Atrial Cardiopathy Associated With Dementia Risk in Older Adults

Atrial cardiopathy is associated with an increased risk for dementia in community-dwelling older adults, according to a study in the Journal of the American Heart Association.

A prospective cohort analysis was conducted in participants from the Atherosclerosis Risk in Communities study who were originally recruited between 1987 and 1989 from 4 communities in the United States. The analysis included participants who returned for visit 5 (2011-2013) and did not have dementia and also had echocardiography, electrocardiography (ECG), and serum amino N-terminal pro–brain natriuretic peptide (NT-proBNP) measurement performed during the visit.

The primary independent variable was atrial cardiopathy, which was defined as having 1 or more of the following:

• P-wave terminal force greater than 5000 mV·ms in ECG lead V1
• NT-proBNP concentration greater than 250 pg/mL
• Left atrial volume index of 34 mL/m² or higher measured by transthoracic echocardiography

The primary outcome was dementia onset after visit 5 through December 31, 2019, or censoring owing to death.

The final study population included 5078 participants. Of these patients, 1709 met the criteria for atrial cardiopathy and 3369 did not have atrial cardiopathy. Before exclusion, patients with atrial cardiopathy had a mean age of 77±5.2 years and 56% were women, and those without atrial cardiopathy had a mean age of 74±4.6 years and 60.1% were women. Of the cohort, 478 participants had atrial cardiopathy when 2 or more biomarkers were required to be present.

A total of 763 participants had dementia after visit 5 through the end of the follow-up, and the mean time at risk was 6.12 years. The absolute incidence rates of dementia were increased in participants with atrial cardiopathy (3.69 per 1000 person-years) vs those without atrial cardiopathy (1.86 per 1000 person-years).

Atrial cardiopathy was significantly associated with an increased risk for dementia (hazard ratio [HR], 1.35; 95% CI, 1.16-1.58) compared with not having atrial cardiopathy after adjustment for confounders in the primary analysis of the full cohort at visit 5.

The association was stronger with use of a stricter definition in which participants had to have 2 or more biomarkers to have a diagnosis of atrial cardiopathy with strengthening of the effect estimate (HR, 1.54; 95% CI, 1.25-1.89).

The findings were comparable in participants without a history of atrial fibrillation (AF) at visit 5 (n=4691). A significantly increased risk for dementia was found in participants with atrial cardiopathy (adjusted HR [aHR], 1.30; 95% CI, 1.10-1.53), with an attenuation of effect and slight widening of CIs when participants with prevalent AF were excluded.

When participants with prevalent AF or prevalent stroke were excluded, a significant association was still observed with an increased risk for dementia in those with atrial cardiopathy (aHR, 1.28; 95% CI, 1.09-1.52), with a similar magnitude of effect to the primary analysis. This finding also was observed when the stricter definition of atrial cardiopathy was used (aHR, 1.52; 95% CI, 1.19-1.95).

AF significantly mediated the association between atrial cardiopathy and incident dementia (P =.008), and the proportion of effect was 4% (0.0076/0.2017). The proportion of effect mediated by stroke was 9% (0.0015/0.0160, P =.048).

Among several study limitations, asymptomatic AF or silent cerebral infarction may have been missed, and another definition of atrial cardiopathy could be superior to the one that is used. Also, some participants who died without having dementia may have been censored before dementia was observed, and some participants with milder symptoms during the follow-up may have been missed. Furthermore, residual confounding and survival bias are possible.

“These findings reveal that a state of atrial cardiopathy, which precedes AF and stroke, contributes to the risk of dementia, independent of AF and stroke,” wrote the researchers. “We cautiously suggest that an understanding of this relationship might provide a basis for new interventional strategies to help thwart the development of dementia.”

Disclosure: One of the study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.

This article originally appeared on The Cardiology Advisor