Principal Findings:

The primary composite endpoint occurred in 508 losartan (23.8 per 1000 patient-years) and 588 atenolol patients (27.9 per 1000 patient-years; relative risk 0.87, 95% CI 0.77-0.98, p=0.021). 204 losartan and 234 atenolol patients died from cardiovascular disease (0.89, 0.73-1.07, p=0.206); 232 and 309, respectively, had fatal or non-fatal stroke (0.75, 0.63-0.89, p=0.001); and myocardial infarction (non-fatal and fatal) occurred in 198 and 188, respectively (1.07, 0.88-1.31, p=0.491). These reductions were independent of blood pressure decreases. Losartan was better tolerated than atenolol. A recent report evaluated the effect of LVH in this cohort. There was a significant decrease in left ventricular mass over the course of the study in both arms with the magnitude of reduction being greater in the losartan group (p=0.02). When stratified for left ventricular hypertrophy, the composite endpoint was significantly lower in patients without LVH. (p=0.008; [HR 0.58, 95% CI 0.38-0.68]). Cardiovascular mortality and stroke but not myocardial infarction were each individually lower in patients without LVH. Losartan also led to a decrease in left atrial size compared to atenolol and afer adjusting for age and blood pressure reduction, the stroke rate in patients with atrial fibrillation was lower in patients treated with losartan (p=0.018; [HR 0.51, 95% CI 0.29-0.89].