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The objective of this case report was to identify a second-hit gene that may promote Moyamoya disease (MMD)-like vascular formation in an individual having theWe performed magnetic resonance imaging and genetic analyses ofWe identified bilateral periventricular nodular heterotopia (PNH) as the cause of seizures and MMD-like vascular formation in the patient. The patient had theThe family study suggested that the

Background and purpose The impact of the paraoxonase-1 (PON1) polymorphism, Q192R, on platelet inhibition in response to clopidogrel remains controversial. We aimed to investigate the association between carrier status of PON1 Q192R and high platelet reactivity (HPR) with clopidogrel in patients undergoing elective neurointervention. Methods Post-clopidogrel platelet reactivity was measured using a VerifyNow® P2Y12 assay in P2Y12 reaction units (PRU) for consecutive patients before the treatment. Genotype testing was performed for PON1 Q192R and CYP2C19*2 and *3 (no function alleles), and *17. PRU was corrected on the basis of hematocrit. We investigated associations between factors including carrying ≥1 PON1 192R allele and HPR defined as original and corrected PRU ≥208. Results Of 475 patients (232 men, median age, 68 years), HPR by original and corrected PRU was observed in 259 and 199 patients (54.5% and 41.9%), respectively. Carriers of ≥1 PON1 192R allele more frequently had HPR by original and corrected PRU compared with non-carriers (91.5% vs 85.2%, P = 0.031 and 92.5% vs 85.9%, P = 0.026, respectively). In multivariate analyses, carrying ≥1 PON1 192R allele was associated with HPR by original (odds ratio [OR] 1.96, 95% confidence interval [CI] 1.03–3.76) and corrected PRU (OR 2.34, 95% CI 1.21–4.74) after adjustment for age, sex, treatment with antihypertensive medications, hematocrit, platelet count, total cholesterol, and carrying ≥1 CYP2C19 no function allele. Conclusions Carrying ≥1 PON1 192R allele is associated with HPR by original and corrected PRU with clopidogrel in patients undergoing elective neurointervention, although alternative results related to other genetic polymorphisms cannot be excluded.

Background: We aimed to clarify associations between pre-admission risk scores (CHADS2, CHA2DS2-VASc, and HAS-BLED) and 2-year clinical outcomes in ischemic stroke or transient ischemic attack (TIA) patients with non-valvular atrial fibrillation (NVAF) using a prospective, multicenter, observational registry. Methods: From 18 Japanese stroke centers, ischemic stroke or TIA patients with NVAF hospitalized within 7 days after onset were enrolled. Outcome measures were defined as death/disability (modified Rankin Scale score ≥3) at 2 years, 2-year mortality, and ischemic or hemorrhagic events within 2 years. Results: A total of 1,192 patients with NVAF (527 women; mean age, 78 ± 10 years), including 1,141 ischemic stroke and 51 TIA, were analyzed. Rates of death/disability, mortality, and ischemic or hemorrhagic events increased significantly with increasing pre-admission CHADS2 (p for trend p for trend = 0.024 for events), CHA2DS2-VASc (p for trend p for trend = 0.004 for death/disability, p for trend p for trend = 0.024 for events) scores. Pre-admission CHADS2 (OR per 1 point, 1.52; 95% CI 1.35–1.71; p p p = 0.016 for events), CHA2DS2-VASc (1.55, 1.41–1.72, p < 0.001; 1.21, 1.12–1.30, p < 0.001; 1.17, 1.07–1.27, p < 0.001; respectively), and HAS-BLED (1.33, 1.17–1.52, p < 0.001; 1.23, 1.10–1.38, p < 0.001; 1.18, 1.05–1.34, p = 0.008; respectively) scores were independently associated with all outcome measures. Conclusions: In ischemic stroke or TIA patients with NVAF, all pre-admission risk scores were independently associated with death/disability at 2 years and 2-year mortality, as well as ischemic or hemorrhagic events within 2 years.

