Midlife CV risk may cause decline in brain metabolism in subclinical atherosclerosis
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CV risk factors, particularly hypertension, were linked to impaired brain metabolism tied to cognitive decline and were identifiable at midlife among asymptomatic patients with subclinical atherosclerosis, researchers reported.
“We think that cardiovascular risk factors that affect the large vessels carrying blood from the heart to the brain also affect the small vessels in the brain. We found that the same risk factors that damage the heart and the large arteries, and especially hypertension, are closely linked to the decline in brain metabolism years before the appearance of symptoms,” Valentin Fuster, MD, PhD, physician-in-chief of the Mount Sinai Hospital and director of Mount Sinai Heart in New York, said in a press release. “Although everybody knows about the importance of caring for ourselves and controlling cardiovascular risk factors in order to avoid a heart attack, the association of these same risk factors with cognitive decline may increase awareness of the need to acquire healthy habits from the earliest stages of life.”
The study, published in the Journal of the American College of Cardiology, included 547 asymptomatic participants with evidence of subclinical atherosclerosis from the PESA cohort (mean age, 50 years; 82% men). Each patient underwent 18F-fluorodeoxyglucose PET, and researchers assessed the association between cerebral metabolism with CV risk factors and atherosclerotic plaque burden in carotid and femoral arteries as shown on 3D vascular ultrasound.
According to the study, global brain 18F-fluorodeoxyglucose uptake was found to have an inverse correlation with 30-year Framingham Risk Score (beta = 0.15; P < .001), which researchers determined was mainly driven by the presence of hypertension (Cohen’s d = 0.36; P < .001).
Moreover, carotid plaque burden was also inversely associated with global brain 18F-fluorodeoxyglucose uptake (beta = 0.16; P < .001), even after adjustment for 30-year Framingham Risk Score.
“When brain metabolism declines, the brain’s ability to handle adverse events can be compromised. Depending on the brain area affected, this can lead to a range of distinct problems,” Marta Cortés-Canteli, PhD, Miguel Servet fellow and investigator at the Centro Nacional de Investigaciones Cardiovasculares, said in another press release. “The next step will be to determine whether individuals with subclinical atherosclerosis in the carotid arteries and low brain metabolism at the age of 50 go on to experience cognitive decline 10 years later.”
Brain areas affected by vascular disease
According to the study, voxel-wise analyses determined the brain areas most strongly affected by hypometabolism associated with 30-year Framingham Risk Score, hypertension and carotid plaque burden were the parietotemporal regions, including the angular, supramarginal and inferior/middle temporal gyri, and the cingulate gyrus.
“The brain areas showing low metabolism in participants with higher cardiovascular risk are the same areas affected in Alzheimer’s disease, suggesting that these individuals may have higher than normal vulnerability to this disease,” Juan Domingo Gispert, PhD, head of the neuroimaging group at the Barcelona Beta Brain Research Center in Barcelona, Spain, said in the release. “There is abundant evidence linking cardiovascular risk factors and Alzheimer’s disease. If we can gain a more precise understanding of this relationship at asymptomatic disease stages, we will be in a position of design new strategies to prevent Alzheimer’s, matching the success of current strategies to prevent cardiovascular disease.”
Focus on early markers of vascular disease
“These findings provide valuable insights into the impact of midlife cardiovascular risk factors and carotid atherosclerosis on cognitive brain health. The regional hypometabolism pattern seen with high midlife 30-year Framingham Risk Score and high carotid atherosclerosis burden implicates these factors in Alzheimer’s disease decades before the typical age of symptom onset,” Neal S. Parikh, MD, MS, assistant professor of neurology at Weill Cornell Medicine, and Rebecca F. Gottesman, MD, PhD, professor of neurology at Johns Hopkins School of Medicine, wrote in a related editorial. “Furthermore, these data suggest that carotid atherosclerosis — carotid atherosclerosis alone, and above and beyond comorbid cardiovascular risk factors — may be detrimental to brain health even when it is subclinical and non-stenosing.
“Although the midlife time window has been emphasized in previous studies of cardiovascular risk factors, the current study’s focus on carotid atherosclerosis in midlife provides new insight into early markers of vascular disease and their relevance,” Parikh and Gottesman wrote.
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This important new work adds to the growing body of evidence that BP in midlife is critically important relative to the future development of cognitive impairment. Elevated BP raises risk for early brain aging and even Alzheimer’s disease later in life. The message to our patients is clear: Check your BP regularly and don’t ignore elevated numbers, particularly at younger ages, simply because you have no symptoms. This should be posted in our offices to remind our patients.
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