ABSTRACT NUMBER: ESOC2026A2241 CARDIAC TROPONIN AS A BIOMARKER OF ACUTE ISCHAEMIC STROKE SUBTYPE

Abstract Background and aims Atrial dysfunction or cardiomyopathy, defined by the presence of specific serum biomarkers, ECG findings, or echocardiographic findings, increase the risk of atrial fibrillation, which has been implicated as a key risk factor for ischaemic stroke. There is now growing body of evidence which suggest that early positive troponin after ischaemic stroke may be independently associated with a cardiac embolic source. We hypothesize that early elevated troponin is a predictor of cardiac source of embolus in patients with embolic stroke subtypes (cardioembolic stroke (CE) and embolic stroke of unknown source (ESUS)) as compared with non-cardioembolic stroke subtypes (NCE). Methods Data was retrospectively extracted from patients recruited to the MiND study with confirmed diagnosis of acute ischaemic stroke within 12 hours of symptoms onset having also undergone high-sensitivity troponin testing. Data were dichotomised as normal troponin (<14ng/L) and elevated troponin (≥14ng/L). Results Univariate regression analysis revealed a significant association between elevated troponin and severe stroke (admission NIHSS >12, (OR(CI), 4.13(1.21–14.09), p=0.024)), and unfavourable outcome (day 7 mRS >2, (OR(CI), 3.47(1.04–11.55), p=0.042)). Unadjusted logistic regression analysis revealed a positive association between CE stroke subtype and elevated troponin (OR(CI), 3.94(1.20–12.17), p=0.024) and a negative association between elevated troponin and NCE (OR(CI), 0.63 (0.18-2.17), p=0.46), and ESUS (OR(CI), 0.24(0.05-1.21), p=0.08) stroke subtypes. Conclusions Our analysis suggests potential utility of early elevated troponin after ischaemic stroke as a biomarker of cardioembolic subtype. Conflict of interest Jorin Bejleri: nothing to disclose; Karen Doyle: nothing to disclose; David J Williams: nothing to disclose; Shona Pfeiffer: nothing to disclose