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22. European Stroke Conference 11 Etiology of stroke and risk factors B 16:40 - 16:50 Do blood biomarkers predict long term risk of recurrent vascular events? H.C. Segal1, A.I. Burgess2, D.L. Poole3, L.E. Silver4, Z. Mehta5, P.M. Rothwell6 Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, Univer-sity of Oxford, Oxford, UNITED KINGDOM1,Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM2, Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM3, Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM4, Stroke Pre-vention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM5, Stroke Prevention Research Unit, Nuffield Department of Clin-ical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM6 BACKGROUND: There are few validated tools for prediction of the long term risk of recurrent stroke and other vascular events after TIA or stroke, partly because traditional vascular risk fac-tors appear to be of limited prognostic value. We aimed to determine whether a panel of blood biomarkers might help long-term prognostication. METHODS: We studied 14 haemostatic, in-flammatory and cell damage biomarkers (table 1A) in consecutive patients with TIA and stroke in a population-based study (Oxford Vascular Study). These were measured in plasma using an automated coagulation analyser (Sta, Stago, Asniers, France) and commercial enzyme immuno-assay systems including the Randox biochip analyser (Randox Laboratories Ltd, Co. Antrium, UK). Levels of biomarkers in the whole cohort and separately in TIA, minor stroke (NIHSS score ≤3) and major stroke were related to the 5 year risk (hazard ratio per decile increase in biomarker level) of recurrent stroke or MI after adjustment for age and sex. RESULTS: 1206 patients with biomarkers measured at baseline had 151 recurrent strokes and 41 MI during 5-year follow-up. Table 1A shows that CRP (HR= 1.08, 95%CI 1.01-1.16, p=0.025) and IL6 (1.08, 1.02-1.15, p=0.01) predicted recurrent stroke, although most of their value derived from patients with major stroke at baseline. Otherwise, only D-dimer predicted recurrent stroke after TIA (1.16, 1.02-1.33, p=0.026), but showed no association with recurrent stroke after minor or major stroke. For prediction of MI (table 1B), only IL-6 (1.17, 10.04-1.32, p=0.01) and NGAL (1.14, 1.00-1.29, p= 0.049) were predictive overall. CONCLUSION: In the first large popula-tion- based study of this type, we found that IL-6 showed some potential for prediction of both recurrent stroke and MI independently of age and sex. Further research is required to validate these observations and to see whether predictive value adds to simple clinical predictors. 16:30-18:00 Oral Session Room 9,10 Etiology of stroke and risk factors B Chairs: A. Carolei, Italy and E. Berge, Norway 10 Etiology of stroke and risk factors B 16:30 - 16:40 Clinical and physiological validity of maximum blood pressure on multi-day home mea-surement versus single-day ambulatory monitoring: frequency versus duration? A.J.S. Webb1, M Wilson2, NLM Paul3, U Fischer4, P.M. Rothwell5 Stroke Prevention Research Unit, Department of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM1,Stroke Prevention Research Unit, Department of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM2, Stroke Pre-vention Research Unit, Department of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM3, Stroke Prevention Research Unit, Department of Clinical Neuroscienc-es, University of Oxford, Oxford, UNITED KINGDOM4, Stroke Prevention Research Unit, De-partment of Clinical Neurosciences, University of Oxford, Oxford, UNITED KINGDOM5 BACKGROUND: Maximum (max) SBP predicts stroke independently of mean SBP when derived from several clinic visits, but not when derived from 24-h ambulatory monitoring (ABPM). It may be that single-day recording (i.e. ABPM) misses clinically important, physio-logically determined fluctuations seen over a longer period. We contrasted the validity of max SBP on high-frequency single-day ABPM vs prolonged home Bluetooth monitoring (HBPM) by the strength of their associations with hypertensive arteriopathy (aortic stiffness), end-organ damage (creatinine and leukoaraiosis) and premorbid clinic BP. METHODS: Max SBP was determined in consecutive patients with TIA or minor stroke (Ox-ford Vascular Study) on 1-month (from day 7) HBPM (3 BPs, 3 times daily) and on 24-h ABPM at one month. Markers of arteriopathy were aortic stiffness (pulse wave velocity) and moderate/severe leukoaraiosis (MRI). Max premorbid SBP was based on all BPs in primary care over the last 10-years. Associations with max SBP were determined by linear and logistic regression. RESULTS: In 500 patients, max SBP on HBPM was associated with creatinine, but max SBP on ABPM was not (combined model with age and sex: r2=0.191 p<0.001 vs 0.046 p=0.25). Max SBP on HBPM was also more strongly associated with aortic stiffness (r2=0.05 p=0.006 vs 0.001 p=0.78), leukoaraiosis (HR per 10mmHg =1.24, 1.12-1.37 p<0.001 vs 1.02, 0.93-1.13 p=0.6), and premorbid max SBP (r2=0.165 p<0.0001 vs 0.017 p=0.008). The associations with max SBP on HBPM were partly accounted for by duration (1 vs 7 vs all days of monitoring): creatinine (r2= 0.12 vs 0.15 vs 0.19), aortic stiffness (r2=0.003 vs 0.03 vs 0.05), leukoaraiosis (HR 1.13 vs 1.22 vs 1.24) and premorbid max SBP (r2=0.10 vs 0.16 vs 0.17). CONCLUSIONS: Compared with ABPM, max SBP on HBPM is more strongly associated with markers of hypertension and end-organ damage, due mainly to the longer duration of recording, with implications for recurrent stroke risk stratification. 72 © 2013 S. Karger AG, Basel Scientific Programme


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