2 September 2019

Lower blood pressure to slow brain ageing: study

Cardio Clinical Neurology

The link between hypertension and dementia is growing, but treatment caution is still urged

Keeping blood pressure down slows down the formation of white matter lesions in the brain, a risk factor for cognitive decline and dementia, according to a substudy of the Systolic Blood Pressure Intervention Trial (SPRINT).

This has implications for the management of elderly patients, but must be done with great care and on carefully chosen patients to avoid adverse effects, says University of Western Australia Geriatrics Professor Leon Flicker AO.

SPRINT is a large longitudinal randomised study examining the cardiovascular benefits of keeping systolic blood pressure below 120mmHg, rather than the currently recommended goal of  under140mmHg.

In 2015, the group reported a 25% reduction in rates of heart attack, heart failure and stroke in the intensive treatment group. In January it reported less cognitive decline in the intensive group, but not significantly less dementia.

In the substudy published in the Journal of the American Medical Association this month, 449 participants, about half of them whose systolic blood pressure was treated to a target of <120mmHg, had the extent of white matter lesions and brain volume assessed by MRI  over an average period of about 3.5 years. White matter lesions are present in in small vessel ischaemic disease, which causes vascular dementia.

The intensive group had significantly fewer white matter lesions compared with the standard group, although the authors say “the differences were small”.

Men in the intensive arm experienced a decline in total brain volume while the women did not.

Professor Flicker, who has seen the results presented, said the paper did not make clear just how careful the researchers were to ensure patients in the intensive treatment group did not suffer adverse events.

“They were aggressively treating people so that if at six months they hadn’t reached the target they gave them more drugs.

“But every time they did they followed them up and if they got side-effects [or orthostatic hypotension] they backed off. It’s really a very intensive monitoring process to make sure you do this safely.

“You have to have lots of appointments. In GP land, in routine care, patients don’t always come back each time you ask them, right?

“And that’s not the GPs’ fault by any means. You’ve got to have very motivated patients who are happy to do all this.”

Professor Flicker said while an association had previously been shown between white matter lesions and cognitive impairment, this was one of very few intervention studies to date.

While some research groups were still targeting amyloid plaques as the cause of Alzheimer’s disease, and trying to catch it earlier, he said, it was time to consider changing the hypothesis to one with a vascular component.

“When you test a hypothesis and you keep getting them the same answer, which is that it doesn’t seem to work, then what you have to do is change the hypothesis,” Professor Flicker  said.

“And it may be that the amyloid is in association with dementia, but it may not be pathogenic, it may be an epiphenomenon, it may be a product of the brain’s repair mechanism.”

JAMA, 13 August