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London, United Kingdom 2013 Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 527 453 Small vessel stroke and white matter disease The Ambulatory Arterial Stiffness Index is not associated with markers of cerebral small ves-sel disease in first-ever lacunar stroke patients P. Klarenbeek1, R.J. van Oostenbrugge2, J. Staals3 Maastricht University Medical Centre, Maastricht, THE NETHERLANDS1, Maastricht Uni-versity Medical Centre, Maastricht, THE NETHERLANDS2, Maastricht University Medical Centre, Maastricht, THE NETHERLANDS3 Background In recent years, the ambulatory arterial stiffness index (AASI) was introduced as a novel measure representing the dynamic relationship between systolic and diastolic blood pressure (BP). Although it was introduced as a measure of arterial stiffness, the exact pathophysiological background of this index remains unclear. This measure consistently predicts cardiovascular outcome (especially stroke) and is associated with target organ damage in kidney and heart. Because of the association with microvascular damage in other organs we hypothesized that AASI would be associated with markers of cerebral small vessel disease on brain MRI in lacunar stroke patients. Methods We performed 24-hour ambulatory BP monitoring and brain MR in 129 first-ever lacunar stroke pa-tients. AASI was defined as 1 minus the regression slope of diastolic on systolic BP values derived from the 24-hour BP data. In logistic regression analyses, we investigated the association of the AASI (as a continuous variables and in tertiles) with the presence of different MRI markers of cere-bral small vessel disease. Results Asymptomatic lacunar infarcts, white matter lesions, enlarged basal ganglia perivascular spaces and deep cerebral microbleeds were present in 82 (63%), 41 (32%), 83 (64%) and 24 (19%) patients re-spectively. 24-hour systolic and diastolic BP levels were associated with the presence of asymptom-atic lacunar infarcts, enlarged perivascular spaces and deep cerebral microbleeds, but not with white matter lesions. AASI was associated with white matter lesions in unadjusted analyses, but not after correction for age and sex. The other MRI markers were not associated with AASI. Conclusion We found no association of the AASI with MRI markers of cerebral small vessel disease. A possible explanation is that other factors, such as systemic vascular resistance, influence AASI. Our study suggests that AASI has no added value over standard 24-hour BP monitoring in cerebral small ves-sel disease. 454 Small vessel stroke and white matter disease Do reduced leptomeningeal collaterals in humans result in leukoaraiosis, lacunes and brain at-rophy? V. Nambiar1, O. Volny2, S.I. Sohn3, M. Goyal4, A.M. Demchuk5, B.K. Menon6 University of Calgary, Calgary, CANADA1, University of Calgary, Calgary, CANADA2, Keimyung University, Daegu, SOUTH KOREA3, University of Calgary, Calgary, CANADA4, Uni-versity of Calgary, Calgary, CANADA5, University of Calgary, Calgary, CANADA6 Introduction: We seek to identify if reduction in leptomeningeal collaterals results in leukoaraiosis, lacunar disease and brain atrophy. In addition, we seek to explore an association between amyloid angiopathy and reduced leptomeningeal collaterals. Methods: Data are from the Keimyung Stroke Registry. Consecutive patients with M1 segment mid-dle cerebral artery (MCA) ± intracranial internal carotid artery (ICA) occlusions on baseline CT-an-giography (CTA) from May 2004 to July 2009 were included. Only patients with baseline CTA and MRI (FLAIR, T1 and GRE) were included in the current study. Two raters assessed leptomeningeal collaterals on baseline CTA by consensus, using a previously validated regional leptomeninge-al score (rLMC). Brain volume=(FLAIR hemispheric volume – FLAIR intraventricular volume) / (Total intracranial volume on CT), volume of periventricular hyperintensity on FLAIR (PVH), number of lacunes (T1) and microbleeds (GRE) were assessed by consensus, blinded to collateral assessment. Brain volumes were measured using Quantomo and data analyzed using Stata 12.1. Results: Baseline characteristics (n=120) were: mean age 67.3 years, median baseline NIHSS 14 (IQR 10) and median stroke symptom onset to CTA 118.5 minutes (IQR 117). There was a signifi-cant difference in PVH in those with poor collateral status vs. those without (median volume 7. 5 ml vs 4.4 ml, p=0.04). No difference was noted in brain volume, number of lacunes or number of mi-crobleeds by collateral status. (Table 1) Nonetheless, we noted significant correlation between brain volume, PVH and number of lacunes. (Table 2) Cerebral microbleeds were not associated with col-lateral status, PVH, brain atrophy and lacunes. Conclusion: Our results establish an association between poor collateral status and leukoaraiosis. Correlation between leukoaraiosis, brain atrophy and number of lacunes points towards a common pathophysiological mechanism with reduced collateral status potentially being causal.


Karger_ESC London_2013
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