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Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy: the losartan intervention for endpoint reduction in hypertension (LIFE) study
Glostrup University Hospital, Glostrup, Denmark.
Rigshospitalet, Copenhagen, Denmark.
City Hospital, Birmingham, UK.
Sahlgrenska University Hospital/Östra, Göteborg, Sweden.
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2009 (Engelska)Ingår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 27, nr 3, s. 567-574Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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.

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2009. Vol. 27, nr 3, s. 567-574
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URN: urn:nbn:se:umu:diva-38999DOI: 10.1097/HJH.0b013e32831daf96Scopus ID: 2-s2.0-67649562235OAI: oai:DiVA.org:umu-38999DiVA, id: diva2:387555
Tillgänglig från: 2011-01-14 Skapad: 2011-01-14 Senast uppdaterad: 2023-03-24Bibliografiskt granskad

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