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Dementia is a rapidly increasing global clinical and public health issue in aging populations, and insights from observation and clinical assessment aided by pathology consistently suggest that modifying cardiovascular risk factors may prevent cognitive decline.1 Such an approach was tested in the third Health Outcomes Prevention Evaluation (HOPE-3) trial,2 as reported in this issue of Neurology®, in which an assessment of cognitive outcomes was included in an older subgroup (age ≥70 years) of 12,705 participants who had intermediate cardiovascular risk but had no prior cardiovascular events who were randomized to blood pressure (BP) lowering with a combination of candesartan and hydrochlorothiazide and cholesterol lowering with rosuvastatin. Of the initial 3,086 (24%) participants eligible for the cognitive substudy by age, 2,361 (77%) agreed to participate, and 1,626 (69%) were able to complete a series of tests emphasizing various aspects of cognitive function at baseline and at study end: the Digit Symbol Substitution Test (DSST), the modified Montreal Cognitive Assessment (mMoCA), and the Trail Making Test Part B (TMT-B). Despite reasonable reductions in systolic BP (by 6.0 mm Hg) and low-density lipoprotein cholesterol (LDL-C; 24.8 mg/dL) over a median of 5.7 years, there were no differences in any of the cognitive outcomes compared to placebo. However, in a post hoc analysis of the small group of participants (n = 181) at highest cardiovascular risk, defined by the highest tertiles of baseline systolic BP (>145 mm Hg) and LDL-C (>140 mg/dL), who were treated the most intensively with a combination of BP and cholesterol lowering, there was a reduction in cognitive decline on the DSST. What does this mean, and where do we go next?
Footnotes
Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.
See page 606
- © 2019 American Academy of Neurology
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