Mid-life hypertension is a risk factor for cognitive decline. A 10 mm Hg rise in systolic pressure led to an intermediate cognitive decline in 7% of the cohort on follow-up.
For years, an appropriate emphasis has been placed on a cause-and-effect relationship between hypertension and strokes. At the 2013 American Society of Hypertension (ASH) annual meeting, a troubling CNS complication of untreated hypertension was discussed-dementia.
The Honolulu-Asia Aging Study, brought to a close in 2012, looked at mid-life hypertension as a risk factor for cognitive decline. A 10 mm Hg rise in systolic pressure led to an intermediate cognitive decline in 7% of the cohort on follow-up. An additional 9% of the same group developed poor cognitive function compared with individuals without hypertension. If the systolic pressure exceeded 160 mm Hg, cognitive decline was 4.8 times more likely than in matched individuals with systolic pressures between 110 and 139 mm Hg.
My first response was that the CNS damage was correlated with development of vascular dementia. I was only partially correct.
Both vascular dementia and Alzheimer-type dementia increased later in midlife hypertensive individuals. Dr Fernando Testai of the University of Illinois Chicago looked at contributing factors.
Hypertension at midlife is associated with white matter damage. This is a pathologic process usually expected later in life. With hypertension, the seeds are planted much earlier. Plaque deposition, lacunar infarcts, and small bleeds are a consequence of hypertension. Hypertension can cause progressive atrophy of the neocortex, hippocampus, and amygdala without clinical evidence for a stroke. Hypertension also has more subtle effects demonstrated by basic science techniques. Elevated blood pressure injures the neurovascular units, thereby altering the blood-brain barrier. As a result, blood flow changes, amyloid deposition can increase, and later lead to dementia. In general, all of these factors contribute to more than one variety of dementia in hypertensive individuals.
If these data are not disturbing enough, diabetes makes the hypertensive injuries even worse.
Serum insulin, higher in people with type 2 diabetes mellitus (DM2) with insulin resistance, degrades choline acetyltransferase. DM2 adds oxidative stress, mitochondrial dysfunction, and amyloid and P-tau deposition to the pathologic injuries. Also, advanced glycation end products have receptors in the brain. They are a consequence of elevated sugars and reach a chemical point where they cannot be metabolized. Their presence is pro-inflammatory and can increase neurofibrillary tangles. Again, hypertension plus DM2 makes both kinds of dementia-vascular and Alzheimer type-more likely (that is where the tangles, amyloid, and tau proteins enter the picture).
For years, medicine has focused on blood pressure as the culprit in cerebrovascular disease manifesting as strokes. We may have focused on the combination of blood pressure and strokes as an “older person’s” problem. What does this “hot off the press” data from ASH have to add?
The damage is occurring in typical middle-aged persons with hypertension who come to primary care offices every day.
Even minimal systolic hypertension in this group is setting the stage not only for vascular dementia later, but also for the rising tide of folks with Alzheimer-type dementia. If these individuals have concomitant DM2, the damage is accelerated.
If we did not have enough incentive before this to treat blood pressure effectively and earlier as well, this data should redirect our efforts even more intensely. The damage done to the brain today will haunt later years as dementia.