Key result
Impairments in baseline cognitive function were associated with a significantly higher incidence of elevated hs-cTnT (OR 1.511) and NT-proBNP (OR 1.929) in older adults without known cardiovascular disease.
Why the study?
The association between cognition impairment and CVD risk is inconsistent, and it is unknown whether pathways contributing to CVD are caused by impaired cognition.
Does cognitive impairment increase the risk of subclinical cardiovascular disease (elevated hs-cTnT and NT-proBNP) in older adults?
Cohort (n=9,216)
Yes
Does cognitive impairment increase the risk of subclinical cardiovascular disease (elevated hs-cTnT and NT-proBNP) in older adults?
Effect estimate: OR 1.511 (95% CI 1.093-2.088)
p-value: p=0.013
Impairments in baseline cognitive function are independently associated with an increased risk of subclinical myocardial damage and wall strain in older adults.
May warrant integrated cognitive-cardiac screening in older adults; extends bidirectional observations but leaves causality and interventions open.
Background Clinical cardiovascular disease (CVD) and cognition impairment are common and often coexist in aging populations, and CVD is associated with greater cognition impairment risk; however, the association between cognition impairment and CVD risk is inconsistent. It is unknown if pathways that contribute to CVD are caused by impaired cognition. We hypothesized that cognition impairment would be associated with greater subclinical CVD including subclinical myocardial damage [assessed by high-sensitivity cardiac troponin T (hs-cTnT)] and cardiac strain or dysfunction [assessed by N-terminal pro-B-type natriuretic peptide (NT-proBNP)]. Methods This analysis included Atherosclerosis Risk in Communities Study (ARIC) participants who underwent global cognition z -score tests between 1991 and 1993. Cardiac biomarkers were measured from stored plasma samples collected between 1996 and 1999. Logistic regression models were used to determine the association of cognitive function with subclinical CVD risk. Results There were 558/9216 (6.1%) and 447/9097 (5.0%) participants with incident elevated hs-CTnT (≥14 ng/L) and NT-proBNP (≥300 pg/mL) levels, respectively. Comparing the lowest and highest quartiles of global cognition z -scores, a higher incidence of elevated hs-CTnT [odds ratio (OR) = 1.511, 95% confidence interval (CI): 1.093–2.088, P = 0.013] and NT-proBNP (OR = 1.929, 95% CI: 1.350–2.755, P < 0.001) were observed, respectively. In structural equation modeling, the indirect effect of global cognition z -score on major adverse cardiac events was 42.1% ( P < 0.05). Conclusion Impairments in baseline cognitive function were associated with subclinical myocardial damage or wall strain. Although future studies are warranted to investigate the pathophysiological mechanisms behind these associations, our study suggests common pathways between cognitive and cardiac dysfunction.
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Li et al. (2022) conducted a cohort in Subclinical cardiovascular disease (n=9,216). Cognitive impairment (lowest quartile of global cognition z-score) vs. Highest quartile of global cognition z-score was evaluated on Incident elevated hs-cTnT (≥14 ng/L) (OR 1.511, 95% CI 1.093-2.088, p=0.013). Impairments in baseline cognitive function were associated with a significantly higher incidence of elevated hs-cTnT (OR 1.511) and NT-proBNP (OR 1.929) in older adults without known cardiovascular disease.
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