Key result
Lower LA conduit function linked to ~39% higher risk of cortical brain infarcts per SD.
Why the study?
Atrial cardiomyopathy has been associated with ischemic stroke, but whether its markers are independently associated with specific incident brain infarct subtypes of probable embolic etiology remained unclear.
Do markers of atrial cardiomyopathy associate independently with incident cortical and non-cortical brain infarct subtypes on MRI in older adults?
Cohort (n=780)
Yes
Do markers of atrial cardiomyopathy associate independently with incident cortical and non-cortical brain infarct subtypes on MRI in older adults?
Impaired left atrial conduit function is independently associated with incident MRI-defined cortical brain infarcts and greater cortical infarct burden, supporting a specific link between atrial cardiomyopathy and cardioembolic brain infarcts even in the absence of prevalent atrial fibrillation.
May aid cortical infarct risk stratification in AF; extends atrial cardiomyopathy data but should not yet change practice.
Background Atrial cardiomyopathy, characterized by structural and electromechanical abnormalities of the left atrium, has been associated with ischemic stroke. However, its relationship with specific brain infarct subtypes remains unclear. Purpose To determine whether markers of atrial cardiomyopathy are independently associated with incident brain infarct subtypes related to a probable embolic aetiology. Methods We studied participants from the Atherosclerosis Risk in Communities (ARIC) Study who attended Visit 5 (2011–2013) and had brain MRI at Visit 5 with at least one follow-up brain MRI through 2025. At Visit 5, the following were assessed: Left atrial (LA) structure and function, using echocardiographic volume and strain parameters, electrocardiographic P-wave parameters, and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Incident infarcts were identified on follow-up brain MRI using standardized ARIC protocols and classified as cortical or non-cortical. Multivariable logistic regression was used to evaluate associations with incident brain infarcts, and Poisson regression was used to assess infarct burden. Results Among 780 participants (mean [SD] age 74 [5] years at Visit 5, 58% women, 27% Black), at least one incident cortical infarct was detected in 78 individuals (10%), 37 of whom had >1 infarct. At least one non-cortical infarct was detected in 158 individuals (20%). In multivariable models adjusted for CHA₂DS₂-VA score, sex, smoking, creatinine and left ventricular ejection fraction, lower LA conduit function (expressed as absolute value) was independently associated with incident cortical infarcts (OR per 1-SD decrease 1.39, 95% CI 1.04-1.89, p=0.03; Figure 1). Each 1-SD decrease in the absolute value of LA conduit strain was associated with a 67% higher expected number of cortical infarcts (incidence rate ratio 1.67, 95% CI 1.22–2.29, p =0.001). LA conduit < 11.0%, a cut-off proposed by a previous ARIC analysis,1 was present in 25% of patients and was associated with a 112% increase in the risk of incident cortical infarcts (OR 2.12, 95% CI 1.30-3.45, p<0.01). Findings were consistent in sensitivity analyses restricted to participants free of prevalent atrial fibrillation. No significant associations were observed for non-cortical infarcts (Figure 1). Conclusions Among multiple markers of atrial cardiomyopathy, impaired LA conduit is associated with MRI-defined brain infarcts with a probable embolic origin and greater infarct burden. These findings support a specific link between atrial cardiomyopathy and cardioembolic brain infarcts.
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Masini et al. (2026) conducted a cohort in Atrial cardiomyopathy and incident brain infarcts (n=780). Lower left atrial conduit function (per 1-SD decrease) vs. Higher left atrial conduit function was evaluated on Incident cortical brain infarcts (OR 1.39, 95% CI 1.04-1.89, p=0.03). Lower left atrial conduit function was independently associated with incident cortical brain infarcts (OR per 1-SD decrease 1.39, 95% CI 1.04-1.89, p=0.03), but not non-cortical infarcts.
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