Objective:\ud It is not known whether patients with atrial fibrillation (AF) with ischemic stroke despite oral anticoagulant therapy are at increased risk for further recurrent strokes or how ongoing secondary prevention should be managed.\ud \ud Methods:\ud We conducted an individual patient data pooled analysis of 7 prospective cohort studies that recruited patients with AF and recent cerebral ischemia. We compared patients taking oral anticoagulants (vitamin K antagonists [VKA] or direct oral anticoagulants [DOAC]) prior to index event (OACprior ) with those without prior oral anticoagulation (OACnaive ). We further compared those who changed the type (ie, from VKA or DOAC, vice versa, or DOAC to DOAC) of anticoagulation (OACchanged ) with those who continued the same anticoagulation as secondary prevention (OACunchanged ). Time to recurrent acute ischemic stroke (AIS) was analyzed using multivariate competing risk Fine-Gray models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).\ud \ud Results:\ud We included 5,413 patients (median age = 78 years [interquartile range (IQR) = 71-84 years]; 5,136 [96.7%] had ischemic stroke as the index event, median National Institutes of Health Stroke Scale on admission = 6 [IQR = 2-12]). The median CHA2 DS2 -Vasc score (congestive heart failure, hypertension, age≥ 75 years, diabetes mellitus, stroke/transient ischemic attack, vascular disease, age 65-74 years, sex category) was 5 (IQR = 4-6) and was similar for OACprior (n = 1,195) and OACnaive (n = 4,119, p = 0.103). During 6,128 patient-years of follow-up, 289 patients had AIS (4.7% per year, 95% CI = 4.2-5.3%). OACprior was associated with an increased risk of AIS (HR = 1.6, 95% CI = 1.2-2.3, p = 0.005). OACchanged (n = 307) was not associated with decreased risk of AIS (HR = 1.2, 95% CI = 0.7-2.1, p = 0.415) compared with OACunchanged (n = 585).\ud \ud Interpretation:\ud Patients with AF who have an ischemic stroke despite previous oral anticoagulation are at a higher risk for recurrent ischemic stroke despite a CHA2 DS2 -Vasc score similar to those without prior oral anticoagulation. Better prevention strategies are needed for this high-risk patient group.

Background We aimed to clarify associations between prior anticoagulation and short‐ or long‐term clinical outcomes in ischemic stroke or transient ischemic attack patients with nonvalvular atrial fibrillation. Methods and Results A total of 1189 ischemic stroke or transient ischemic attack patients with nonvalvular atrial fibrillation who were hospitalized within 7 days after onset were analyzed. Of these, 813 patients (68.4%) received no prior anticoagulation, 310 (26.1%) received prior warfarin treatment with an international normalized ratio ( INR ) INR ≥2 on admission, and the remaining 38 (3.2%) received prior direct oral anticoagulant treatment. Prior warfarin treatment was associated with a lower risk of death or disability at 3 months compared with no prior anticoagulation ( INR P =0.001; INR ≥2: adjusted odds ratio: 0.40; 95% CI, 0.16–0.97; P =0.043) but was not associated with a lower risk of death or disability at 2 years. Prior warfarin treatment with an INR ≥2 on admission was associated with a higher risk of ischemic events within 2 years compared with no prior anticoagulation (adjusted hazard ratio: 2.94; 95% CI, 1.20–6.15; P =0.021). Conclusions Prior warfarin treatment was associated with a lower risk of death or disability at 3 months but was not associated with a lower risk of death or disability at 2 years in ischemic stroke or transient ischemic attack patients with nonvalvular atrial fibrillation. Prior warfarin treatment with an INR ≥2 on admission was associated with a higher risk of ischemic events within 2 years. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unique identifier: NCT 01581502.

