Incident myocardial infarction (MI) was associated with accelerated long-term cognitive decline, but not with an acute decrease in cognition.
Over a median follow-up of 6.4 years, people with incident heart attacks experienced faster, more persistent drops in global cognition (-0.15 points per year, 95% CI -0.21 to -0.10) compared with people who never had MI, reported Michelle Johansen, MD, PhD, of Johns Hopkins University School of Medicine in Baltimore, and co-authors.
Memory (-0.13 points per year, 95% CI -0.22 to -0.04) and executive function (-0.14 points per year, 95% CI -0.20 to -0.08) scores also fell faster over time in those with incident MI.
"We also quantified the magnitude of post-MI cognitive change; the decline in global cognition after incident MI was equivalent to 6 to 13 years of cognitive aging, representing an important public health problem," Johansen and colleagues wrote in .
Race (P=0.02) and sex (P=0.04) appeared to modify global cognitive decline after MI, with steeper annual declines in white compared with Black individuals, and in men compared with women.
The observational cohort study of more than 30,000 adults did not show an acute decline after MI in global cognition (-0.18 points, 95% CI -0.52 to 0.17), executive function (-0.17 points, 95% CI -0.53 to 0.18), or memory (0.62 points, 95% CI -0.07 to 1.31).
The slope of cognitive decline after MI could not be explained by stroke or new atrial fibrillation, noted Eric Smith, MD, MPH, of the University of Calgary in Canada, and Lisa Silbert, MD, MCR, of the Oregon Health & Science University in Portland, in an .
"The lack of an immediate decrease in cognition and the steeper decline in subsequent years suggests that the MI was associated with a slower, progressive process that accelerated cognitive decline, rather than an acute process," Smith and Silbert wrote.
"One possibility is that there may be progressive cardiac dysfunction due to ischemic cardiomyopathy, with alterations in blood pressure and cardiac output leading to brain ischemia," they observed. Patients with MI may be vulnerable to post-MI arrhythmias, they suggested, or to subclinical disease or ongoing inflammation. In addition, MI may increase depression risk, which is associated with dementia.
"Even though the mechanism for post-MI cognitive decline is unclear, the risk seems real," Smith and Silbert said.
"Patients with history of MI should be asked about cognitive symptoms periodically, with follow-up cognitive screening for patients in whom symptoms are endorsed by themselves or an informant," they suggested. "Referral to a cognitive specialist or neuropsychologist may be warranted in select cases."
Johansen and co-authors studied 30,465 adults without MI, dementia, or stroke at the time of their first cognitive assessment from six U.S. cohort studies from 1971 to 2019: the Atherosclerosis Risk in Communities ( Study, Coronary Artery Risk Development in Young Adults Study (), Cardiovascular Health Study (), Framingham Offspring Study (), Multi-Ethnic Study of Atherosclerosis (), and Northern Manhattan Study ().
Incident MI was measured during cohort follow-up. The primary outcome measure was change in global cognition; secondary outcomes were changes in memory and executive function. Outcomes were standardized as mean T scores of 50; a 1-point difference represented a 0.1-standard deviation difference in cognition. The average number of global cognitive assessments after incident MI was 2.63.
Mean age was 60 at the time of first cognitive assessment. Most participants (56%) were female; 23% were Black, 8% were Hispanic, and 69% were white. Overall, 1,033 participants had one or more incident MI and 237 participants had two. In people with a second MI event, there was no acute drop in global cognition after the second MI, but there was an acute decrease in executive function.
Measures of post-MI cognition may have occurred months after the event, which may have led to an underestimation of acute cognitive changes, Johansen and co-authors acknowledged.
In addition, some demographic data, such as occupation, and some clinical factors, such as depressive symptoms, were unknown. The number of post-MI cognitive assessments was also a study limitation.
Disclosures
This study was supported by the grants from the NIH through the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA).
Johansen has received grants from NINDS and NIA. Co-authors reported relationships with the NIH, the Yale University Open Data Access Project funded by Johnson & Johnson, and the American Heart Association.
Smith reported personal fees for consulting from Eli Lilly and Alnylam. Silbert reported grants from NIH and the Department of Defense Peer-Reviewed Alzheimer's Research Program, and having a patent to identify perivascular spaces in MRI.
Primary Source
JAMA Neurology
Johansen MC, et al "Association between acute myocardial infarction and cognition" JAMA Neurol 2023; DOI: 10.1001/jamaneurol.2023.1331.
Secondary Source
JAMA Neurology
Smith EE, Silbert LC "Myocardial infarction bends the curve of age-related cognitive decline, but how?" JAMA Neurol 2023; DOI: 10.1001/jamaneurol.2023.0466.