Body build and risk of cardiovascular events in hypertension and left ventricular hypertrophy: the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study.
BACKGROUND
Obesity may independently increase the risk of adverse events in hypertension with target-organ damage. We investigated whether body build was independently associated with higher cardiovascular risk and whether treatment with losartan relative to atenolol influenced the impact of body build on the primary composite end point of cardiovascular death, stroke, and myocardial infarction and on cardiovascular death in patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study.


RESULTS
The population of 9079 patients was divided as follows: thin (body mass index [BMI] <20 kg/m2, 2%), normal weight (BMI 20 to 24.9, 24%), overweight (BMI 25 to 29.9, 45%), and obese (class I: BMI 30 to 34.9, 21%; class II: BMI 35 to 39.9, 6%; class III: BMI > or =40, 2%). Incident diabetes increased progressively with BMI and was somewhat higher in the atenolol arm. Differences in gender and race were detected among the body build groups. Rates (Cox proportional hazard analysis) of the primary composite end point did not differ among body build groups after adjustment for age, gender, race, smoking habit, prevalent cardiovascular disease, and left ventricular hypertrophy. Cardiovascular death was more frequent among thin (P<0.05) and pooled class II-III obesity (both P<0.04) than normal-weight groups. Risk was not attenuated significantly by losartan treatment, nor did it interfere with the greater benefit of losartan- as opposed to atenolol-based treatment.


CONCLUSIONS
In the LIFE study, stratification for classes of body build identified increased risk of cardiovascular mortality in both thin and moderately-to-severely obese individuals. This risk was not attenuated significantly by losartan treatment, nor did it interfere with the greater benefit of losartan-based treatment as opposed to atenolol-based treatment.
de Simone
Giovanni
G
Department of Clinical and Experimental Medicine, Federico II University Hospital, via S. Pansini, No. 5, 80131 Naples, Italy. simogi@unina.it
Wachtell
Kristian
K
Palmieri
Vittorio
V
Hille
Darcy A
DA
Beevers
Gareth
G
Dahlöf
Björn
B
de Faire
Ulf
U
Fyhrquist
Frej
F
Ibsen
Hans
H
Julius
Stevo
S
Kjeldsen
Sverre E
SE
Lederballe-Pedersen
Ole
O
Lindholm
Lars H
LH
Nieminen
Markku S
MS
Omvik
Per
P
Oparil
Suzanne
S
Devereux
Richard B
RB
D000368:Aged; D001262:Atenolol / Q000627:therapeutic use; D015992:Body Mass Index; D001835:Body Weight; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000503:physiopathology*; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009765:Obesity; D016016:Proportional Hazards Models; D018570:Risk Assessment; D013008:Somatotypes / Q000502:physiology*
D001262:Atenolol; D019808:Losartan