Background and purpose The aim of this study was to evaluate the anticoagulation intensity of dabigatran for acute ischemic stroke patients and hemorrhagic/ischemic events after early initiation of dabigatran. Methods Acute ischemic stroke/transient ischemic attack (TIA) patients admitted to our hospital who started dabigatran from January 2012 to December 2017 were studied. Blood samples were drawn just before (0 h) and 4 h after dabigatran at a median of 5 days after starting dabigatran to measure dabigatran concentrations (C0h, C4h) based on the thrombin clotting time assay (Hemoclot®). Results Of the 70 patients (54 men, 69 ± 9 y), 14 started dabigatran after a TIA, and 56 started it after an ischemic stroke a median of 5 days after onset. C0h, C4h was 82.5 ± 58.0, 143.1 ± 98.2 ng/dl (150 mg BID, 35 patients) and 50.6 ± 40.9, 91.2 ± 64.7 ng/ml (110 mg BID, 35 patients). During a median follow-up of 382 (IQR 109–688) days of all 70 patients, five had clinical events. Three patients had bleeding events, two with nasal bleeding (C0h, C4h: 50, 80 ng/ml, C0h, C4h: 91, 173 ng/ml) and one with GI bleeding (C0h, C4h: 5, 5 ng/ml). Two patients had ischemic events, one with ischemic stroke (C0h, C4h: 10, 50 ng/ml) and another with acute myocardial infarction (C0h, C4h: 40, 40 ng/ml). Conclusions There was no obvious relationship between dabigatran concentration and hemorrhagic/ischemic events in this study. Larger sample study will be needed to examine the relationship between the concentration and events in clinical practice.

BACKGROUND Measuring anti-Xa activity (AXA) has been reported as useful for predicting future risk of hemorrhagic and ischemic events in stroke patients taking direct factor Xa inhibitors. We evaluated AXA levels of rivaroxaban or apixaban in acute stroke patients with non-valvular atrial fibrillation. Methods and Results: This was a single-center, prospective, observational study. Consecutive patients with acute ischemic stroke or transient ischemic attack who were admitted within 7 days of onset and started taking rivaroxaban or apixaban for NVAF between January 2012 and April 2017 were enrolled. AXA was measured at 2 time points: just before (AXAtrough) and 4 h after (AXApeak) taking rivaroxaban or apixaban on the 2nd day or later of administration. Of 156 patients taking rivaroxaban, hemorrhagic events occurred in 13. Patients with hemorrhagic events had higher AXApeak than those without [median (interquartile range): 1.93 (1.11-3.75) vs. 1.35 (0.80-2.00) IU/mL; P

Background and purposeHemorrhagic complications during neurointerventional procedures have various etiologies and can result in severe morbidity and mortality. This study investigated the possible association between low platelet reactivity measured by the VerifyNow assay and increased hemorrhagic complications during elective neurointervention under dual antiplatelet therapy.MethodsFrom May 2010 to April 2013 we recorded baseline characteristics, P2Y12 reaction units (PRU), and aspirin reaction units using VerifyNow. The primary endpoint was post-procedural hemorrhagic complications.ResultsA total of 279 patients were enrolled and 31 major hemorrhagic complications (11.1%) were identified. From receiver-operating characteristic curve analysis, PRU values could discriminate between patients with and without major hemorrhagic complications (area under the curve 0.63). Aspirin reaction unit values had no association with the primary outcome. The optimal cut-off for the primary outcome (PRU ≤175) was used to identify the low platelet reactivity group. The incidence of hemorrhagic complications was 20.0% in this group and 8.9% in the non-low platelet reactivity group. Multivariate analysis identified low platelet reactivity as an independent predictor for hemorrhagic complications.ConclusionsThe risk of hemorrhagic complications during elective neurointervention including cerebral aneurysm coil embolization and carotid artery stenting under dual antiplatelet therapy is associated with the response to clopidogrel but not to aspirin. A PRU value of ≤175 discriminates between patients with and without hemorrhagic complications. Future prospective studies are required to validate whether a specific PRU value around 170–180 is predictive of hemorrhagic complications.

