ABSTRACT
Objective Cerebral small vessel disease is closely related to kidney disease .Chronic kidney disease ( CKD) may increase the risk of hemorrhage stroke .However, its impact on hemorrhage-prone small vessel disease represented by cerebral microb-leeds( CMBs) remains unclear .The purpose of this study was to investigate the relationship of CKD with the presence and location of CMBs in patients with acute lacunar stroke . Method Consecutive patients with acute lacunar stroke within 7 days from onset were enrolled retrospectively from January 2014 to July 2016 and scanned by gradient-echo T2*-weighted imaging (GRE-T2*WI).Their demographic, clinical, laboratory and imaging data were collected .Estimate glomerular filtration rate (eGFR) was calculated individu-ally by the following chronic kidney disease epidemiology collaboration (CKD-EPI) equation for the Asian population .CKD was defined as the level of eGFR<60 mL/min/1.73 m2. Results Finally, 308 patients (mean age:65.79±8.67 years; median NHISS:3(2-5);42.2%Female) with lacunar ischemic stroke were enrolled in the final analysis .Among these patients, CMBs were present in 116 patients ( 37.7%) and CKD in 62 patients ( 20.1%) .Patients were divided into CKD group and normal group according to GFR level . The result of univariate analysis showed that patients with CKD had higher prevalence of diabetes ( P=0.014) and higher degrees of CMBs (P=0.001) compared with normal group.CMBs were refined by its location .The result of multivariable analysis showed that CMBs in deep brain [ OR=7.61, 95%CI 4.18-16.55, P=0.001] were sig-nificantly associated with CKD incidence , while no significant rela-tionship was found in CKD incidence and CMBs in the lobe and mixed location of brain . Conclusion The CKD incidence in patients with acute lacunar stroke is in dependent relationship with CMBs in deep brain and without significant correlation with CMBs in the lobe and mixed location of brain .
ABSTRACT
Objective To investigate the correlation between the indicators of common carotid artery mechanical dynamics, a circumferential wal tension (CWT) and a shear stress (SS), and cerebral smal vessel disease (SVD). Methods The neurological outpatients without obvious cardiovascular disease were enrol ed consecutively. The inner diameters of carotid arteries and blood flow velocity of the patients w ere measured by ultrasound examination, and their CWT and SS w ere calculated. Lacunar infarction and/or leukoaraiosis w ere determined according to the findings of MRI. Results A total of 296 patients w ere enrol ed, 163 of them had lacunar infarction and 132 had leukoaraiosis. Univariate analysis show ed that there w ere significant differences in the distributions of age, hypertension, diabetes, systolic blood pressure, diastolic blood pressure, CWT, and SS betw een the lacunar infarction group and the non-lacunar infarction group, as wel as between the leukoaraiosis group and the non-leukoaraiosis group (al P<0.05). After adjusting for relevant risk factors, multivariate logistic regression analysis show ed that the peak systolic CWT (odds ratio [OR] 3.60, 95% confidence interval [CI] 1.48-8.30) and end diastolic CWT (OR 1.22, 95%CI 1.21-1.25) w ere the independent risk factors for lacunar infarction, w hile the peak systolic SS (OR 0.90, 95%CI 0.75-0.95 ) and end diastolic SS ( OR 0.87, 95%CI 0.84-0.98 ) w ere the independent protective factors for lacunar infarction; the peak systolic CWT (OR 4.67, 95%CI 2.05-10.52) and end diastolic CWT (OR 1.25, 95%CI 1.22-1.47) were the independent risk factors for leukoariosis, w hile the peak systolic SS (OR 0.93, 95%CI 0.75-0.94) and end diastolic SS (OR 0.91, 95%CI 0.85-0.98) w ere the independent protective factors for leukoaraiosis. Conclusions The common carotid artery mechanical stress w as associated w ith the occurrence of SVD.
ABSTRACT
Apoptosis is one of the important forms during cerebral ischemia.Phosphoinositide-3 kinase (PI3K)/serine/threonine kinase (Akt) is the important cell survival signaling pathway,while c-jun N-terminal kinase (JNK) is the important pro-apoptotic signaling pathway.The dynamic equilibrium of the two signal transduction pathways maintains cell survival and apoptosis under the physiological state.Stimulation during cerebral ischemia breaks this physiological balance and results in the apoptosis of massive neurons.A variety of proved neuroprotective factors are associated with the amplification of enhancement of cell survival signal or inhibition of apoptosis signal,and thrus maintain the balance between the two signal pathways.