title: Sex-related difference in regression of left ventricular hypertrophy with antihypertensive treatment: the LIFE study.
abstract: While left ventricular (LV) structure and function differ between hypertensive women and men, it remains unclear whether sex affects regression of LV hypertrophy with antihypertensive treatment. We analysed paired echocardiograms in 500 men and 347 women enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study at baseline and after 12 months of antihypertensive treatment with either losartan or atenolol. At enrollment, 177 women and 242 men were randomized to losartan-based treatment and 161 women and 247 men were randomized to atenolol-based treatment (sex difference=NS). After 12 months of antihypertensive treatment, blood pressure was lowered similarly in women (152/83 from 174/97 mmHg) and men (149/85 from 173/99 mmHg; both P<0.001, sex difference=NS), without significant change in body weight in either sex. Cardiac output and pulse pressure/stroke volume were equivalently reduced in both sexes (-0.2 vs -0.1 l/min and both -0.20 mmHg/ml/m(2), respectively; both P=NS). Absolute LV mass change after 12 months of antihypertensive treatment was greater in men than in women (-30 vs -24 g, P=0.01). However, after adjusting for baseline LV mass and randomized study treatment, LV mass reduction was greater in women than in men (-33 vs -23 g, P=0.001). LV mass regression was greater in women, by 8.0+/-2.8 g, after adjusting for baseline LV mass and randomized study treatment. After consideration of baseline LV mass and randomized study treatment, antihypertensive treatment regressed LV hypertrophy more in women. Further studies are needed to identify the mechanisms and prognostic implications of this sex-related difference.
authors.affiliation: Weill Medical College of Cornell University, New York, NY, USA. jonnbella@earthlink.net
authors.forename: J N
authors.initials: JN
authors.lastname: Bella
authors.forename: V
authors.initials: V
authors.lastname: Palmieri
authors.forename: K
authors.initials: K
authors.lastname: Wachtell
authors.forename: J E
authors.initials: JE
authors.lastname: Liu
authors.forename: E
authors.initials: E
authors.lastname: Gerdts
authors.forename: M S
authors.initials: MS
authors.lastname: Nieminen
authors.forename: M J
authors.initials: MJ
authors.lastname: Koren
authors.forename: M
authors.initials: M
authors.lastname: Zabalgoitia
authors.forename: J T
authors.initials: JT
authors.lastname: Wright
authors.forename: B
authors.initials: B
authors.lastname: Dahlöf
authors.forename: R B
authors.initials: RB
authors.lastname: Devereux
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use*; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging* / Q000188:drug therapy; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D012074:Remission Induction; D012737:Sex Factors; D013997:Time Factors; D014463:Ultrasonography
chemical_list: D000959:Antihypertensive Agents; D001262:Atenolol; D019808:Losartan