title: Midlife pulse pressure and incidence of dementia: the Honolulu-Asia Aging Study.
abstract: OBJECTIVE
  Previous studies have shown that midlife systolic blood pressure (SBP) predicts late-life cognitive decline and incident dementia. This study explores whether this association is attributable to the pulsatile, ie, pulse pressure (PP), or the nonpulsatile component of blood pressure (BP).
  
  
  METHODS
  Data are from the Honolulu-Asia Aging Study, a community-based study of Japanese American men. Midlife BP was measured in 1971 to 1974 and dementia assessment was conducted in late-life. The 2505 men who were dementia free in 1991 and had complete follow-up data were re-examined for incident dementia in 1994 to 1996 and 1997 to 1999. Their age ranged from 71 to 93 years. Survival analysis with age as the time scale was performed to estimate the risk (hazard ratio [HR] and 95% CI) for incident dementia associated with mid- and late-life tertiles of PP and mean arterial BP, as well as SBP and diastolic BP categories.
  
  
  RESULTS
  Over a mean of 5.1 years of follow-up, 189 cases (7.5%) of incident Alzheimer disease or vascular dementia were identified. After adjustment for cerebrovascular risk factors, dementia was significantly associated with SBP (HR 1.77; 95% CI, 1.10 to 2.84, for SBP > or =140 mm Hg compared with SBP <120 mm Hg), but not with PP tertiles. Limiting the analysis to those never treated with antihypertensives, high levels of all 4 BP components were significantly associated with dementia. In models with 2 BP components, only SBP remained significant in both the total sample and the never-treated subgroup (HR 2.29; 95% CI, 1.23 to 4.25, for SBP > or =140 mm Hg in total sample), whereas PP was not significantly associated with the risk for dementia.
  
  
  CONCLUSIONS
  Midlife PP is not independently associated with dementia incidence. Midlife SBP is the strongest BP component predicting incident dementia.
authors.affiliation: Laboratory of Epidemiology, Demography and Biometry, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: Michael H
authors.initials: MH
authors.lastname: Freitag
authors.forename: Rita
authors.initials: R
authors.lastname: Peila
authors.forename: Kamal
authors.initials: K
authors.lastname: Masaki
authors.forename: Helen
authors.initials: H
authors.lastname: Petrovitch
authors.forename: G Webster
authors.initials: GW
authors.lastname: Ross
authors.forename: Lon R
authors.initials: LR
authors.lastname: White
authors.forename: Lenore J
authors.initials: LJ
authors.lastname: Launer
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging; D000544:Alzheimer Disease / Q000453:epidemiology / Q000473:pathology; D001794:Blood Pressure; D003071:Cognition; D015331:Cohort Studies; D003704:Dementia / Q000453:epidemiology* / Q000208:ethnology / Q000473:pathology*; D015140:Dementia, Vascular / Q000453:epidemiology / Q000473:pathology; D006801:Humans; D015994:Incidence; D007564:Japan; D015233:Models, Statistical; D016016:Proportional Hazards Models; D011674:Pulse; D012306:Risk; D020521:Stroke; D013997:Time Factors; D014481:United States