Blood pressure lowering is often performed as a part of general acute management in acute intracerebral hemorrhage (ICH) patients. The relationship between relative blood pressure reduction and clinical outcomes is not fully known.Hyperacute (3 h from onset) ICH patients with initial SBP more than 180 mmHg were included in the observational study. All patients received intravenous antihypertensive treatment based on a predefined protocol to lower and maintain SBP between 120 and 160 mmHg. The relative SBP reduction was defined as the ratio of SBP reduction to the admission SBP in the first 24 h, and associations between the relative SBP reduction and neurological deterioration (≥2 points decrease in the Glasgow Coma Scale score or ≥4 increase in the National Institutes of Health Stroke Scale score), hematoma expansion (33% increase), and unfavorable outcome (modified Rankin scale score 4-6 at 3 months) were assessed with multivariate logistic regression analyses.Of the 211 patients [81 women, median age 65 (interquartile range 58-74) years, and median initial National Institutes of Health Stroke Scale score 13 (8-17)] enrolled, 17 (8%) showed neurological deterioration, 36 (17%) showed hematoma expansion, and 87 (41%) had an unfavorable outcome. On multivariate regression analyses, relative SBP reduction was independently and inversely associated with neurological deterioration (odds ratio 0.053, 95% confidence interval 0.011-0.254 per 10% increment), hematoma expansion (0.289, 0.099-0.841), and unfavorable outcome (0.254, 0.095-0.680) after adjusting for known predictive factors.Insufficient relative SBP reduction after standardized antihypertensive therapy in hyperacute ICH was independently associated with poor clinical outcomes. Aggressive antihypertensive treatment may improve clinical outcomes.

For optimal acute stroke management and secondary prevention, discrimination of stroke etiology is crucial. We hypothesized that a low Alberta Stroke Program Early CT Score (ASPECTS) on diffusion-weighted imaging (DWI) immediately after stroke onset was associated with the presence of atrial fibrillation (AF).Consecutive patients admitted within 24h from stroke onset with an occlusion at the horizontal segment of the middle cerebral artery (M1) on initial MRA were retrospectively enrolled. AF was diagnosed based on continuous electrocardiogram monitoring during acute hospitalization or its confirmed history.Of the 206 patients (95 women, median age 77 [IQR 69-85] years, NIHSS score 18 [13-23]) enrolled, AF was identified in 138 patients (AF group): chronic AF in 89, known paroxysmal AF (pAF) in 13, and masked pAF on admission in 36. The ASPECTS score on the initial DWI, performed a median of 2.5h after onset, was lower in the AF group than in the others (4 [2-6] vs. 7 [4-8], p0.001). With the optimal cut-off value of ≤ 6 (sensitivity, 78%; specificity, 57%; area under the ROC curve, 0.682), DWI-ASPECTS was independently associated with the presence of any AF (OR 5.05, 95%CI 2.36 to 10.8), as well as the presence of any pAF (OR 8.64, 95%CI 3.00 to 24.9) and that of masked pAF on admission (OR 10.0, 95%CI 3.06 to 32.9).Extensive early ischemic change assessed by DWI-ASPECTS predicts the presence of AF, even initially masked pAF, in acute stroke patients with M1 occlusion.

