Objective-We performed an association study to identify gene polymorphisms for assessing the genetic risk of ischemic or hemorrhagic stroke. Methods and Results-The study population comprised 3151 unrelated Japanese individuals: 1141 stroke patients (636 with atherothrombotic cerebral infarction, 282 with intracerebral hemorrhage, and 223 with subarachnoid hemorrhage) and 2010 controls. The genotypes for 202 polymorphisms of 152 genes were determined by suspension array technology. Multivariable logistic regression analysis with adjustment for conventional risk factors revealed that the -572G3 C polymorphism of the interleukin-6 (IL-6) gene (IL6) was significantly (PϽ0.001) associated with both atherothrombotic cerebral infarction and intracerebral hemorrhage and that the -55C3

N ovel oral anticoagulants (NOACs) reduce incidence of stroke and intracerebral hemorrhage (ICH) in patients with nonvalvular atrial fibrillation.1 Several studies demonstrated hematoma expansion in patients with ICH occurring during warfarin therapy and poor clinical outcomes.2 However, information regarding hematoma size, its expansion, and functional and vital outcomes of patients with ICH occurring during NOAC treatment have been limited and remain largely unclear.Cerebral microbleeds (CMBs) are said to be predictive of the occurrence of ICH or ischemic stroke 3 and to increase the risk of warfarin-associated ICH. 4 Furthermore, a considerable interest has been shown in association between CMBs and subsequent ICH in patients treated with NOACs. 5 In the present study, we investigated clinical and neuroradiological characteristics of patients with ICH occurring during NOAC treatment. MethodsFrom April 2011 through October 2013, 585 patients (342 men) with ICH were admitted to the Hirosaki Stroke and Rehabilitation Center for acute therapy <7 days after the onset (n=329) and for further rehabilitation therapy <60 days after the onset from other hospitals (n=256). Of all, 5 patients (1%) had ICH during NOAC treatment with nonvalvular atrial fibrillation, 56 (10%) during warfarin, and the other 524 (89%) during Background and Purpose-Neuroradiological characteristics and functional outcomes of patients with intracerebral hemorrhage (ICH) during novel oral anticoagulant treatment were not well defined. We examined these in comparison with those during warfarin treatment. Methods-The consecutive 585 patients with ICH admitted from April 2011 through October 2013 were retrospectively studied. Of all, 5 patients (1%) had ICH during rivaroxaban treatment, 56 (10%) during warfarin, and the other 524 (89%) during no anticoagulants. We focused on ICH during rivaroxaban and warfarin treatments and compared the clinical characteristics, neuroradiological findings, and functional outcomes. Results-Patients in the rivaroxaban group were all at high risk for major bleeding with hypertension, abnormal renal/ liver function, stroke, bleeding history or predisposition, labile international normalized ratio, elderly, drugs/alcohol concomitantly (HAS-BLED) score of 3 and higher rate of past history of ICH. Moreover, multiple cerebral microbleeds (≥4) were detected more frequently in rivaroxaban group than in warfarin (80% versus 29%; P=0.04). Hematoma volume in rivaroxaban group was markedly smaller than that in warfarin (median: 4 versus 11 mL; P=0.03). No patient in the rivaroxaban group had expansion of hematoma and surgical treatment. Rivaroxaban group showed lower modified Rankin Scale at discharge relative to warfarin, and the difference between modified Rankin Scale before admission and at discharge was smaller in rivaroxaban than in warfarin (median: 1 versus 3; P=0.047). No patient in the rivaroxaban group died during hospitalization, whereas 10 (18%) warfarin patients died. Conclusions-Rivaroxaban-associated ICH occur...

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Abstract. Metabolic syndrome is a risk factor for cardiovascular disease. The aim of the present study was to identify genetic variants that confer susceptibility to atherothrombotic cerebral infarction among individuals with metabolic syndrome in order to allow prediction of genetic risk for this condition. The study population comprised 1284 unrelated Japanese individuals with metabolic syndrome, including 313 subjects with atherothrombotic cerebral infarction and 971 controls. The genotypes for 296 polymorphisms of 202 candidate genes were determined with a method that combines the polymerase chain reaction and sequence-specific oligonucleotide probes with suspension array technology. The Chisquare test, multivariable logistic regression analysis with adjustment for age, sex, body mass index, and the prevalence of hypertension, hypercholesterolemia, and diabetes mellitus, as well as a stepwise forward selection procedure revealed that the 2445G¨A (Ala54Thr) polymorphism (rs1799883) of FABP2, the -108/3G¨4G polymorphism of IPF1 (S82168), the A¨G (Thr94Ala) polymorphism (rs2241883) of FABP1, the G¨A (Asp2213Asn) polymorphism (rs529038) of ROS1, the -11377C¨G polymorphism (rs266729) of ADIPOQ, the 162A¨C polymorphism (rs4769055) of ALOX5AP, the -786T¨C polymorphism (rs2070744) of NOS3, and the 3279C¨T polymorphism (rs7291467) of LGALS2 were associated (P<0.05) with the prevalence of atherothrombotic cerebral infarction. Among these polymorphisms, the 2445G¨A (Ala54Thr) polymorphism of FABP2 was most significantly associated with this condition. Our results suggest that FABP2, IPF1, FABP1, ROS1, ADIPOQ, ALOX5AP, NOS3, and LGALS2 are susceptibility loci for atherothrombotic cerebral infarction among Japanese individuals with metabolic syndrome. Genotypes for these polymorphisms, especially for the 2445G¨A (Ala54Thr) polymorphism of FABP2, may prove informative for the prediction of genetic risk for atherothrombotic cerebral infarction among such individuals.

Muscle volume decreases in the hemiplegic side in stroke patients.