RISK OF FATAL STROKE ACCORDING TO BLOOD-PRESSURE LEVEL - AN 18-YEAR FOLLOW-UP OF THE OSLO STUDY

Citation
Ll. Haheim et al., RISK OF FATAL STROKE ACCORDING TO BLOOD-PRESSURE LEVEL - AN 18-YEAR FOLLOW-UP OF THE OSLO STUDY, Journal of hypertension, 13(8), 1995, pp. 909-913
Citations number
21
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
02636352
Volume
13
Issue
8
Year of publication
1995
Pages
909 - 913
Database
ISI
SICI code
0263-6352(1995)13:8<909:ROFSAT>2.0.ZU;2-Y
Abstract
Objective: To determine how blood pressure level predicts the incidenc e of fatal stroke. Design: The Oslo Study is a prospective cohort stud y of preventive and epidemiological aspects of cardiovascular disorder s in middle-aged men. Of 25915 men invited, 16209 aged 40-49 years att ended the screening. A 7% random sample of men aged 20-39 years were a lso invited to attend. Methods: The screening started in May 1972 and the analysis presented is an 18-year follow-up for fatal strokes. Men with a history of stroke were excluded from the analyses. Results: Of 16173 men with no history of stroke 85 died from stroke. Results from Cox proportional hazards regression analysis confirm diastolic (DBP) a nd systolic blood pressure (SEP) as strong independent risk factors of fatal stroke, with DBP being the stronger predictor. Analyses of risk of fatal stroke by quintile values show SEP to give significantly inc reased risk from the third quintile (136 mmHg), and DBP from the fifth quintile (95 mmHg) relative to the first quintile. No levelling off a t highest levels can be seen when analysing decile values. No J-shape of the curve was evident. Men on drug treatment for hypertension with no stroke history (n = 440) had 4.7-fold (crude) and 2.8-fold (adjuste d for age and DBP) the rate of stroke mortality of men not on drug tre atment for hypertension. Conclusion: DBP was a stronger predictor than SEP, with increasing risk from the fifth quintile of DBP and the thir d quintile of SEP. Men on drug treatment for hypertension at screening were at increased risk during the follow-up period, indicating that t heir treatment did not sufficiently reduce their risk of stroke.