Specific inflammatory profile of acute ischemic stroke patients with left atrial enlargement

Front Cardiovasc Med. 2023 Jul 19:10:1190857. doi: 10.3389/fcvm.2023.1190857. eCollection 2023.

Abstract

Background: The inflammatory process underlying atrial myopathy may affect the inflammatory response activated in acute ischemic stroke (AIS).

Objectives: We aimed to assess whether left atrial enlargement (LAE) as a marker of atrial myopathy is associated with a different profile of circulating inflammatory markers in AIS patients.

Methods: HIBISCUS-STROKE is a cohort study including anterior circulation AIS patients treated with mechanical thrombectomy following MRI. Ten circulating inflammatory markers were measured at admission and 6, 24, and 48 h after admission. LAE was defined as a left atrial volume index (LAVi) ≥34 ml/m2. A multiple logistic regression model was performed to detect an independent association between the area under the curve (AUC) of these markers and LAE.

Results: We included 143 patients. Of them, 85 (59.4%) had LAE. On univariable analysis, we found that patients with LAE had higher soluble form suppression of tumorigenicity 2 (sST2), soluble tumor necrosis factor receptor I (sTNFR1), and vascular cellular adhesion molecule-1 (VCAM-1) AUC, were older, mostly female, had a higher National Institutes of Health Stroke Scale (NIHSS) score and blood glucose level at admission, had more often hypertension, and a cardioembolic source of AIS, such as atrial fibrillation, while they were less frequently current smokers and had a lower rate of tandem occlusion than patients without LAE. On multivariable analysis, we found that among circulating inflammatory markers, only high VCAM-1 (OR: 9.13, 95% CI: 3.21-25.9) and sST2 (OR: 3.40, 95% CI: 1.68-6.86) AUC remained associated with LAE.

Conclusions: High VCAM-1 and sST2 levels within the first 48 h are associated with LAE in AIS patients.

Keywords: SST2; VCAM-1; inflammatory; ischemic stroke; left atrial enlargement.

Grants and funding

This work was supported by the RHU MARVELOUS (ANR-16-RHUS-0009) of Université de Lyon, within the program “Investissements d'Avenir” operated by the French National Research Agency.