- Calcium build-up in blood vessels outside the brain may be associated with brain changes linked to future risk of dementia and stroke.
- The results may help understand how atherosclerosis affects brain function and ultimately the risk of developing dementia and stroke.
DALLAS — Greater calcium build-up in blood vessels outside the brain may be associated with brain changes linked to future risk of dementia and stroke, according to new research in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association.
“The relationship between calcium in atherosclerotic plaque and brain changes exists on top of the effect of classic cardiovascular risk factors such as high blood pressure, smoking and diabetes,” said Meike W. Vernooij, M.D., Ph.D., senior study author and assistant professor of epidemiology and radiology at the Erasmus Medical Center in Rotterdam, the Netherlands.
Furthermore, the amount of hardened, calcified plaque provided more information about the extent of brain changes than traditional ultrasound measures of the presence of plaque in the carotid artery.
The researchers studied 885 people, average age 67, participating in the Rotterdam Study, which includes varying types of imaging to better understand the causes and predictors of dementia and stroke. They used computed X-ray tomography (CT) scans to measure calcification in four blood vessel areas: the coronary arteries that feed the heart; the aortic arch (part of the body’s largest artery that delivers blood from the heart into the general circulation); and the extracranial and intracranial carotid arteries that carry blood through the neck into the brain.
Researchers used magnetic resonance imaging or MRI of the brain to visualize small brain infarctions, microbleeds (tiny brain bleeds) and bright areas called white matter lesions. White matter in the brain refers to the fiber tracts that carry information to and from the brain. White matter lesions are more commonly seen in patients who have risk factors such as a history of hypertension, diabetes and high cholesterol.
“These subclinical brain changes, apparent on MRI, do not necessarily cause symptoms right away but are frequently seen in patients with stroke or dementia and over the long term may be associated with worse cognitive performance,” Vernooij said.
Among the results:
- Calcium build-up in each of the four arteries scanned was associated with the presence of small brain infarctions and white matter lesions in the brain.
- No associations were found between microbleeds in the brain and calcification in any of the arteries studied.
- As predicted, the amount of calcification in vessels closer to the brain — the extracranial and intracranial carotids — had the strongest relationship to MRI markers of vascular brain disease.
- The most prominent associations were found between intracranial carotid calcification and the volume of white matter lesions, and extracranial carotid calcification and brain infarctions.
“The distinction between the impact of calcification in the extracranial and intracranial carotids adds to the current belief that white matter lesions mainly result from disease in smaller intracranial vessels, while brain infarctions are thought to be mainly caused by larger vessel disease,” Vernooij said.
The results will be used to advance the understanding of how atherosclerosis affects brain function and ultimately the risk of developing dementia and stroke.
“We are a long way from using CT-assessed calcification to screen individuals for brain lesions and dementia risk,” Vernooij said.
Unanswered questions include whether treatment can reduce calcification in blood vessels and whether doing so would improve cognitive health or lower the risk of dementia and stroke.
However, if a physician has performed a heart CT scan to assess heart attack risk, the results may provide information that extends beyond the reason for the examination.
“Though far away from the brain, calcification in coronary arteries may indicate the presence of subclinical brain disease as well,” Vernooij said.
Co-authors are: Daniel Bos, M.D.; M. Arfan Ikram, M.D., Ph.D..; Suzette E. Elias-Smale, M.D., M.Sc.; Gabriel P. Krestin, M.D., Ph.D.; Albert Hofman, M.D., Ph.D.; Jacqueline C.M. Witteman, Ph.D.; and Aad van der Lugt, M.D., Ph.D. Author disclosures and funding sources are on the manuscript.
Statements and conclusions of study authors published in American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect the association’s policy or position. The association makes no representation or guarantee as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at www.americanheart.org/corporatefunding.
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