Affiliation:
1. Western Australian Heart Research Institute, Department of Medicine, University of Western Australia
2. Royal Perth Hospital, Wellington Street, GPO Box X22I3, Perth 6001, Western Australia
Abstract
1. β-blockers improve morbidity and mortality after myocardial infarction, probably by several mechanisms. We investigated potentially relevant effects of β-blockers in vivo and in vitro on plasma lipid oxidizability. Forty-two healthy men were randomized to receive placebo (13), metoprolol (14) or propranolol (15).
2. At 4 weeks, the effects on heart rate, blood pressure and lipids appeared similar and subjects taking a β-blocker were combined. Compared with placebo, those on a β-blocker gained 0.5 kg in weight (P = 0.04), heart rate fell from 63 to 52 beats/min (P < 0.0001) and blood pressure fell from 116/74 to 113/69 mmHg (P < 0.005); high-density lipoprotein (HDL)-cholesterol fell from 1.26 to 1.11 mmol/l (P = 0.005), there being no change in the ratio of free to esterified cholesterol in HDL, and there was an apparent rise in serum triacylglycerols from 1.18 to 1.43 mmol/l (P = 0.15 when adjusted for weight gain). Low-density lipoprotein (LDL)-cholesterol and lipoprotein (a) did not change. In this study, the oxidizability of LDL was unaffected by β-blocker therapy. β-blockade was not associated with any change in LDL fatty acid profile, or β-carotene or α-tocopherol content which might account for the reduced LDL oxidizability previously reported in patients treated with β-blockers. Furthermore, neither atenolol nor propranolol, at concentrations up to 100 μmol/l, had any effect on in vitro oxidizability of LDL obtained from healthy volunteers.
3. In contrast to the favourable haemodynamic effects conferred by β-blockers, the effects on weight and serum triacylglycerols and HDL-cholesterol appear to be adverse and we did not demonstrate any changes in lipid oxidizability which might be relevant to the protective effects of β-blockers in patients with coronary disease.
Cited by
11 articles.
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