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Hypertension. 2005;45:580-585
doi: 10.1161/01.HYP.0000161186.55933.6b
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(Hypertension. 2005;45:580.)
© 2005 American Heart Association, Inc.


Original Articles

Pulse Pressure and Effects of Losartan or Atenolol in Patients With Hypertension and Left Ventricular Hypertrophy

Frej Fyhrquist; Björn Dahlöf; Richard B. Devereux; Sverre E. Kjeldsen; Stevo Julius; Gareth Beevers; Ulf de Faire; Hans Ibsen; Krister Kristianson; Ole Lederballe-Pedersen; Lars H. Lindholm; Markku S. Nieminen; Per Omvik; Suzanne Oparil; Darcy A. Hille; Paulette A. Lyle; Jonathan M. Edelman; Steven M. Snapinn; Hans Wedel for the LIFE Study Group

From Helsinki University Central Hospital (F.F.) and Minerva Institute for Medical Research, Helsinki, Finland; Sahlgrenska University Hospital/Östra (B.D.), Gothenburg, Sweden; Weill Medical College of Cornell University (R.B.D.), New York, NY; Ullevaal University Hospital (S.E.K.), Oslo, Norway; University of Michigan (S.J., S.E.K.), Ann Arbor, Mich; City Hospital (G.B.), Birmingham, United Kingdom; Karolinska University Hospital (U.d.F.), Stockholm, Sweden; Glostrup University Hospital (H.I.), Glostrup, Denmark; Merck Research Laboratories Scandinavia (K.K.), Stockholm, Sweden; Viborg Hospital (O.L.-P.), Viborg, Denmark; Umeå University (L.H.L.), Umeå, Sweden; Helsinki University Central Hospital (M.S.N.), Helsinki, Finland; Haukeland University Hospital (P.O.), Bergen, Norway; University of Alabama (S.O.), Birmingham, Ala; Merck & Co, Inc (D.A.H., P.A.L., J.M.E., S.M.S.), Whitehouse Station, NJ; The Nordic School of Public Health (H.W.), Gothenburg, Sweden.

Correspondence to Dr Frej Fyhrquist, Helsinki University Central Hospital, Department of Medicine, Haartmansgatan 4, 00290 Helsinki, Finland. E-mail frej.fyhrquist{at}helsinki.fi

In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, the primary composite end point of cardiovascular death, stroke, and myocardial infarction was reduced by losartan versus atenolol in patients with hypertension and left ventricular hypertrophy. The objective of this post hoc analysis was to determine the influence of pulse pressure on outcome. Patients were divided into quartiles of baseline pulse pressure. Cox regression, including baseline Framingham risk score as a covariate, was used to compare risk in the quartiles. In the atenolol group, there were significantly higher risks in the highest versus lowest quartile for the composite end point 28% (confidence interval [CI], 2% to 62%; P=0.035), stroke 84% (CI, 32% to 157%; P<0.001), and total mortality 41% (CI, 7% to 84%; P=0.013). Risk for myocardial infarction was 44% higher (CI, –5% to 120%; P=0.089). The risks in the losartan group also increased with increasing quartile, but were lower than in the atenolol group, and differences between the highest and lowest quartiles were not significant: composite end point 12% (CI, –13% to 44%; P>0.2), stroke –5% (CI, –34% to 37%; P>0.2), myocardial infarction 30% (CI, –13% to 94%; P>0.2), and total mortality 32% (CI, –1% to 76%; P=0.062). In patients with hypertension and left ventricular hypertrophy in the LIFE study, there were significantly higher risks, adjusted for the Framingham risk score, for the primary composite end point, stroke, and total mortality in the highest versus lowest quartile of pulse pressure with atenolol-based treatment. The risks in the losartan group also increased with increasing pulse pressure quartile, but were lower than those in the atenolol group, and were not significant.


Key Words: pulse • hypertension • losartan




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