| Objective: With the development of magnetic resonance imaging techniques, the prevalence of cerebral microbleeds(CMBs) are increasing in different populations. As a bleeding-prone microangiopathy, CMBs are not only closely related intracranial hemorrhage but also associated with ischemic stroke, leukoaraiosis, vascular cognitive impairment, and Alzheimer’s disease(AD). The present studys are generally recognized that microangiopathy caused by cerebral amyloid angiopathy(CAA), hypertension, and atherosclerosis may be the pathogenesis of CMBs. Although currently there are numerous studys about risk factors and other clinical problems of CMBs, its exact pathogenesis and clinical implications remains incompletely clear. In this study we aimed to investigate the risk factors for CMBs and its relationship with cerebral ischemic events and carotid plaque in neurological hospitalized patients.Methods: One hundred and ninety-eight patients(age range:36-88; mean age:66.3±10.6) hospitalized between December 2013 and December 2014 were included in this study. Cranial computed tomography(CT), brain magnetic resonance imaging(MRI)(including T1-weighted imaging, T2-weighted imaging, T2-FLAIR imaging, diffusion weighted imaging, susceptibility-weighted imaging), and carotid ultrasound were performed after admission. For each patient the age, gender, poor lifestyles, past medical history, and laboratory tests data were recorded. The occurrence, number, location, and grade of the CMBs, white matter lesions(WML), and lacunar infarcts were recorded. With regard to the counting for the number and grade of CMBs, we firstly counted the total number of two hemispheres and then graded. Next, we counted and graded the left and right hemisphere separately. We recorded the carotid plaque and divided it into four echo types: low echo, mixed echo, equivalent echo, and strong echo. According to the different composition the echo represented, we defined low echo and mixed echo as vulnerable plaque, and defined equivalent echo and strong echo as stable plaque.In this study, we regarded the carotid and cerebral hemisphere of each side as an independent unit. We defined the hemisphere that had acute cerebral infarction or transient ischemic attack(TIA) as ischemic group, and the hemisphere that had not acute cerebral infarction or TIA as non-ischemic group.Results:1 The overall prevalence of CMBs in all patients was 47%, the prevalence of CMBs among men and women were 46.8% and 47.3%, respectively. The incidence of CMBs increased with age, and the incidence of CMBs in patients older than 80 years was the highest(66.7%). The number of CMBs ranged 1 to 82 and the median(first quartile,third quartile) of numbers of CMBs was 3(1,6) in all patients with CMBs. In all the CMBs positive patients, the cases of CMBs from grade 1 to grade 3 were 48(51.6%), 30(32.3%), and 15(16.1%), respectively. A total of 725 CMBs were found in all the CMBs positive patients, the number of CMBs in cortical-subcortical region, the basal ganglia and the thalamus, and infratentorial region were 348(48%), 273(37.7%), and 104(14.3%), respectively.2 Univariate analysis of CMBs: Age and body mass index(BMI) in the patients with CMBs were significantly higher than the patients without CMBs(P=0.004 and P=0.000, respectively). History of cerebral infarction and the use of antithrombotic drugs were more common in patients with CMBs than those without(P<0.05). The prevalence of hypertension, WML, and lacunar infarcts in patients with CMBs were significantly higher than the patients without CMBs(P<0.05). Triglyceride and very low density lipoprotein(VLDL) levels were significantly lower in patients with CMBs than in those without CMBs(P<0.05).3 Multivariate analysis of CMBs: The use of antithrombotic drugs(P=0.004; OR=2.852; 95%CI:1.411-5.767), elevated BMI(P=0.000; OR=3.505; 95%CI:2.065-5.948), and lacunar infarcts(P=0.000; OR=6.100; 95%CI:2.381-15.632) were independent risk factors for CMBs. Age(P=0.011; OR=1.510; 95%CI:1.098-2.077), history of Intracerebral haemorrhage(P=0.023; OR=4.474; 95%CI:1.232-16.248), and history of cerebral infarction(P=0.000; OR=3.528; 95%CI:1.837-6.778) were independent risk factors for cortic-alsubcortical CMBs. The use of antithrombotic drugs(P=0.001; OR=3.284; 95%CI:1.640-6.577) and hypertension(P=0.002; OR=4.233; 95%CI:1.732-10.345) were independent risk factors for basal ganglia and thalamus CMBs. History of cerebral infarction was an independent risk factor for infratentorial CMBs(P=0.001; OR=3.892; 95%CI:1.778-8.523), high fibrinogen level was a protective factor for infratentorial CMBs(P=0.020; OR=0.616; 95%CI:0.409-0.927).4 The prevalence of CMBs in ischemic group was 47.3%, whereas the prevalence was 32.4% in non-ischemic group, the difference was statistically significant(P=0.005; OR=1.875; 95%CI:1.200-2.930). The number of CMBs in ischemic group was significantly higher than the non-ischemic group(P=0.009).The prevalences of CMBs from grade 1 to grade 3 in ischemic group were higher than the non-ischemic group, whereas the prevalence of grade 0 CMBs was lower than the non-ischemic group, the difference was statistically significant(P=0.010). The prevalence of CMBs on the side of mixed echo plaque was the highest(64%) and significantly higher than other three types of plaques(P=0.000). The prevalence of CMBs on the side of vulnerable plaque was significantly higher than the stable plaque(P=0.000; OR=2.465; 95%CI: 1.473-4.126).Conclusions: The use of antithrombotic drugs, elevated BMI, and lacunar infarcts were independent risk factors for CMBs. Age, history of Intracerebral haemorrhage, and history of cerebral infarction were independent risk factors for corticalsubcortical CMBs. The use of antithrombotic drugs and hypertension were independent risk factors for CMBs. History of cerebral infarction was an independent risk factor for infratentorial CMBs,high fibrinogen level was a protective factor for infratentorial CMBs. CMBs may be associated with cerebral ischemic events, carotid mixed echo plaque, and carotid vulnerable plaque. |
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