Markus Arnold1, Juliane Schweizer1, Christos T Nakas2,3, Valerie Schütz1, Laura P Westphal1, Corinne Inauen1, Thomas Pokorny1, Andreas Luft1, Alexander Leichtle2, Marcel Arnold4, Antonela Bicvic1,4, Urs Fischer4, Gian Marco De Marchis5, Leo H Bonati5, Mandy D Müller5, Timo Kahles6, Krassen Nedeltchev6, Carlo W Cereda7, Georg Kägi8, Alejandro Bustamante9, Joan Montaner9, George Ntaios10, Christian Foerch11, Katharina Spanaus12, Arnold von Eckardstein12, Mira Katan1. 1. Department for Neurology, University Hospital Zurich, Zurich, Switzerland. 2. Department of Clinical Chemistry, Inselspital, University Hospital and University of Bern, Bern, Switzerland. 3. Laboratory of Biometry, University of Thessaly, Volos, Greece. 4. Department for Neurology, Inselspital, University Hospital and University of Bern, Bern, Switzerland. 5. Department for Neurology & Stroke Center, University Hospital of Basel & University of Basel, Basel, Switzerland. 6. Department of Neurology, Cantonal Hospital Aarau, Switzerland. 7. Neurocentro della Svizzera Italiana, Stroke Center EOC, Lugano, Switzerland. 8. Department of Neurology, Cantonal Hospital St, Gallen, Switzerland. 9. Department for Neurology, Vall d'Hebron Institute of Research (VHIR), Universitat Autónoma de Barcelona, Spain. 10. Department of Internal Medicine, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece. 11. Department of Neurology, University Hospital of Frankfurt, Frankfurt am Main, Germany. 12. Institute of Clinical Chemistry, University Hospital Zurich, Zurich, Switzerland.
Abstract
AIMS: Lipoprotein(a) [Lp(a)] is a recognized causal risk factor for atherosclerotic cardiovascular disease but its role for acute ischaemic stroke (AIS) is controversial. In this study, we evaluated the association of Lp(a) with large artery atherosclerosis (LAA) stroke and risk of recurrent cerebrovascular events in AIS patients. METHODS AND RESULTS: For this analysis of the prospective, observational, multicentre BIOSIGNAL cohort study we measured Lp(a) levels in plasma samples of 1733 primarily Caucasian (98.6%) AIS patients, collected within 24 h after symptom onset. Primary outcomes were LAA stroke aetiology and recurrent cerebrovascular events (ischaemic stroke or transient ischaemic attack) within 1 year. We showed that Lp(a) levels are independently associated with LAA stroke aetiology [adjusted odds ratio 1.48, 95% confidence interval (CI) 1.14-1.90, per unit log10Lp(a) increase] and identified age as a potent effect modifier (Pinteraction =0.031) of this association. The adjusted odds ratio for LAA stroke in patients aged <60 years was 3.64 (95% CI 1.76-7.52) per unit log10Lp(a) increase and 4.04 (95% CI 1.73-9.43) using the established cut-off ≥100 nmol/l. For 152 recurrent cerebrovascular events, we did not find a significant association in the whole cohort. However, Lp(a) levels ≥100 nmol/l were associated with an increased risk for recurrent events among patients who were either <60 years [adjusted hazard ratio (HR) 2.40, 95% CI 1.05-5.47], had evident LAA stroke aetiology (adjusted HR 2.18, 95% CI 1.08-4.40), or had no known atrial fibrillation (adjusted HR 1.60, 95% CI 1.03-2.48). CONCLUSION: Elevated Lp(a) was independently associated with LAA stroke aetiology and risk of recurrent cerebrovascular events among primarily Caucasian individuals aged <60 years or with evident arteriosclerotic disease. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Lipoprotein(a) [Lp(a)] is a recognized causal risk factor for atherosclerotic cardiovascular disease but its role for acute ischaemic stroke (AIS) is controversial. In this study, we evaluated the association of Lp(a) with large artery atherosclerosis (LAA) stroke and risk of recurrent cerebrovascular events in AISpatients. METHODS AND RESULTS: For this analysis of the prospective, observational, multicentre BIOSIGNAL cohort study we measured Lp(a) levels in plasma samples of 1733 primarily Caucasian (98.6%) AISpatients, collected within 24 h after symptom onset. Primary outcomes were LAA stroke aetiology and recurrent cerebrovascular events (ischaemic stroke or transient ischaemic attack) within 1 year. We showed that Lp(a) levels are independently associated with LAA stroke aetiology [adjusted odds ratio 1.48, 95% confidence interval (CI) 1.14-1.90, per unit log10Lp(a) increase] and identified age as a potent effect modifier (Pinteraction =0.031) of this association. The adjusted odds ratio for LAA stroke in patients aged <60 years was 3.64 (95% CI 1.76-7.52) per unit log10Lp(a) increase and 4.04 (95% CI 1.73-9.43) using the established cut-off ≥100 nmol/l. For 152 recurrent cerebrovascular events, we did not find a significant association in the whole cohort. However, Lp(a) levels ≥100 nmol/l were associated with an increased risk for recurrent events among patients who were either <60 years [adjusted hazard ratio (HR) 2.40, 95% CI 1.05-5.47], had evident LAA stroke aetiology (adjusted HR 2.18, 95% CI 1.08-4.40), or had no known atrial fibrillation (adjusted HR 1.60, 95% CI 1.03-2.48). CONCLUSION: Elevated Lp(a) was independently associated with LAA stroke aetiology and risk of recurrent cerebrovascular events among primarily Caucasian individuals aged <60 years or with evident arteriosclerotic disease. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Paul Philipp Heinisch; Maks Mihalj; Markus Huber; Joerg C Schefold; Alexander Hartmann; Michael Walter; Elisabeth Steinhagen-Thiessen; Juerg Schmidli; Frank Stüber; Lorenz Räber; Markus M Luedi Journal: Cells Date: 2021-10-21 Impact factor: 6.600
Authors: Jun-Xu Gu; Juan Huang; Shan-Shan Li; Li-Hua Zhou; Ming Yang; Yang Li; Ai-Min Zhang; Yue Yin; Na Zhang; Mei Jia; Ming Su Journal: Sci Rep Date: 2022-03-04 Impact factor: 4.379