title: Influence of beta 2 agonism and beta 1 and beta 2 antagonism on adverse effects and plasma lipoproteins: results of a multicenter comparison of dilevalol and metoprolol.
abstract: Dilevalol combines vasodilation due to selective beta 2 agonism and nonselective beta antagonism. We studied 311 patients randomized to dilevalol and 138 to metoprolol in a multicenter trial. After a 4-week placebo washout, dilevalol was titrated from 200 to 1,600 mg once daily and metoprolol from 100 to 400 mg to a goal supine diastolic blood pressure less than 90 and greater than or equal to 10 mm Hg decrease from baseline. Responders were followed for 1 year. The average age of patients was 51 years; 72% were men and 54% were white. Both drugs reduced blood pressure effectively to a similar level. Fewer patients discontinued dilevalol than did those taking metoprolol (9 vs 16%; p less than 0.03). More metoprolol-treated patients withdrew because of depression (6 vs less than 1%; p = 0.03) and impotence (5 vs less than 1%; p = 0.03). Lipoprotein levels before and after treatment were measured in 99 patients treated for 53.5 weeks with dilevalol (mean dose 438 mg). Dilevalol increased high-density lipoprotein (HDL) cholesterol by 2.5 mg/dl to 47.2 (p = 0.05), reduced low-density lipoprotein (LDL) cholesterol by 2.5 mg/dl, increased HDL/LDL by 0.03, and decreased total cholesterol/HDL cholesterol by 0.18. Triglycerides increased by 21 mg/dl (p = 0.06). In patients with an initial HDL cholesterol less than 35 mg/dl, dilevalol increased it by 9 mg/dl. In patients treated with metoprolol, the only significant change (p = 0.02) was a 41.9-mg/dl increase in triglyceride levels.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: University of Miami Medical School, Florida.
authors.forename: B J
authors.initials: BJ
authors.lastname: Materson
authors.forename: N D
authors.initials: ND
authors.lastname: Vlachakis
authors.forename: S P
authors.initials: SP
authors.lastname: Glasser
authors.forename: C
authors.initials: C
authors.lastname: Lucas
authors.forename: K B
authors.initials: KB
authors.lastname: Ramanathan
authors.forename: S
authors.initials: S
authors.lastname: Ahmad
authors.forename: J H
authors.initials: JH
authors.lastname: Morledge
authors.forename: E
authors.initials: E
authors.lastname: Saunders
authors.forename: L J
authors.initials: LJ
authors.lastname: Lutz
authors.forename: H W
authors.initials: HW
authors.lastname: Schnaper
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000368:Aged; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000209:etiology; D004311:Double-Blind Method; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006852:Hydrochlorothiazide / Q000494:pharmacology; D006973:Hypertension / Q000097:blood / Q000188:drug therapy*; D007741:Labetalol / Q000009:adverse effects / Q000627:therapeutic use; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008790:Metoprolol / Q000009:adverse effects / Q000627:therapeutic use; D008875:Middle Aged; D015337:Multicenter Studies as Topic; D011897:Random Allocation; D012307:Risk Factors; D013484:Supination; D014280:Triglycerides / Q000097:blood
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D008074:Lipoproteins; D014280:Triglycerides; D006852:Hydrochlorothiazide; D002784:Cholesterol; D008790:Metoprolol; D007741:Labetalol