Apostolos Safouris1, Christos Krogias1, Vijay K Sharma1, Aristeidis H Katsanos1, Simon Faissner1, Andromachi Roussopoulou1, Christina Zompola1, Janina Kneiphof1, Odysseas Kargiotis1, Spyridon Deftereos1, Georgios Giannopoulos1, Nikos Triantafyllou1, Konstantinos Voumvourakis1, Konstantinos Vadikolias1, Georgios Tsivgoulis2. 1. From the Second Department of Neurology, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens, Greece (A.S., A.H.K., A.R., C.Z., K.V., G.T.); Acute Stroke Unit, Metropolitan Hospital, Pireus, Greece (A.S., O.K.); Department of Neurology, St. Josef-Hospital, Ruhr University, Bochum, Germany (C.K., S.F., J.K.); Yong Loo Lin School of Medicine, National University of Singapore (V.K.S.); Division of Neurology, National University Hospital, Singapore (V.K.S.); Department of Neurology, University Hospital of Ioannina, School of Medicine, University of Ioannina, Greece (A.H.K.); Second Department of Cardiology, Attikon University Hospital, National and Kapodistrian University of Athens, Greece (S.D., G.G.); First Department of Neurology, University of Athens, School of Medicine, Eginition University Hospital, Greece (N.T.); and Department of Neurology, Alexandroupolis University Hospital, School of Medicine, Democritus University of Thrace, Greece (K.V.). 2. From the Second Department of Neurology, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens, Greece (A.S., A.H.K., A.R., C.Z., K.V., G.T.); Acute Stroke Unit, Metropolitan Hospital, Pireus, Greece (A.S., O.K.); Department of Neurology, St. Josef-Hospital, Ruhr University, Bochum, Germany (C.K., S.F., J.K.); Yong Loo Lin School of Medicine, National University of Singapore (V.K.S.); Division of Neurology, National University Hospital, Singapore (V.K.S.); Department of Neurology, University Hospital of Ioannina, School of Medicine, University of Ioannina, Greece (A.H.K.); Second Department of Cardiology, Attikon University Hospital, National and Kapodistrian University of Athens, Greece (S.D., G.G.); First Department of Neurology, University of Athens, School of Medicine, Eginition University Hospital, Greece (N.T.); and Department of Neurology, Alexandroupolis University Hospital, School of Medicine, Democritus University of Thrace, Greece (K.V.). tsivgoulisgiorg@yahoo.gr.
Abstract
OBJECTIVE: Although statin pretreatment (SP) is associated with better outcomes in patients with acute cerebral ischemia after an ischemic stroke/transient ischemic attack, data on the underlying mechanism of this beneficial effect are limited. APPROACH AND RESULTS: We sought to evaluate the potential association between SP and microembolic signal (MES) burden in acute cerebral ischemia because of large artery atherosclerosis (LAA). We prospectively evaluated consecutive patients with first-ever acute cerebral ischemia because of LAA in 3 tertiary stroke centers over a 2-year period. All patients underwent continuous 1-hour transcranial Doppler monitoring of the relevant vessel at baseline (≤24 hours). SP was recorded and dichotomized as high dose or low-to-moderate dose. SP was documented in 43 (41%) of 106 LAA patients (mean age, 65.4±10.3 years; 72% men; low-to-moderate dose, 32%; high dose, 8%). There was a significant (P=0.022) dose-dependent effect between SP and MES prevalence: no SP (37%), SP with low-to-moderate dose (18%), and SP with high dose (0%). Similarly, a significant (P=0.045) dose-dependent effect was documented between SP and MES burden: no SP (1.1±1.8), SP with low-to-moderate dose (0.7±1.6), and SP with high dose (0±0). In multivariable logistic regression analysis adjusting for demographics, vascular risk factors, location of LAA, stroke severity, and other prevention therapies, SP was associated with lower likelihood of MES presence (odds ratio, 0.29; 95% confidence interval, 0.09-0.92; P=0.036). In addition, SP was found also to be independently related to higher odds of functional improvement (common odds ratio, 3.33; 95% confidence interval, 1.07-10.0; P=0.037). CONCLUSIONS: We found that SP in patients with acute LAA is related with reduced MES presence and lower MES burden with an apparently dose-dependent association.
OBJECTIVE: Although statin pretreatment (SP) is associated with better outcomes in patients with acute cerebral ischemia after an ischemic stroke/transient ischemic attack, data on the underlying mechanism of this beneficial effect are limited. APPROACH AND RESULTS: We sought to evaluate the potential association between SP and microembolic signal (MES) burden in acute cerebral ischemia because of large artery atherosclerosis (LAA). We prospectively evaluated consecutive patients with first-ever acute cerebral ischemia because of LAA in 3 tertiary stroke centers over a 2-year period. All patients underwent continuous 1-hour transcranial Doppler monitoring of the relevant vessel at baseline (≤24 hours). SP was recorded and dichotomized as high dose or low-to-moderate dose. SP was documented in 43 (41%) of 106 LAA patients (mean age, 65.4±10.3 years; 72% men; low-to-moderate dose, 32%; high dose, 8%). There was a significant (P=0.022) dose-dependent effect between SP and MES prevalence: no SP (37%), SP with low-to-moderate dose (18%), and SP with high dose (0%). Similarly, a significant (P=0.045) dose-dependent effect was documented between SP and MES burden: no SP (1.1±1.8), SP with low-to-moderate dose (0.7±1.6), and SP with high dose (0±0). In multivariable logistic regression analysis adjusting for demographics, vascular risk factors, location of LAA, stroke severity, and other prevention therapies, SP was associated with lower likelihood of MES presence (odds ratio, 0.29; 95% confidence interval, 0.09-0.92; P=0.036). In addition, SP was found also to be independently related to higher odds of functional improvement (common odds ratio, 3.33; 95% confidence interval, 1.07-10.0; P=0.037). CONCLUSIONS: We found that SP in patients with acute LAA is related with reduced MES presence and lower MES burden with an apparently dose-dependent association.
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