypertensive therapy on cardiovascular morbidity and mortality. 7,8 It has recently been suggested that moxonidine seems to be a logical choice for hypertensive patients with coexistent glucose intolerance or dyslipidaemia, 20 as in clinical studies moxonidine has been proved to have neutral or even beneficial effects on lipid and carbohydrate metabolism.…”

“…[1][2][3][4] Additionally, it has been shown that beta-blocker use may predispose to expression of a relatively atherogenic lipoprotein subclass profile, as it is associated with a predominance of smaller, denser, low-density lipoprotein (LDL) particles and less HDL mass. 5,6 Since an overview of all hypertension trials has shown that antihypertensive treatment does lead to a less than expected reduction in coronary heart disease (CHD) event rates, 7,8 it is tempting to suggest that the adverse effects of the study drugs on lipid metabolism may have offset the potential benefit of blood pressure (BP) reduction.…”