Original Article

Journal of Human Hypertension advance online publication 5 November 2009; doi: 10.1038/jhh.2009.77

Effects of losartan vs candesartan in reducing cardiovascular events in the primary treatment of hypertension
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S E Kjeldsen1, J Stålhammar2, P Hasvold3, J Bodegard3, U Olsson4 and D Russell5

  1. 1Department of Cardiology, Oslo University Hospital, Ullevål, Oslo, Norway
  2. 2Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden
  3. 3Medical Department, AstraZeneca AS, Oslo, Norway
  4. 4Statisticon AB, Uppsala, Sweden
  5. 5Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway

Correspondence: Professor SE Kjeldsen, Department of Cardiology, Oslo University Hospital, Ullevål, Kirkeveien 166, N-0407 Oslo, Norway.

Received 25 July 2009; Revised 23 August 2009; Accepted 3 September 2009; Published online 5 November 2009.

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Abstract

Although angiotensin receptor blockers have different receptor binding properties no comparative studies with cardiovascular disease (CVD) end points have been performed within this class of drugs. The aim of this study was to test the hypothesis that there are blood pressure independent CVD-risk differences between losartan and candesartan treatment in patients with hypertension without known CVD. Seventy-two primary care centres in Sweden were screened for patients who had been prescribed losartan or candesartan between the years 1999 and 2007. Among the 24 943 eligible patients, 14 100 patients were diagnosed with hypertension and prescribed losartan (n=6771) or candesartan (n=7329). Patients were linked to Swedish national hospitalizations and death cause register. There was no difference in blood pressure reduction when comparing the losartan and candesartan groups during follow-up. Compared with the losartan group, the candesartan group had a lower adjusted hazard ratio for total CVD (0.86, 95% confidence interval (CI) 0.77–0.96, P=0.0062), heart failure (0.64, 95% CI 0.50–0.82, P=0.0004), cardiac arrhythmias (0.80, 95% CI 0.65–0.92, P=0.0330), and peripheral artery disease (0.61, 95% CI 0.41–0.91, P=0.0140). No difference in blood pressure reduction was observed suggesting that other mechanisms related to different pharmacological properties of the drugs may explain the divergent clinical outcomes.

Keywords:

epidemiology, heart failure, cardiovascular diseases, blood pressure

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