| Objective:By retrospective analysis of the differences between patients with and without Silent brain infarction（SBI）in patients with first-episode symptomatic cerebral infarction,to explore the prevalence,TOAST etiology type,risk factors and clinical significance of Silent brain infarction in patients with first-episode symptomatic cerebral infarction.In order to better guide the clinical understanding,prevention and treatment of silent brain infarction.Methods:In this study,patients with acute cerebral infarction admitted to our hospital during2020-2021 were selected as the main screening object,and 252 patients with first symptomatic cerebral infarction were included in the study.According to whether silent brain infarction was complicated,they were divided into SBI group and non-SBI group,including 206 cases in SBI group and 46 cases in non-SBI group.General clinical data,laboratory examination results（glycosylated hemoglobin,fasting blood glucose,blood lipids（including TC,TG,LDL-C,HDL-C）,uric acid,homocysteine levels,creatinine,etc.）and imaging examination results（head CT,head MRI,MRA,brain color,neck color,electrocardiogram,etc.）were collected and collated.The differences of general clinical data,laboratory examination and imaging examination between the SBI group and the non-SBI group were compared and analyzed,and the distribution characteristics of infarct foci in silent brain infarction in the SBI group were summarized and analyzed,and the research conclusions were drawn.Results:1.There were 252 patients with first symptomatic cerebral infarction,including206 patients（81.7%）in the SBI group and 46 patients（18.3%）in the non-SBI group.There were 139 males（67.5%）and 67 females（32.5%）in the SBI group,and 29males（63.0%）and 17 females（37.0%）in the non-SBI group,the difference was not statistically significant（P > 0.05）.The mean age of patients in the SBI group was62.85±11.07 years old,while that in the non-SBI group was 51.50±12.77 years old,the difference was statistically significant（P < 0.001）.2.Comparison of TOAST etiological types: In the SBI group,108 patients（54.2%）were LAA type,86 patients（41.8%）were SAA type,and 12 patients（5.8%）were other types.In the non-SBI group,there were 28 patients（60.8%）were LAA type,17 patients（37.0%）were SAA type,and 1 patients（2.2%）were other types.The prevalence of LAA type in SBI group and non-SBI group was higher than that in SAA type,and there was no statistical significance（P > 0.05）.3.There were 130 patients（63.1%）with hypertension in SBI group,and 29patients（63.0%）with hypertension in non-SBI group,the difference was not statistical significance（P > 0.05）.There were 141 patients（68.4%）in SBI group with diabetes,and 24 patients（52.2%）in non-SBI group with diabetes,the difference was statistically significant（P < 0.05）.145 patients（70.4%）with hyperlipidemia in SBI group,and 24patients（52.2%）with hyperlipidemia in non-SBI group,the difference was statistically significant（P < 0.05）.116 patients（56.3%）with hyperhomocysteine in SBI group,and12 patients（26.1%）with hyperhomocysteine in non-SBI group,the difference was statistically significant（P < 0.001）.The level of uric acid（umol /L）in SBI group303（249,369）was lower than that in non-SBI group 306（256.5,406）,and the difference was not statistically significant by rank sum test（P > 0.05）.The creatinine（umol /L）level in SBI group 71（61.00,86.00）was lower than that in non-SBI group 73（62.50,84.40）,and the difference was not statistically significant by rank sum test（P > 0.05）.4.There were 198 patients（96.1%）with carotid atherosclerosis in SBI group,and36 patients（78.3%）with carotid atherosclerosis in non-SBI group,the difference was statistically significant（P < 0.001）.There were 153 patients（74.3%）with carotid intima-media thickening in SBI group,and 28 patients（60.9%）with carotid intima-media thickening in non-SBI group,the difference was not statistically significant（P > 0.05）.There were 180 patients（87.4%）with carotid atherosclerotic plaque in SBI group,and 30 patients（65.2%）with carotid atherosclerotic plaque in non-SBI group,the difference was statistically significant（P < 0.001）.There were 32 patients（15.5%）with carotid artery stenosis in SBI group,and 2patients（4.3%）with carotid artery stenosis in non-SBI group,with statistically significant differences（P < 0.05）.There were 32 patients with SBI combination combined with carotid artery stenosis,and there were 116 SBI in total,among which 88 were anterior circulation SBI,including 54（46.6%）in ipsilateral carotid artery stenosis and 34（29.3%）in contralateral carotid artery stenosis,and the prevalence of SBI in the ipsilateral side of carotid stenosis was higher than that in the contralateral side,and the difference was statistically significant（P < 0.05）.5.There were 12 patients（5.8%）with atrial fibrillation in SBI group,and 1 patient（2.2%）with atrial fibrillation in non-SBI group,with no statistical difference（P > 0.05）.6.In SBI group,there were 771 silent brain infarction lesions,including 246（31.91%）in the basal ganglia,218（28.27%）in the radial corona,74（9.60%）in the thalamus,73（9.47%）in the brainstem,and 31（4.02%）in the cerebellum.129（16.73%）were located in the cerebral lobes.The highest percentage of infarct foci were located in the basal ganglia and the radiological crown.7.Multivariate Logistic regression analysis showed that age and carotid atherosclerosis were independent risk factors for asymptomatic cerebral infarction.Conclusion:1.The prevalence of silent brain infarction in patients with first symptomatic cerebral infarction is high and the onset age is older.2.Patients with first-symptom cerebral infarction complicated with SBI have a high prevalence of diabetes,hyperlipidemia,hyperhomocysteinemia,carotid atherosclerosis,carotid atherosclerotic plaque and carotid artery stenosis.The prevalence of ipsilateral SBI was higher in patients with carotid stenosis than in the contralateral side.3.Age and carotid atherosclerosis are independent risk factors for silent brain infarction.4.The infarct foci of silent brain infarction were mainly distributed in the intracranial basal ganglia and radiographic coronal region. |
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