ESPITE SUBSTANTIAL BENefits from lowering blood pressure (BP), conventional treatment does not normalize the risk of major cardiovascular (CV) events in patients with hypertension. 1-5 Progress has been made in predicting risk of hypertension by evaluating preclinical CV disease. 6 Left ventricular hypertrophy (LVH), ie, pathologically increased left ventricular mass, independently predicts adverse outcomes in diverse populations, 7-12 including patients with hypertension. 7,11 These findings suggest that the level of left ventricular mass and mass reduction during treatment of hypertension may provide independent information about disease progression or control. This hypothesis has been supported by data from some, 13,14 but not other, 15,16 electrocardiographic studies. Echocardio-See also pp 2343 and 2396 and Patient Page.

EFT VENTRICULAR HYPERTROphy (LVH) detected by 12lead electrocardiogram (ECG) 1-3 and by echocardiography 4-8 are common manifestations of preclinical cardiovascular (CV) disease that strongly predict CV morbidity and mortality. Antihypertensive therapy aimed at reducing blood pressure (BP) can produce regression of LVH 3,4,9-15 and reduces but does not entirely eliminate the increased risk of major CV events. 16-20 However, whether regression of electrocardiographic LVH per se is associated with improved prognosis independent of improvements in See also pp 2350 and 2396 and Patient Page.

Lower Cornell product electrocardiographic LVH during antihypertensive therapy is associated with a lower likelihood of new-onset AF, independent of blood pressure lowering and treatment modality in essential hypertension. These findings suggest that antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may reduce the incidence of new-onset AF.

Background-An echocardiographic substudy of the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial was designed to test the ability of losartan to reduce left ventricular (LV) mass more than atenolol. Methods and Results-A total of 960 patients with essential hypertension and LV hypertrophy (LVH) on screening ECG were enrolled at centers in 7 countries and studied by echocardiography at baseline and after 1, 2, 3, 4, and 5 years' randomized therapy. Clinical examination and blinded readings of echocardiograms in 457 losartan-treated and 459 atenolol-treated participants with Ն1 follow-up measurement of LV mass index (LVMI) were used in an intention-totreat analysis. Losartan-based therapy induced greater reduction in LVMI from baseline to the last available study than atenolol with adjustment for baseline LVMI and blood pressure and in-treatment pressure (Ϫ21.7Ϯ21.8 versus Ϫ17.7Ϯ19.6 g/m 2 ; Pϭ0.021). Greater LVMI reduction with losartan was observed in women and men, participants Ͼ65 or Ͻ65 years of age, and with mild or more severe baseline hypertrophy. The difference between treatment arms in LVH regression was due mainly to reduced concentricity of LV geometry in both groups and lesser increase in LV internal diameter in losartan-treated patients. Conclusions-Antihypertensive treatment with losartan, plus hydrochlorothiazide and other medications when needed for pressure control, resulted in greater LVH regression in patients with ECG LVH than conventional atenolol-based treatment. Thus, angiotensin receptor antagonism by losartan has superior efficacy for reversing LVH, a cardinal manifestation of hypertensive target organ damage.