In-treatment reduced left atrial diameter during antihypertensive treatment is associated with reduced new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy: The LIFE Study.
OBJECTIVE
It is unclear whether improvement of left atrial (LA) and ventricular (LV) structure results in reduction in new-onset atrial fibrillation (AF). The aim of the present study was to examine whether changes in-treatment LA diameter were related to changes in risk of new-onset AF.


METHODS
We followed 939 hypertensive patients with electrocardiographic LV hypertrophy randomized to atenolol or losartan-based regimens in the LIFE Study for a mean of 4.8 years with echocardiograms at enrolment and annually during treatment.


RESULTS
New-onset AF occurred in 46 patients (10.2/1000 patient-years of follow-up). At baseline, patients with new-onset AF were older, had higher systolic blood pressure and heart rate as well as higher prevalence of LA dilatation, but had similar prevalences of LV hypertrophy and mitral or aortic valve disease. In univariate Cox analysis baseline LA diameter (HR=4.67 per cm increase [95% CI 2.86-7.65], p<0.001) and LV mass index (HR=1.11 per 10 g/m(2) increase [95% CI 1.02-1.22], p<0.05) both predicted new-onset AF. In multivariate analysis, increased baseline LA diameter increased the risk of new-onset AF (HR=5.16 per cm [95% CI 2.85-9.35], p<0.001) whereas reduction of in-treatment LA diameter reduced the risk (HR=0.21 per cm lower LA diameter during treatment [95% CI 0.14-0.32], p<0.001) with adjustment for in-treatment LV mass in-treatment systolic blood pressure, age and Framingham risk score.


CONCLUSIONS
LA diameter at baseline and during antihypertensive treatment were equally strong predictors of new-onset AF independent of the level of arterial pressure, LV mass and other covariates. Prevention of AF during antihypertensive treatment may be improved by antihypertensive therapy that reduces LA size in addition to controlling blood pressure.
Wachtell
Kristian
K
Department of Cardiology, Rigshospitalet, Denmark. kristian@wachtell.net
Gerdts
Eva
E
Aurigemma
Gerard P
GP
Boman
Kurt
K
Dahlöf
Björn
B
Nieminen
Markku S
MS
Olsen
Michael Hecht
MH
Okin
Peter M
PM
Palmieri
Vittorio
V
Rokkedal
Jens E
JE
Devereux
Richard B
RB
D000368:Aged; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000188:drug therapy; D001262:Atenolol / Q000494:pharmacology / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000453:epidemiology / Q000517:prevention & control*; D001794:Blood Pressure / Q000187:drug effects; D006332:Cardiomegaly / Q000150:complications / Q000188:drug therapy; D002318:Cardiovascular Diseases / Q000150:complications / Q000188:drug therapy; D004562:Electrocardiography; D005260:Female; D006325:Heart Atria / Q000503:physiopathology; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D012306:Risk
D000959:Antihypertensive Agents; D001262:Atenolol; D019808:Losartan