TY - JOUR
T1 - Hypertension and longitudinal changes in cerebral blood flow
T2 - The SMART-MR study
AU - Muller, Majon
AU - van der Graaf, Yolanda
AU - Visseren, Frank L.
AU - Mali, Willem P. Th. M.
AU - Geerlings, Mirjam I.
PY - 2012/6
Y1 - 2012/6
N2 - Objective: Cerebral hypoperfusion is among the mechanisms that may explain the association of high blood pressure (BP) with dementia. However, few data are available on the longitudinal association of hypertension and cerebral perfusion. Methods: We examined the longitudinal association of hypertension, BP, and antihypertensive drugs with change in parenchymal cerebral blood flow (pCBF) in 575 patients with manifest atherosclerotic disease (mean age, 57 6 10 years) from the SMART-MR study. Total CBF was measured at baseline and at follow-up with magnetic resonance (MR) angiography and was expressed per 100ml brain volume as an indicator of cerebral perfusion. Automated brain segmentation was used to quantify brain tissue volumes and cerebrospinal fluid on MR imaging. Results: Mean (standard deviation [SD]) baseline pCBF was 52.3 (9.8) ml/min/100ml and after 3.9 years (range, 3.0-5.8 years) of follow-up declined to 50.7 (10.3) ml/min/100ml. Regression analyses adjusted for age, sex, follow-up time, and vascular risk showed that untreated and poorly controlled hypertension and higher levels of systolic and diastolic BP (per SD) were significantly associated with a decline in pCBF; mean differences in decline (95% confidence interval) were -2.2 (-4.4 to 0.0), -1.0 (-1.8 to -0.1), and -1.0 (-1.8 to -0.2) ml/min/100ml. In addition, within hypertensive patients (n = 469), patients using angiotensin receptor blockers (ARBs) did not show a decline in pCBF, whereas patients using other antihypertensive drugs did show a decline in pCBF. Interpretation: Untreated hypertension, poorly controlled hypertension, and high BP levels are associated with a decline in pCBF. In addition, treatment with ARBs might result in less decline in pCBF than other antihypertensive treatment. © 2012 American Neurological Association.
AB - Objective: Cerebral hypoperfusion is among the mechanisms that may explain the association of high blood pressure (BP) with dementia. However, few data are available on the longitudinal association of hypertension and cerebral perfusion. Methods: We examined the longitudinal association of hypertension, BP, and antihypertensive drugs with change in parenchymal cerebral blood flow (pCBF) in 575 patients with manifest atherosclerotic disease (mean age, 57 6 10 years) from the SMART-MR study. Total CBF was measured at baseline and at follow-up with magnetic resonance (MR) angiography and was expressed per 100ml brain volume as an indicator of cerebral perfusion. Automated brain segmentation was used to quantify brain tissue volumes and cerebrospinal fluid on MR imaging. Results: Mean (standard deviation [SD]) baseline pCBF was 52.3 (9.8) ml/min/100ml and after 3.9 years (range, 3.0-5.8 years) of follow-up declined to 50.7 (10.3) ml/min/100ml. Regression analyses adjusted for age, sex, follow-up time, and vascular risk showed that untreated and poorly controlled hypertension and higher levels of systolic and diastolic BP (per SD) were significantly associated with a decline in pCBF; mean differences in decline (95% confidence interval) were -2.2 (-4.4 to 0.0), -1.0 (-1.8 to -0.1), and -1.0 (-1.8 to -0.2) ml/min/100ml. In addition, within hypertensive patients (n = 469), patients using angiotensin receptor blockers (ARBs) did not show a decline in pCBF, whereas patients using other antihypertensive drugs did show a decline in pCBF. Interpretation: Untreated hypertension, poorly controlled hypertension, and high BP levels are associated with a decline in pCBF. In addition, treatment with ARBs might result in less decline in pCBF than other antihypertensive treatment. © 2012 American Neurological Association.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84863395276&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/22447734
U2 - https://doi.org/10.1002/ana.23554
DO - https://doi.org/10.1002/ana.23554
M3 - Article
C2 - 22447734
SN - 0364-5134
VL - 71
SP - 825
EP - 833
JO - Annals of neurology
JF - Annals of neurology
IS - 6
ER -