Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy: The Losartan Intervention for Endpoint reduction in hypertension study

Michael Hecht Olsen, Kristian Wachtell, Gareth Beevers, Björn Dahlöf, Giovanni De Simone, Richard B. Devereux, Ulf De Faire, Frej Fyhrquist, Hans Ibsen, Sverre E. Kjeldsen, Ole Lederballe-Pedersen, Lars H. Lindholm, Paulette A. Lyle, Markku S. Nieminen, Per Omvik, Suzanne Oparil, Hans Wedel

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    Abstrakt

    OBJECTIVE: Beta-blockers and angiotensin II receptor blockers have different effects on lipids. METHODS: We examined lipid levels in the Losartan Intervention For Endpoint reduction in hypertension study and their impact on the primary composite endpoint of cardiovascular death, myocardial infarction, or stroke. We measured total and high-density lipoprotein cholesterol at baseline and annually during 4.8 years of losartan-based compared with atenolol-based treatment in 8611 patients with hypertension and left ventricular hypertrophy. RESULTS: Patients randomized to losartan-based or atenolol-based treatment had similar baseline total (6.04 ± 1.12 vs. 6.05 ± 1.13 mmol/l, NS) and high-density lipoprotein (HDL) cholesterol (1.50 ± 0.44 vs. 1.49 ± 0.44 mmol/l, NS). Total cholesterol decreased significantly but equally (-0.37 ± 1.05 vs. -0.34 ± 1.09 mmol/l, NS), whereas HDL cholesterol decreased less during the first 2 years in patients randomized to losartan compared with atenolol (-0.13 ± 0.24 vs. -0.19 ± 0.25 mmol/l) and remained higher each year (1.38, 1.37, 1.42, 1.47, and 1.48 mmol/l vs. 1.32, 1.30, 1.36, 1.40, and 1.42 mmol/l, all P < 0.001) independent of hydrochlorothiazide or statin treatment. In Cox regression analysis, baseline total cholesterol [hazard ratio (HR) = 1.08 (1.02-1.14) per mmol/l, P < 0.01], HDL cholesterol [HR = 0.56 (0.48-0.66) per mmol/l, P < 0.001], and treatment allocation [HR = 0.86 (0.76-0.98), P < 0.05] predicted composite endpoint independently. Using time-varying analyses, the predictive strength of HDL cholesterol was increased [HR = 0.36 (0.30-0.44) per mmol/l, P < 0.001], whereas that of total cholesterol [HR = 1.03 (0.97-1.09) per mmol/l, NS] and treatment allocation [HR = 0.91 (0.80-1.03), NS] were reduced. CONCLUSION: Losartan blunted the decrease in HDL cholesterol during antihypertensive treatment in the LIFE study. Higher intreatment HDL cholesterol was associated with fewer composite endpoints and may partly explain the better outcome of losartan-based treatment.

    OriginalsprogEngelsk
    Sider (fra-til)567-574
    Antal sider8
    TidsskriftJournal of Hypertension
    Vol/bind27
    Udgave nummer3
    DOI
    StatusUdgivet - 1 mar. 2009

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    Udforsk hvilke forskningsemner 'Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy: The Losartan Intervention for Endpoint reduction in hypertension study' indeholder.

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