Dyslipidemic effects of cigarette smoking on beta-blocker-induced serum lipid changes in systemic hypertension.

To assess the effects of beta blockers on lipids and apolipoproteins in cigarette smokers and nonsmokers, 330 patients with systemic hypertension received 1 month of placebo and 6 months of beta-blocker monotherapy. Serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoproteins A1 and B were measured. Total cholesterol increased with propranolol (smokers vs nonsmokers, 8 vs 2%); increased for smokers and decreased for nonsmokers with atenolol (8 vs -3%), metoprolol (6 vs -1%) and pindolol (7 vs -6%); and decreased for both groups with celiprolol (-3 vs -10%). HDL cholesterol decreased with propranolol (smokers vs nonsmokers, -8 vs -18%), atenolol (-7 vs -2%) and metoprolol (-12 vs -1%); increased for smokers and decreased for nonsmokers with pindolol (11 vs -2%); and increased for both groups with celiprolol (5 vs 6%). Similar trends were observed with LDL cholesterol and the total/HDL cholesterol ratio. It is concluded that early noncardioselective beta blockers such as propranolol have significant dyslipidemic effects in both smokers and nonsmokers. Cardioselective drugs such as atenolol and metoprolol, or drugs with partial agonist activity such as pindolol, have variable effects. Celiprolol, a new, highly cardioselective beta 1 blocker with partial beta 2 agonist activity and vasodilatory properties, has favorable effects on lipids and minimizes the dyslipidemic effects associated with smoking.