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
| Autor: | Hans Ibsen, Gareth Beevers, Giovanni de Simone, Per Omvik, Hans Wedel, Ulf de Faire, Kristian Wachtell, Richard B. Devereux, Björn Dahlöf, Suzanne Oparil, Markku S. Nieminen, Frej Fyhrquist, Sverre E. Kjeldsen, Lars H Lindholm, Ole Lederballe-Pedersen, Michael H. Olsen, Paulette A. Lyle |
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| Rok vydání: | 2009 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Physiology Diastole Blood Pressure Left ventricular hypertrophy Losartan Muscle hypertrophy Electrocardiography chemistry.chemical_compound Internal medicine Internal Medicine Humans Multicenter Studies as Topic Medicine Antihypertensive Agents Aged Randomized Controlled Trials as Topic Dose-Response Relationship Drug medicine.diagnostic_test business.industry Cholesterol Cholesterol HDL Middle Aged Lipid Metabolism medicine.disease Atenolol Angiotensin II Treatment Outcome Endocrinology chemistry Cardiovascular Diseases Hypertension Cardiology Female Hypertrophy Left Ventricular lipids (amino acids peptides and proteins) Cardiology and Cardiovascular Medicine business Follow-Up Studies medicine.drug |
| Zdroj: | Journal of Hypertension. 27:567-574 |
| ISSN: | 0263-6352 |
| DOI: | 10.1097/hjh.0b013e32831daf96 |
| Popis: | Beta-blockers and angiotensin II receptor blockers have different effects on lipids.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.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 P0.001) 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, P0.01], HDL cholesterol [HR = 0.56 (0.48-0.66) per mmol/l, P0.001], and treatment allocation [HR = 0.86 (0.76-0.98), P0.05] 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, P0.001], 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.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. |
| Databáze: | OpenAIRE |
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