Work

Association Between Stroke Lesion Size and Atrial Fibrillation Detected After Stroke: An Observational Cohort Study

Year: 2024

Type: article

Abstract: Background Atrial fibrillation detected after stroke (AFDAS) is considered to be a distinct entity influenced by cardiogenic and neurogenic factors. We hypothesized that patients with AFDAS have larger stroke lesions than patients without atrial fibrillation (AF) and with known AF (KAF). Methods and Results Consecutive patients with magnetic resonance imaging–confirmed acute ischemic stroke admitted to a university hospital between October 2020 and January 2023 were prospectively registered. We categorized patients as AFDAS, no AF or KAF upon hospital discharge. We manually segmented diffusion‐weighted imaging lesions to determine lesion volume. We analyzed 1420 patients (median age, 78; 47.2% women, median National Institutes of Health Stroke Scale score, 3; median hospital stay, 5 days). Of these, 81 had AFDAS (5.7%), 329 had KAF (23.2%) and 1010 had no AF (71.1%). Lesion volume was larger in patients with AFDAS (median, 5.4 mL [interquartile range, 1.0–21.6]) compared with patients with no AF and KAF (median, 0.7 [interquartile range,0.2–4.4] and 2.0 [interquartile range,0.3–11.1] mL, respectively; both P <0.001). Lesion volume was independently associated with AFDAS compared with no AF (adjusted odds ratio, 1.37 [95% CI, 1.20–1.58] per log mL) and KAF (adjusted odds ratio, 1.22 [95% CI, 1.07–1.41] per log mL). Patients in the highest lesion volume quartile (>6.5 mL) were more likely to be diagnosed with AFDAS compared with the lowest quartile (<0.22 mL, 13.6% versus 2.1%; adjusted odds ratio, 5.88 [95% CI, 2.30–17.40]). These associations were more pronounced when excluding 151 patients with nonembolic lesion pattern and similar when excluding 199 patients with KAF on oral anticoagulation. Conclusions Larger stroke lesions were independently associated with AFDAS diagnosis during index stroke hospitalization highlighting a potential neurogenic contribution to AFDAS pathogenesis.

Source: Journal of the American Heart Association

DOI: 10.1161/jaha.124.035285