title: Regression of electrocardiographic left ventricular hypertrophy predicts regression of echocardiographic left ventricular mass: the LIFE study.
abstract: The electrocardiogram (ECG) is widely used for detection of left ventricular hypertrophy (LVH). However, whether changes in ECG LVH during antihypertensive therapy predict changes in LV mass remains unclear. Baseline and year-1 ECGs and echocardiograms were assessed in 584 hypertensive patients with ECG LVH by Sokolow-Lyon or Cornell voltage-duration product criteria at entry into the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy. A >/=25% decrease in Cornell product defined regression of ECG LVH; a <25% decrease defined no significant regression; and an increase defined progression of ECG LVH. Regression of echocardiographic LVH was defined by a >/=20% reduction in LV mass. After 1 year of therapy, 155 patients (27%) had regression of ECG LVH, 286 (49%) had no significant change, and 143 (25%) had progression of ECG LVH. Compared with patients with progression of ECG LVH, patients with no significant decrease and patients with regression of ECG LVH had stepwise greater absolute decreases in LV mass (-16+/-33 vs -29+/-37 vs -32+/-41 g, P<0.001), greater percent reductions in LV mass (-5.7+/-14.6 vs -11.3+/-13.6 vs -12.3+/-15.6%, P<0.001), and were more likely to decrease LV mass by >/=20% (11.2 vs 24.8 vs 36.1%, P<0.001), even after adjusting for possible effects of baseline and change in systolic and diastolic pressures. Compared with progression of ECG LVH, regression of the Cornell product ECG LVH is associated with greater reduction in LV mass and a greater likelihood of regression of anatomic LVH.
authors.affiliation: Department of Medicine, Division of Cardiology, Weill Medical College of Cornell University, New York, NY 10021, USA. pokin@mail.med.cornell.edu
authors.forename: P M
authors.initials: PM
authors.lastname: Okin
authors.forename: R B
authors.initials: RB
authors.lastname: Devereux
authors.forename: J E
authors.initials: JE
authors.lastname: Liu
authors.forename: L
authors.initials: L
authors.lastname: Oikarinen
authors.forename: S
authors.initials: S
authors.lastname: Jern
authors.forename: S E
authors.initials: SE
authors.lastname: Kjeldsen
authors.forename: S
authors.initials: S
authors.lastname: Julius
authors.forename: K
authors.initials: K
authors.lastname: Wachtell
authors.forename: M S
authors.initials: MS
authors.lastname: Nieminen
authors.forename: B
authors.initials: B
authors.lastname: Dahlöf
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001262:Atenolol / Q000627:therapeutic use; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000503:physiopathology*; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012074:Remission Induction; D013997:Time Factors
chemical_list: D000959:Antihypertensive Agents; D001262:Atenolol; D019808:Losartan