title: Hypertension and longitudinal changes in cerebral blood flow: the SMART-MR study.
abstract: 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 ± 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Internal Medicine, VU University Medical Center Amsterdam, Amsterdam, the Netherlands.
authors.forename: Majon
authors.initials: M
authors.lastname: Muller
authors.forename: Yolanda
authors.initials: Y
authors.lastname: van der Graaf
authors.forename: Frank L
authors.initials: FL
authors.lastname: Visseren
authors.forename: Willem P Th M
authors.initials: WP
authors.lastname: Mali
authors.forename: Mirjam I
authors.initials: MI
authors.lastname: Geerlings
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D015992:Body Mass Index; D020520:Brain Infarction / Q000209:etiology; D002540:Cerebral Cortex / Q000098:blood supply* / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000473:pathology* / Q000628:therapy; D016014:Linear Models; D008137:Longitudinal Studies; D018810:Magnetic Resonance Angiography; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology*; D012189:Retrospective Studies
chemical_list: D000959:Antihypertensive Agents