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Autopsy study shows link between untreated elevations in SBP, cerebrovascular damage

Monday, December 14 2009 | Comments

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What's This? New data from the Adult Changes in Thought (ACT) study suggest elevated systolic blood pressure (SBP) may be a risk factor for the development of cerebral microinfarcts. However, findings from the study also suggest that treatment for hypertension may modify this association.

The ACT study is a prospective cohort study of individuals aged 65 years or older at enrollment. In the current analysis, researchers evaluated the link between BP and dementia-related pathologic changes (cystic macroscopic infarcts, microinfarcts, neuritic plaques, neurofibrillary tangles, and cortical Lewy bodies) in 250 ACT participants who provided BP data at baseline and underwent autopsy after a mean follow-up of 7.7 years.

The data showed that the presence of >2 microinfarcts on autopsy was independently associated with baseline SBP in younger participants (aged 65-80 years), but not in older participants (aged older than 80 years). In the younger subgroup, mean baseline SBP was 11.5 mm Hg higher (95% CI, 1.7-21.3 mm Hg) among those with >2 microinfarcts relative to those with <=2 microinfarcts, yielding a relative risk (RR) for >2 microinfarcts of 1.15 (95% CI, 1.00-1.33) for each 10 mm Hg increase in baseline SBP in an analysis adjusted for age, sex, and duration of follow-up.

The data also suggested that antihypertensive treatment significantly modified this association. Specifically, among untreated participants aged 65 to 80 years, the RR for >2 microinfarcts was 1.48 (95% CI, 1.21-1.81) with each 10 mm Hg increase in SBP. However, there was no significant association between SBP and microinfarcts among those who had received antihypertensive therapy.

The study authors acknowledged that ACT participants who underwent autopsy differed from participants who died but did not undergo autopsy. When the data were weighted to account for the selection bias, the relationship between SBP and microinfarcts among younger participants was attenuated (mean difference in baseline SBP, 5.1 mm Hg; 95% CI, -6.4 to +15.8 mm Hg). However, the relationship between SBP and microinfarcts remained significant among untreated participants in this age group (RR, 1.38; 95% CI, 1.05-1.94).

SBP was not significantly associated with cystic macroscopic infarcts, cortical Lewy bodies, or Alzheimer's disease-related pathologic changes (neuritic plaques and neurofibrillary tangles). In addition, there was no association between diastolic BP and measures of brain injury. (Wang LY, et al. J Am Geriatr Soc 2009;57:1975-1981.)

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