August 25, 2009 — Higher diastolic blood pressure (DBP) levels, but not systolic blood pressure (SBP) levels, can impair cognitive status in individuals without prior history of stroke or transient ischemic attack, according to the results of a large study reported in the August 25 issue of Neurology.
"Although both higher [pulse pressure] and SBP values were related to cognitive impairment in unadjusted analyses, these associations were no longer significant after accounting for demographics, health behaviors, and vascular risk factors," write Georgios Tsivgoulis, MD, from the Comprehensive Stroke Center at the University of Alabama in Birmingham, and colleagues.
"The present study indicates that elevated [DBP] levels are linearly and cross-sectionally associated with a higher likelihood of impaired cognitive status. If this association is causally established in future longitudinal studies, than reducing elevated BP levels may result in reducing the incidence of dementia," Dr. Tsivgoulis told Medscape Neurology.
The study authors write that the prevalence of dementia is estimated at approximately 8% and the prevalence of hypertension approximately 65% among individuals aged 65 years or older. Although the relationship among BP, cognitive function, and dementia has received a lot of attention in recent years, the findings have varied greatly.
In this study, the investigators sought to evaluate the cross-sectional relationship of BP components (SBP, DBP, and pulse pressure) with cognitive impairment after adjusting for potential confounders.
Dr. Tsivgoulis and colleagues looked at data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a national, population-based, longitudinal cohort study evaluating stroke risk in 30,228 black and white men and women aged 45 years or older.
From REGARDS, the investigators selected 19,836 participants (mean age, 64.6 years; 57.7% white, 60.8% female), who were enrolled from December 2003 to March 2007, had no prior history of stroke or transient ischemic attack, and completed baseline home physical evaluations.
During the in-home visit, BP measurements were taken as the average of 2 measurements using a standard aneroid sphygmomanometer.
The participants also completed the 6-Item Screener, which was administered either in-person or by telephone, to assess cognitive status, as well as the Center for Epidemiologic Studies-Depression 4-Item version to evaluate depressive symptoms.
Incremental logistic models were used to examine baseline relationships among SBP, DBP, and pulse pressure with impaired cognitive status.
At the end of the study, results showed that higher DBP levels were associated with impaired cognitive status after adjusting for demographic and environmental characteristics, risk factors, depressive symptoms, and antihypertensive medications. An increment of 10 mm Hg in DBP was associated with 7% (95% confidence interval [CI], 1% – 14%; P = .0275) higher odds of cognitive impairment.
However, no independent association was identified between impaired cognitive status and SBP (odds ratio [OR], 1.02; 95% CI, 0.99 – 1.06) or pulse pressure (OR, 0.99; 95% CI, 0.95 – 1.04).
"We were surprised by the fact that DBP and not SBP or [pulse pressure] was related to cognitive impairment after adjusting for potential confounders," said Dr. Tsivgoulis. "We attributed these intriguing findings to a potential association between diastolic hypertension and accelerated stiffening of cerebral small vessels that are profoundly affected by DBP."
"These vascular changes...result in a reduction of luminal diameter, which in turn causes increased resistance to flow and decline in cerebral perfusion. Such hypoperfusion may produce discrete regions of small cerebral infarctions and diffuse ischemic changes in the periventricular and deep white matter (leukoaraiosis), causing vascular cognitive impairment and also contributing to the pathogenesis of Alzheimer's disease by destabilizing neurons and synapses," the authors write.
The results showed no evidence of nonlinear relationships between any of the BP components and impaired cognitive status and no interaction between age and the relationship of impaired cognitive status with SBP (P = .827), DBP (P = .1333), or pulse pressure (P = .827) levels. Also, no interaction was identified between race and the relationship of impaired cognitive status with SBP (P = .899), DBP (P = .966), or pulse pressure (P = .858) levels.
"Our study showed that higher DBP levels were independently related to a higher likelihood of impaired cognitive status in a large national sample that was nearly balanced with respect to race and gender," said Dr. Tsivgoulis. However, he added, the linear, cross-sectional association needs to be confirmed in a longitudinal analysis.
Laying the Groundwork
"This is a good study," said John Hart, Jr, MD, professor of behavioral and brain sciences and medical science director at the Center for BrainHealth at the University of Texas in Dallas in an interview with Medscape Neurology. Dr. Hart was not involved with the study.
"It's another step in laying the groundwork for some things we're noticing about the vascular effects on cognitive decline with aging," Dr. Hart continued. "It's not necessarily saying we have a definitive answer here. But it is saying that in a large study like this, there appears to be an effect of diastolic BP."
However, he added that the study also has some weaknesses, including its cross-sectional design. In addition, the investigators "report diastolic BP versus cognitive impairment based on only a 6-point test, and from a cognitive point of view, that's pretty minimalistic. Calling someone impaired based just on this test really gives a rudimentary picture of their cognitive status."
In the future, Dr. Hart said that he would like to see a big, definitive, prospective, longitudinal study "with a rich set of cognitive measures and some neuroimaging to correlate with the findings."
"I think this study reaffirms the fact that you want to do your best to screen and treat for vascular risk factors in individuals, not just in what people normally think of (heart disease), but also factors such as strokes or vascular changes that might affect cognition in the brain. It just adds another piece of evidence that says that we should all be treating these risk factors aggressively to prevent long-term effects down the road. That's such a straightforward easy thing to do and it lets you see real differences at the end of the game."
Several of the study authors disclosed financial relationships that are listed at the end of the original article. Dr. Hart has disclosed no relevant financial relationships.
Medscape Medical News © 2009
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