Revisiting Coronary Artery Calcium and Incident Dementia
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
- Alzheimer disease
- coronary calcification
- coronary calcium
- coronary computed tomography
Dementia, defined as a progressive cognitive decline interfering with daily activities and independence,1 is perhaps the most feared of the diseases we associate with aging. Fifteen percent of people over age 70 years are afflicted, with annual costs of ≤$215 billion in the United States.2 Substantial resources have been martialed to understand the pathophysiology of dementia toward prevention and a cure.
See Article by Fujiyoshi et al
It is increasingly recognized that the 2 most common subtypes of dementia, Alzheimer’s disease and vascular dementia, have substantial histopathologic overlap. Several synergistic pathophysiologic mechanisms have been proposed.3,4 One hypothesis is that amyloid-β deposition, the hallmark of Alzheimer’s disease, damages the cerebral vasculature; cerebral vascular disease in turn leads to decreased clearance of amyloid-β. Coronary artery calcium (CAC), arguably the best-studied measure of subclinical atherosclerosis that is quantifiable on computed tomography, has proven to be a powerful predictor of long-term risk for incident cardiovascular events and death.5–7 CAC serves as a surrogate for atherosclerotic burden in other vascular beds, including the cerebral arteries, and, thus, can be used as a tool to probe the link between vascular disease and dementia.
The best cross-sectional evidence for a link comes from the AGES (Age, Gene, Environment Susceptibility)–Reykjavik Study. In AGES-Reykjavik study, 4250 Icelanders underwent neurocognitive testing, CAC computed tomography, and brain magnetic resonance imaging. The AGES-Reykjavik investigators found a dose-dependent association between CAC and dementia, with a suggestion that this relationship was mediated by differences in cognitive performance, as well as brain lesions and volumes, as assessed on magnetic resonance imaging, suggesting a possible mechanism of action.8 AGES-Reykjavik was a cross-sectional study, meaning that all evaluations were …