Pauline Anderson
A new study shows that arterial stiffness is related to the amount of amyloid β (Aβ), a hallmark sign of Alzheimer’s disease (AD) deposited in the brains of elderly persons without dementia, independent of current blood pressure and use of antihypertensive medications.
Further, the researchers report that patients who had cerebrovascular disease, indicated by white matter hyperintensities (WMH), also had increased arterial stiffness.
Those who had both amyloid deposits and WMH had the greatest amount of arterial stiffness, giving clout to the idea that arterial stiffness is independently related to both of these risk factors.
“It might be that there are 2 mechanisms by which arterial stiffness works to lead to amyloid and therefore to cognitive impairment,” said lead author Timothy M. Hughes, PhD, formerly of the University of Pittsburgh, now a postdoctoral fellow at Wake Forest University School of Medicine, Winston-Salem, North Carolina.
The study, which according to Dr. Hughes is the first to test amyloid deposition in living adults without dementia by using precise measures of arterial stiffness, is published online October 16 in Neurology.
GEMS Study
The study included 91 participants from the Pittsburgh site of the Ginkgo Evaluation of Memory Study (GEMS), a multicenter, placebo-controlled, randomized trial of daily use of Gingko biloba in community-dwelling adults aged 72 to 96 years.
The participants in the current analysis had a mean age of 87 years and a body mass index of 26 kg/m2. About a third (33%) were women, 15% were carriers of the APOE 4 risk allele for AD, and 15% were classified as having mild cognitive impairment. About 70% were receiving antihypertensive medications.
These participants had undergone brain MRI and Pittsburgh compound B positron emission tomography after the closeout visit of GEMS. About 2 years later, they were measured for arterial stiffness using pulse-wave velocity (PWV) in the central (carotid-femoral PWV and heart-femoral PWV), peripheral (femoral-ankle PWV) and mixed (brachial-ankle PWV [baPWV]) vascular beds.
The study showed that Aβ deposition was more strongly associated with mixed measures of arterial stiffness (eg, baPWV) than central measures. One standard deviation increase in baPWV resulted in a 2-fold increase in the odds of being Aβ positive (P = .007). Aβ was also associated with systolic blood pressure and mean arterial pressure.
These associations were independent of age, sex, body mass index, APOE 4 status, and antihypertensive medication use. Dr. Hughes noted that the study looked at the use of hypertension medications as far back as the original GEMS in 2000 and still found no effect on the amount of amyloid deposited in the brain.
“Taking antihypertensive medication just decreases your blood pressure now; it doesn’t do anything to reverse the stiffness that you have already developed, and it may not reduce stiffness in the future,” said Dr. Hughes. This is why antihypertension trials such as the Systolic Blood Pressure Intervention Trial (SPRINT) study, are a using blood pressure target below 120 mmHg, he noted. “It is proposed that every unit above that increases your stiffness.”
However, he added, the researchers didn’t know what type of antihypertensive medication the patients in this new study were taking, whether or not they were taking it regularly, or how well controlled their blood pressure was.