Abstract

Recently, we found that increased urine albumin creatinine ratio (UACR) as well as electrocardiographic (ECG) verified left ventricular hypertrophy (LVH) were independent predictors of all cause and cardiovascular mortality as well as a composite cardiovascular end-point consisting of CV death, myocardial infarction and stroke. However, it remains unclear whether treatment of albuminuric patients with a losartan-based protocol results in greater reduction in cardiovascular mortality and composite end-point compared to treatment with atenolol.

ECG and morning spot urine were obtained in 8,029 patients with stage II-III hypertension and LVH determined by ECG (Cornell voltage duration or Sokolow-Lyon voltage criteria) after 14 days placebo treatment. Renal glomerular permeability was evaluated by UACR and was defined as microalbuminuria if >3.5 and macroalbuminuria if >35.

1844 (20.1%) patients had microalbuminuria, 1844 (3.5%) had macroalbuminuria and 5865 (63.8%) patients were normoalbuminuric at baseline. During 61 [95% CI 54-71] months 816 (10%) deaths occurred. Of these 438 (5.5%) were cardiovascular deaths, which were added to myocardial infarction and stroke to compose the composite cardiovascular end-point (n=961, 12.0%).

As the LIFE study at the moment is blinded and will be so until the presentation of the main results in March of 2002, we will, in May 2002, be able to show whether treatment with a losartan as compared to an atenolol-based regimen significantly effects cardiovascular composite endpoint and mortality independent of the blood pressure reduction per se in albuminuric patients.