Relation of QT interval and QT dispersion to regression of echocardiographic and electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan Intervention For Endpoint Reduction (LIFE) study.
BACKGROUND
In hypertensive patients, both echocardiographic and electrocardiographic left ventricular hypertrophy (LVH) increase the risk of sudden death, possibly in part because of LVH-induced proarrhythmic repolarization changes. Experimentally, regression of LVH normalizes ventricular electrophysiology.


METHODS
To assess the relation of regression of LVH to changes in electrocardiographic measures of ventricular repolarization, we studied 317 hypertensive (61.2% men, mean age 65 +/- 7 years) participants in the Losartan Intervention For Endpoint Reduction (LIFE) study with electrocardiographic evidence of LVH, at study baseline, and after 1 year of blood pressure-lowering treatment with losartan or atenolol and hydrochlorothiatzide as the first adjunct therapy if needed to reach target blood pressure of 140/90 mm Hg. As indexes of LVH, we used echocardiographically determined LV mass as well as the Sokolow-Lyon and Cornell voltages from the electrocardiogram. QT interval duration and QT dispersion from the 12-lead electrocardiogram were used as ventricular repolarization measures.


RESULTS
By using tertiles of LV mass change and adjusting for the difference in treatment (losartan or atenolol), shortening of the rate-adjusted QT intervals as well as reduction in QT(apex) dispersion were observed in the tertile showing the greatest decrease in LV mass but not in the tertile without substantial changes in LV mass despite a significant reduction in blood pressure. Similar results were obtained with the use of Sokolow-Lyon and Cornell voltage change tertiles.


CONCLUSIONS
In hypertensive patients with electrocardiographic evidence of LVH, regression of echocardiographically determined LV mass and electrocardiographic indexes of LVH may partially reverse the LVH-induced proarrhythmic repolarization changes. This may have a beneficial impact on the increased incidence of sudden death in these patients.
Oikarinen
Lasse
L
Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. lasse.oikarinen@kolumbus.fi
Nieminen
Markku S
MS
Toivonen
Lauri
L
Viitasalo
Matti
M
Wachtell
Kristian
K
Papademetriou
Vasilios
V
Jern
Sverker
S
Dahlöf
Björn
B
Devereux
Richard B
RB
Okin
Peter M
PM
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; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D012074:Remission Induction; D016037:Single-Blind Method
D000959:Antihypertensive Agents; D006852:Hydrochlorothiazide; D001262:Atenolol; D019808:Losartan