title: Losartan benefits over atenolol in non-smoking hypertensive patients with left ventricular hypertrophy: the LIFE study.
abstract: We studied the impact of smoking in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke and myocardial infarction in hypertensives with left ventricular hypertrophy. We compared hazard ratios in 4656 never-smokers, and 3033 previous and 1499 current smokers, adjusting for gender, age, alcohol intake, exercise and race. Composite endpoint rate was higher in previous (28/1000 years), as well as current (39/1000 years) smokers than in never-smokers (21/1000 years). Composite (hazard ratio 0.78, 95% CI 0.65-0.94, p < 0.01) and stroke (hazard ratio 0.61, 95% CI 0.47-0.80], p < 0.001) risks were lower with losartan than atenolol in never-smokers, but not significantly in previous smokers. Drug regimens did not differ in current smokers (composite hazard ratio 0.99, stroke hazard ratio 0.94). Smoking-treatment interactions were non-significant, but a borderline significant trend (p = 0.05) suggested decreasing benefit of losartan vs atenolol for stroke prevention from never- to previous to current smoking status. Smoking increased cardiovascular risk markedly in the LIFE study. The benefit of losartan vs atenolol is consistent with the overall conclusion of the LIFE study, although the treatment effect appeared largest in non-smokers.
authors.affiliation: Department of Cardiology, Ullevaal University Hospital, Oslo, Norway. henrik.reims@ioks.uio.no
authors.forename: Henrik M
authors.initials: HM
authors.lastname: Reims
authors.forename: Suzanne
authors.initials: S
authors.lastname: Oparil
authors.forename: Sverre E
authors.initials: SE
authors.lastname: Kjeldsen
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
authors.forename: Stevo
authors.initials: S
authors.lastname: Julius
authors.forename: William E
authors.initials: WE
authors.lastname: Brady
authors.forename: Frej
authors.initials: F
authors.lastname: Fyhrquist
authors.forename: Hans
authors.initials: H
authors.lastname: Ibsen
authors.forename: Lars H
authors.initials: LH
authors.lastname: Lindholm
authors.forename: Per
authors.initials: P
authors.lastname: Omvik
authors.forename: Hans
authors.initials: H
authors.lastname: Wedel
authors.forename: Gareth
authors.initials: G
authors.lastname: Beevers
authors.forename: Ulf
authors.initials: U
authors.lastname: de Faire
authors.forename: Krister
authors.initials: K
authors.lastname: Kristianson
authors.forename: Ole
authors.initials: O
authors.lastname: Lederballe-Pedersen
authors.forename: Markku S
authors.initials: MS
authors.lastname: Nieminen
authors.forename: Björn
authors.initials: B
authors.lastname: Dahlöf
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D001262:Atenolol / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy*; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000188:drug therapy*; D015994:Incidence; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000517:prevention & control; D012044:Regression Analysis; D012907:Smoking / Q000009:adverse effects*; D020521:Stroke / Q000209:etiology / Q000517:prevention & control
chemical_list: D001262:Atenolol; D019808:Losartan