Background and Purpose: The optimal timing and safety of early anticoagulation using non-vitamin K antagonist oral anticoagulants after acute stroke or transient ischemic attack (TIA) have not been fully investigated. The aims of this study were (1) to assess the risk-benefit profile of early apixaban initiation in stroke/TIA patients and (2) to determine the association between events and plasma concentration of the early apixaban exposure. Patients and Methods: We studied acute stroke/TIA patients with non-valvular atrial fibrillation admitted to our hospital and started apixaban from May 2013 to March 2015. The blood samples were drawn just before (0h) and 4 hours (4h) after taking apixaban median 5 (4-6) days of initiation to measure apixaban concentration (C0h, C4h) based on anti-FXa chromogenic assay. Results: Of a total 90 patients (66 men, 79±9 y), 8 started apixaban median 3 days (IQR 2-6 days) after TIA, 69 did apixaban median 5 (3-9) days after ischemic stroke, and 13 did median 6 (3-7) days after intracerebral hemorrhage. C0h/C4h was 214±112/320±136 ng/mL in total, 170±100/239±106 ng/ml in 54 patients taking 2.5 mg apixaban BID, and 243±110/375±128 ng/mL in 36 patients taking 5 mg BID. During acute hospitalization (median 19 days), one patient experienced non-fatal gastrointestinal (GI) bleeding (C0h/C4h; 551/546 ng/mL). For median 8.4 (IQR 3.3-12.2) month-follow up in 86 patients who continued apixaban after discharge, three had clinically relevant hemorrhages: 1 subdural hematoma (C0h/C4h; 110/170 ng/mL) and 2 GI bleeding events (331/642, 395/529 ng/mL). The rate of clinically relevant hemorrhages was 6.7 %/year overall. Both C0h and C4h were higher in four patients with bleeding than the others (mean C0h 347 versus 204 ng/mL; p=0.018, C4h 472 versus 308 ng/mL; p=0.012). The receiver operating characteristic curve analysis revealed that C0h over 331 ng/mL predicted the hemorrhagic events with sensitivity 75% and specificity 89% (AUC 0.75). None developed ischemic stroke/TIA during the same period. Conclusion: Early starting apixaban after acute stroke/TIA was safe. Bleeding events could occur in patients with trough apixaban exposure over 331 ng/mL.

Recent studies suggest that a thromboembolic disorder resembling heparin-induced thrombocytopenia (HIT), so-called spontaneous HIT syndrome, can occur in patients without any history of heparin exposure. It is likely due to anti-platelet factor 4 (PF4)/polyanion antibodies induced by other polyanions, such as bacterial surfaces and nucleic acids. We describe an atypical case of spontaneous HIT syndrome. A 70-year-old man suddenly presented with acute cerebral sinus thrombosis (CST). Soon after the initiation of unfractionated heparin (UFH) for the treatment of CST, his platelet count fell precipitously and he developed deep vein thrombosis, a clinical picture consistent with rapid-onset HIT but without any proximate episodes of heparin exposure, infection, trauma, surgery, or other acute illness. Antigen assays and a washed platelet activation assay indicated that the patient already possessed anti-PF4/heparin IgG antibodies with heparin-dependent platelet activation properties on admission. Cessation of UFH and initiation of argatroban resulted in prompt recovery of his platelet count without further thromboembolic events. We identified two similar cases in the literature. However, these patients do not meet the recently proposed criteria for spontaneous HIT syndrome. Even in atypical cases, however, inappropriate or delayed diagnosis of HIT appears to be associated with worse outcomes. We propose that these atypical cases should be included in the category of spontaneous HIT syndrome.

Objective: In Japan, low-dose rivaroxaban [15 mg o.d. and 10 mg o.d. only for CCr 30-49 mL/min] was approved for clinical use to NVAF patients, because of its unique pharmacokinetics in Japanese subjects showing higher rivaroxaban concentration than Caucasian subjects when using the same dosage and the results of the J-ROCKET AF trial (Hori M, et al: Circ J 2012). We aimed to determine the anticoagulation intensity of rivaroxaban and its determinant factors in Japanese NVAF patients, especially in those taking crushed tablets. Methods: Consecutive stroke patients with NVAF admitted between July 2012 and July 2013 were studied. Prothrombin time (PT, Recombiplastin/HemosIL®), activated partial thromboplastin time (aPTT, Actin/Sysmex®), and anti-Xa chromogenic assay (Stago®) were measured just before and 4h and 9 h after the administration at the steady state of rivaroxaban (mean 6th day). We calibrated its plasma concentration based on anti-Xa assay. Results: Of 104 patients (32 women, 74±9 y.o., BW 59±11 kg) involving 36 with CCr Conclusion: Nearly peak concentration of rivaroxaban was similar or a little lower than that in the ROCKET AF and J-ROCKET AF trials (Kaneko M, et al: Drug Metab Pharmacokinet 2013). Tablet crushing may decrease anticoagulation intensity.

