Systolic left ventricular function improves more by beta-blokade than losartan: the life study

Systolic left ventricular (LV) function is a predictor of cardiovascular morbidity and mortality and improvement of systolic LV function improves survival. However, it is unclear how to best improve systolic function. A total of 960 prospectively identified patients with essential hypertension and evidence of LV hypertrophy on a screening electrocardiogram underwent echocardiography at enrolment in the Losartan Intervention For Endpoint prevention in hypertension (LIFE) trial, of whom 939 had measurements at baseline and information about cardiovascular events during the 4.8 years mean follow-up. Comparing baseline with the patients last in-study echocardiogram, both treatments reduced LV relative wall thickness (−0.084±0.64 vs. −0.084±0.062, p=NS) similarly. Atenolol was associated with lesser decrease in endocardial fractional shortening (EFS, −2.5±5.8 vs. −1.6±5.8%, p<0.05) as well as stress-corrected EFS (−7.5±19.8 vs. −2.4±19.9, p<0.001). Treatment with atenolol was associated with greater increase in midwall shortening (MWS, 0.92±2.45 vs. 1.38±2.40%, p<0.01) as well as stress-corrected MWS (6.9±14.3 vs. 10.3±14.2%, p<0.001). Linear regression analyses with LV function measures as the dependent variable showed a trend towards independent effect of atenolol on MWS (β=0.089, p=0.011) and a trend towards independency on EFS (β=0.068, p=0.053) even when taking differences in heart rate into account. In similar linear regression models, adjusting for age, gender and heart rate change, atenolol remained associated with smaller decrease in stress-corrected EFS (−7.5±19.8 vs. −2.4±19.9%, p<0.001) and a greater increase in stress-corrected MWS (6.8±14.3 vs. 10.3±14.2%, p=0.001) compared to losartan. In a double-blind, randomized trial, antihypertensive therapy that reduced LV relative wall thickness reduced endocardial and increased midwall LV function. Atenolol treatment reduced EFS less and raised MWS more than losartan, attributable to greater heart rate reduction and consequent preload increase with atenolol. Losartan treatment increased stress-corrected MWS, an index of LV contractility, but atenolol did so even more, consistent with the additional beneficial effects of beta-blockade in heart failure trials.