ABSTRACT NUMBER: ESOC2026A2275 LIPOPROTEIN(A) AND COGNITIVE FUNCTION IN STROKE: RESULTS FROM THE DEMDAS COHORT STUDY

Abstract Background and aims Elevated Lipoprotein(a) [Lp(a)] levels are associated with a higher stroke risk, yet the relationship with post-stroke cognitive impairment remains unclear. We investigated the association of Lp(a) with cognitive outcomes up to five years after stroke. Methods In this predefined, exploratory analysis of the German Center for Neurological Diseases mechanisms of dementia after stroke (DEMDAS) study (NCT01334749) 599 stroke patients received comprehensive assessments at 6, 12, 36 and 60 months. Cognitive function was assessed in five domains (language, memory, executive function, attention, visuospatial ability). We compared the highest baseline serum Lp(a) quartile with the lower three quartiles and patients with Lp(a)>125nmol/l with lower levels. Multiple linear regression models adjusted for age, sex, education, and stroke severity were performed for each domain at each follow-up. Results In ischemic stroke patients(n=583), Lp(a) was measured in n=498 patients(85.4%; 33% female, mean age: 67.7±11.4 years, median acute NIHSS: 3[IQR1–5]). Median Lp(a) was 19.6(IQR7.4–62.5) nmol/l. Compared with lower quartiles, the highest quartile had statistically significantly lower executive function scores at 6 months(95%CI= -0.52to-0.00;p=0.048). Patients with Lp(a)>125nmol/l(n=63) had lower global cognitive function at 36 months (95%CI=-0.41to-0.01,p=0.036). Complete results for all prespecified variables will be presented at the conference. Conclusions Higher Lp(a) levels were associated with poorer executive function at 6 months and lower global cognition at 36 months after ischemic stroke, suggesting Lp(a) may contribute to post-stroke cognitive decline. Conflict of interest Charlotte Pietrock: nothing to disclose. Xenia Krentz: nothing to disclose. Karin Waegemann: nothing to disclose. Silke Wunderlich: nothing to disclose. Michael Goertler: nothing to disclose. Inga Zerr: nothing to disclose. Gabor Petzold: nothing to disclose. Martin Dichgans: nothing to disclose. Matthias Endres: reports grants from Bayer and Ipsen and fees paid to the Charité from Amgen, AstraZeneca, Bayer Healthcare, BMS, Daiichi Sankyo, all outside the submitted work; A. H. Nave reports on research funding from the Corona Foundation and German Center for Cardiovascular Research (DZHK), as well as on honoraria from Ipsen, Novartis and BMS for lectures and consulting activities, all of which are unrelated to the submitted work. Alexander Nave: AHN has received funding from the Corona Foundation, the German Center for Cardiovascular Research (DZHK), and the Else Kröner-Fresenius-Stiftung (EKFS); and has received honoraria from Novartis, Pvzer/BMS, and Ipsen Pharma, all outside the submitted work.