Blood pressure control to prevent decline in cognition after stroke
Authors Ihle-Hansen H, Thommessen B, Fagerland M, Øksengård A, Wyller T, Engedal K, Fure B
Received 13 February 2015
Accepted for publication 26 March 2015
Published 9 June 2015 Volume 2015:11 Pages 311—316
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Daniel Duprez
Hege Ihle-Hansen,1 Bente Thommessen,2 Morten W Fagerland,3 Anne R Øksengård,4 Torgeir B Wyller,5 Knut Engedal,6 Brynjar Fure7
1Department of Internal Medicine, Vestre Viken Hospital Trust, Bærum Hospital, Bærum, Norway; 2Department of Neurology, Akershus University Hospital, Lørenskog, Norway; 3Oslo Centre for Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital, Norway; 4Department of Internal medicine, Vestre Viken Hospital Trust, Bærum Hospital, Bærum, Norway; 5Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway; 6Norwegian Centre for Dementia Research, Oslo University Hospital, Oslo, Norway; 7Norwegian Knowledge Centre for the Health Services, Oslo, Norway
Background: Treatment of hypertension post-stroke preserves cognition through prevention of recurrent stroke, but it is not clear whether it prevents cognitive decline through other mechanisms. We aimed to describe changes in blood pressure from baseline to 1 year post-stroke and to evaluate the association between achieved blood pressure targets and cognitive function, mild cognitive impairment (MCI), and dementia.
Methods: We included patients with first-ever stroke, and defined achieved blood pressure goals as systolic blood pressure (SBP) in the categories ≤125 mmHg, ≤140 mmHg, and ≤160 mmHg, SBP reduction of ≥10 mmHg, and diastolic blood pressure (DBP) reduction of ≥5 mmHg. The main outcome variables were cognitive assessments 1 year post stroke. Secondary outcomes were diagnoses of MCI or dementia.
Results: Forty-one of 166 patients (25%) reached SBP ≤125 mmHg after 1 year, 92/166 (55%) reached SBP ≤140 mmHg, and 150/166 (90%) reached SBP ≤160 mmHg. SBP was reduced by ≥10 mmHg in 44/150 (29%) and DBP by ≥5 mmHg in 57/150 (38%). We did not find any statistically significant associations between cognitive test performances and different blood pressure goals (P=0.070–1.0). Nor was there any significant association between achieved goal blood pressure or blood pressure reduction after 1 year and the diagnoses of MCI or dementia (P=0.32–0.56).
Conclusion: Treatment of hypertension is important for primary and secondary prevention of stroke. Showing a potential beneficial effect of blood pressure control on cognitive function, however, probably needs longer follow-up.
Keywords: cognitive impairment, hypertension, cerebrovascular disease, risk factor management, secondary prevention
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