Objective: We aimed to determine therapeutic effects of novel oral anticoagulants (NOACs) on cardiac thrombi in acute stroke. Methods: We studied consecutive acute ischemic stroke/TIA patients with non-valvular atrial fibrillation who started to take rivaroxaban or dabigatran and was diagnosed as having cardiac thrombi on transesophageal echocardiography (TEE) within 10 days after the admission between July 2012 and July 2013. All continued to take NOACs without additional antithrombotic agents. Plasma concentrations for rivaroxaban were calibrated based on anti-Xa chromogenic assay for rivaroxaban (Stago®) and thrombin clotting time assay for dabigatran (Hemoclot®) just before (trough) and 4h after medication (peak) at steady state. Results: Eight patients (7 men, 52-83 years old) were studied. Their BW ranged 41.0-88.8 kg, CHADS2 ranged 2-5, and NIHSS ranged 2-18. NOACs were initiated at median 3 days and TEE was performed at median 3 days after admission. As a NOAC, one patient took 15 mg o. d. of rivaroxaban, 5 took 10 mg o.d. of rivaroxaban (officially approved dose in Japan) and the other 2 took 110 mg b.i.d. of dabigatran. For all the patients, the thrombus was identified in the left atrial appendage with median size of 14.7 mm; two of them were hyperechoic, being judged as already-organized. In follow-up TEE examinations median 19 days after admission , 5 thrombi disappeared (rivaroxaban in 3, dabigatran in 2), 1 diminished in size (rivaroxaban), and the other 2, all being initially hyperechoic, did not change (rivaroxaban for both). For 6 patients with absolute/partial dissolution of the thrombi, median peak/trough concentrations of rivaroxaban were 69 (19-255)/10 (range10-20) ng/ml, and those of dabigatran were 100 (40-160)/40 (20-60) ng/ml, median peak/trough aPTT was 42/34.5 s in rivaroxaban users and 45/37 s in dabigatran users, and median peak/trough PT was 20.2/12.9 s and 15.3/13.3 s, respectively. Conclusion: Rivaroxaban and dabigatran have potential to resolve non-organized cardiac thrombi. Monotherapy using NOACs may be enough for early prevention of recurrent stroke in patients with cardioembolic stroke/TIA.

BACKGROUND and PURPOSE: Blood pressure (BP) lowering may be beneficial for patients with hyperacute intracerebral hemorrhage (ICH). Although several trials including INTERACT 2 and ATACH II have a design of the strict BP lowering during the initial 24 hours, shorter duration may be enough since active bleeding may not last 24 hours. We aimed to examine the associations between sequential systolic BP levels during antihypertensive treatment (AHT) and clinical outcomes in acute ICH patients. METHODS: Hyperacute (180 mmHg were registered in a prospective, multicenter, observational study, the SAMURAI-ICH study (Koga J Hypertens 2012;30:2357). All patients received intravenous AHT, based on a predefined standardized protocol to lower and maintain SBP between 120 and 160 mmHg using intravenous nicardipine. BPs were measured hourly in the initial 24 hours. The mean of 8 SBP levels during 1 to 8, 9 to 16, and 17 to 24 hours after the initiation of AHT were calculated, and referred to as the 1st, 2nd and 3rd mSBPs, respectively. The associations between mSBPs and neurological deterioration (a decrease of ≥2 in GCS or an increase of ≥4 in NIHSS score), hematoma expansion (>33% in volume), and unfavorable outcome (modified Rankin Scale score 4-6 at 3 months) were assessed. RESULTS: 211 patients (81 women, median age 65 [IQR, 58-74] years, median initial NIHSS score 13 [8-17]) were included. The baseline hematoma volume was 10.2 (5.6-19.2) mL. Neurological deterioration was observed in 17 patients (8%), hematoma expansion in 36 (17%), and unfavorable outcome in 87 (41%). The 1st, 2nd, and 3rd mSBPs were 132 (126-138), 131 (125-140), and 137 (130-144) mmHg, respectively. The 1st (OR 2.41, 95%CI 1.34-4.69 per 10-mmHg) and 2nd mSBPs (2.08; 1.20-3.80) were independently associated with neurological deterioration (17 patients) and the 2nd (1.40; 1.02-2.00) and 3rd mSBPs (1.45; 1.05-2.05) were associated with unfavorable outcome (87 patients), although no mSBPs were associated with hematoma expansion (36 patients). CONCLUSIONS: Continuation of AHT throughout the initial 24 hours may ameliorate clinical outcomes.

