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Regression of hypertensive left ventricular hypertrophy by losartan compared with atenolol: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial

Devereux, R. B. (författare)
Dahlöf, Björn, 1953 (författare)
Gothenburg University,Göteborgs universitet,Hjärt-kärlinstitutionen,Cardiovascular Institute
Gerdts, E. (författare)
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Boman, K. (författare)
Nieminen, M. S. (författare)
Papademetriou, V. (författare)
Rokkedal, J. (författare)
Harris, K. E. (författare)
Edelman, J. M. (författare)
Wachtell, K. (författare)
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 (creator_code:org_t)
2004
2004
Engelska.
Ingår i: Circulation. - 1524-4539. ; 110:11, s. 1456-62
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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 > or =1 follow-up measurement of LV mass index (LVMI) were used in an intention-to-treat 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 (-21.7+/-21.8 versus -17.7+/-19.6 g/m2; P=0.021). Greater LVMI reduction with losartan was observed in women and men, participants >65 or <65 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.

Nyckelord

Adrenergic beta-Antagonists/*therapeutic use
Aged
Aged
80 and over
Angiotensin II Type 1 Receptor Blockers/*therapeutic use
Antihypertensive Agents/therapeutic use
Atenolol/*therapeutic use
Blood Pressure/drug effects
Double-Blind Method
Female
Follow-Up Studies
Heart Rate/drug effects
Heart Ventricles/drug effects/pathology/ultrasonography
Humans
Hypertension/*complications/drug therapy
Hypertrophy
Left Ventricular/*drug therapy/etiology/ultrasonography
Losartan/*therapeutic use
Male
Middle Aged
Organ Size
Prospective Studies
Treatment Outcome

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