Pulse pressure, left ventricular function and cardiovascular events during antihypertensive treatment (the LIFE study)
Authors:
Eva Gerdtsab; Stanley Franklinc;
shild Rieckb; Vasilios Papademetrioud; Kristian Wachtelle; Markku Nieminenf; Bj
rn Dahl
fg; Richard Blyton Devereuxh
shild Rieckb; Vasilios Papademetrioud; Kristian Wachtelle; Markku Nieminenf; Bj
rn Dahl
fg; Richard Blyton Devereuxh
| Affiliations: | a Institute of Medicine, University of Bergen, |
| b Department of Heart Disease, Haukeland University Hospital, Bergen, Norway | |
| c University of California, Irvine, USA | |
| d Department of Medicine, Washington VA Medical Center, Washington DC, USA | |
| e Heart Center, Rigshospitalet, Copenhagen, Denmark | |
| f Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland | |
g Department of Medicine, Sahlgrenska University Hospital/ stra, Gothenburg, Sweden |
|
| h Department of Medicine, Weill Medical College of Cornell University, New York, NY, USA |
DOI:
10.1080/08037050903047202
Publication Frequency:
6 issues per year
First Published:
August
2009
Subjects:
Hypertension;
Vascular Medicine;
Formats available:
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Abstract
Background. Pulse pressure (PP) has been related to risk of cardiovascular events in hypertension. However, less is known about modification of this risk marker during antihypertensive treatment in patients with left ventricular (LV) hypertrophy. Methods. Associations of in-treatment PP with LV systolic function and cardiovascular events was assessed in 883 patients with electrocardiographic LV hypertrophy during 4.8 years of randomized losartan- or atenolol-based treatment within the echocardiographic substudy of the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Results. PP was similarly reduced by both treatments. In different multiple regression models, lower in-treatment PP was independently associated with lower in-treatment LV ejection fraction (β=0.16), stress-corrected midwall shortening (β=0.20), stroke volume (β=0.11) and cardiac index (β=0.07, all p<0.05). In time-varying Cox regression models, 10mmHg lower in-treatment PP was associated with a 28% higher rate of cardiovascular events [hazard ratio, HR = 1.28 (1.09 - 1.52), p<0.01] independent of in-treatment LV mass and ejection fraction, history of ischemic heart disease, Framingham risk score and study treatment allocation. Conclusion. During systematic antihypertensive treatment in hypertensive patients with electrocardiographic LV hypertrophy, lower in-treatment PP was associated with lower in-treatment LV function and cardiac output as well as higher rate of cardiovascular events.
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| Keywords: Ejection fraction; hypertension; left ventricular hypertrophy; pulse pressure |
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stra, Gothenburg, Sweden
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