Background and Purpose— A short duration ( Methods— In 211 hyperacute ICH patients who underwent AHT based on predefined protocol, the mean of hourly SBP (mSBP) measurements was calculated over 1 to 8 hours (first mSBP), 9 to 16 hours (second mSBP), and 17 to 24 hours (third mSBP) after the initiation of AHT. Outcomes included neurological deterioration (72-hour Glasgow Coma Scale decrease ≥2 or National Instititutes of Health Stroke Scale increase ≥4), hematoma expansion (>33%), and unfavorable outcome (3-month modified Rankin Scale score 4–6). Results— The median first, second, and third mSBPs were 132, 131, and 137 mm Hg, respectively. A higher first mSBP (odds ratio [OR], 2.41; 95% confidence interval [CI], 1.34–4.69 per 10 mm Hg) or second mSBP (OR, 2.08; 95% CI, 1.20–3.80) was independently associated with neurological deterioration, and a higher second mSBP (OR, 1.40; 95% CI, 1.02–2.00) or third mSBP (OR, 1.45; 95% CI, 1.05–2.05) was associated with unfavorable outcome. None of the mSBPs was associated with hematoma expansion. Conclusions— The continuation of AHT throughout the initial 24 hours after ICH may improve outcomes.

apy [2, 3] . Recently, novel oral anticoagulants (NOACs) have emerged as alternative prophylaxis for thromboembolism in patients with nonvalvular AF. However, the effect of NOACs on intracardiac thrombi has not been fully elucidated. Here we report on the dissolution of LAA thrombus in 3 patients with nonvalvular AFrelated stroke receiving rivaroxaban. The clinical and neuroradiological characteristics of the 3 patients are summarized in table 1 .

Background and purpose: Characteristics of reverse MRA-DWI mismatch, defined as large DWI lesion despite absence of the major artery occlusion (MAO), remain unknown, especially in patients treated with IV rt-PA. This study aimed to clarify the frequency, associated factors, and outcomes of patients showing reverse MRA-DWI mismatch prior to IV rt-PA therapy. Methods: From the multicenter (SAMURAI) and additional single-center (NCVC) rt-PA registries, patients with the MCA territorial stroke were included. Early ischemic changes (EIC) were assessed with the Alberta Stroke Program Early CT score (ASPECTS) on pretreatment DWI. MAO was defined as ICA or M1 occlusion on MRA. Patients were divided into 4 groups: the large-EIC match (LM) group (MAO, ASPECTS Results: Of the 486 patients (167 women, median age 74 years) enrolled, reverse MRA-DWI mismatch was observed in 24 (5%, RMM group); 108 belonged to LM, 161 to CMM, and 193 to SM groups. Among clinical characteristics, cardioembolism (RMM 92%, LM 76%, CM 69%, SM 49%) was only independently associated with the RMM group (OR 5.49, 95%CI 1.25-24.1). Median initial NIHSS score was 18 in RMM, 18 in LM, 13 in CMM, and 8 in SM (p Conclusion: Reverse MRA-DWI mismatch was observed in 5% of patients eligible for rt-PA. Cardioembolism was independently associated with reverse mismatch. Patients with reverse mismatch may benefit from thrombolysis, compared to those with extensive EIC with MAO.