BACKGROUND： Some reports indicate that electric and/or chemical stimulation at various brain sites of experimental animals can raise regional cerebral blood flow and improve cerebral circulation; however, its mechani...BACKGROUND： Some reports indicate that electric and/or chemical stimulation at various brain sites of experimental animals can raise regional cerebral blood flow and improve cerebral circulation; however, its mechanism is still unclear.OBJECTIVE： To observe the effects of electric stimulation at cerebellar fastigial nucleus on serum C-reactive protein of patients with acute cerebral infarction.DESIGN： Non-randomized synchronized contrast study.SETTING： The Second People＇s Hospital of Xinxiang City.PARTICIPANTS： A total of 54 patients with acute cerebral infarction were selected from the Department of Neurology, the Second People＇s Hospital of Xinxiang from December 2005 to December 2006. There were 31 males and 23 females, and their ages ranged from 56 to 80 years. All patients met the diagnostic criteria of the Fourth National Cerebrovascular Academic Meeting, were finally diagnosed by using CT examination,and provided the confirmed consent. Based on therapeutic demands, patients were divided into electric stimulation group and routine treatment group with 27 cases in each group. In addition, 21 healthy subjects,including 11 males and 10 females and aging 53 - 78 years, were selected as the control group. All the subjects in the control group did not have any histories of cerebrovascular diseases and severe body diseases.METHODS： Based on routine drug therapy, patients in the electric stimulation group were also treated by using CVFT-010M cerebral circulation function therapeutic device （made in Shanghai）. Electrode was fixed at bilateral mastoid in the first group and at extensible sides of upper limbs in the second group. Electric stimulation was given twice a day and lasted for 30 minutes each time. Ten days were regarded as a course.Parameters of device： mode Ⅲ, frequency 198%, and intensity 90% - 110% （bionic current）. Patients in the routine treatment group received the routine drug treatment. Content of serum C-reactive protein was measured in both electric stimulation group and routine treatment group before treatment and at 20 days after treatment, while in the control group on the exact day of health examination by using immunization.MAIN OUTCOME MEASURES： Level of serum C-reactive protein in the three groups.RESULTS： All 54 patients with acute cerebral infarction and 21 healthy subjects were involved in the final analysis. Level of serum C-reactive protein was higher in both electric stimulation group and routine treatment group than that in the control group before treatment （P 〈 0.01）. While, level of serum C-reactive protein was lower in the electric stimulation group than that in the routine treatment group after electric stimulation at cerebellar fastigial nucleus （P 〈 0.01）.CONCLUSION： Electric stimulation at cerebellar fastigial nucleus can decrease level of serum C-reactive protein in patients with acute cerebral infarction, and this may be one of the therapeutic mechanisms for curing acute cerebral infarction.展开更多
BACKGROUND： Some researches demonstrate that high-sensitivity C-reactive protein may be a risk factor to cause carotid atherosclerosis in patients with cerebral infarction. Inflammatory reaction may participate in fo...BACKGROUND： Some researches demonstrate that high-sensitivity C-reactive protein may be a risk factor to cause carotid atherosclerosis in patients with cerebral infarction. Inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction. OBJECTIVE： To investigate the correlation between levels of serum high-sensitivity C-reactive protein and carotid atherosclerosis in patients with acute cerebral infarction accompanied with carotid atherosclerosis. DESIGN： Contrast observation between two groups. SETTING： Department of Neurology, Zhenzhou Hospital, Shenyang Medical College. PARTICIPANTS： A total of 102 patients with acute cerebral infarction regarded as cerebral infarction group were selected from Department of Neurology, Shenzhou Hospital Affiliated to Shenyang Medical College from February 2005 to September 2006. There were 55 males and 47 females and their ages ranged from 55 to 86 years. All patients met the variously diagnostic points of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were finally diagnosed with CT or MRI examination. Illness course was in an acute phase. A total of 96 healthy subjects were regarded as control group, including 51 males and 45 females aged from 48 to 78 years. All accepted subjects provided the confirmed consent. METHODS： ① Patients in the cerebral infarction group received carotid ultrasound Doppler examination and serum high-sensitivity C-reactive protein detection within 72 hours after onset. IMMAGE immune biochemical system and latex reinforcement particle-enhanced nephelometric ilnmunoassay （PENIA） were used for quantitative detection of serum high-sensitivity C-reactive protein. ② Healthy subjects in the control group received the same detection. SEQUOIA512 color Doppler ultrasound （Siemens Company, USA） was used to detect carotid artery of all subjects so as to observe intima media thickness of artery and formation of artery atherosclerostic plaques. If artery atherosclerostic plaques were formed, their properties and amounts were determined based on the characteristics of light-echo signals. Evaluating criteria： Intima media thickness of artery was the vertical dimension from crossed face between lumen and tunica intima to crossed face between tunica media and tunica adventitia. Intima media thickness ≤ 0.9 into was regarded as normal; 0.9 inm 〈 intima media thickness ≤ 1.2 inm was regarded as thickening; when local eminence thickening was processed towards to lumen, the intima media thickness was more than 1.2 into and plaque of tunica intima was formed at the same time. Properties of plaque were classified into 4 types： steady low-echo lipid malacoplakia, equal-echo fiber plaque, strong-echo or sound-imaging calcification hard plaque and unsteady-echo ulcer mixed plaque. Fiber plaque and calcification hard plaque were steady but malacoplakia and mixed plaque were unsteady. MAIN OUTCOME MEASURES： Thickness of tunica media, characteristics of plaque and level of serum high-sensitivity C-reactive protein in carotid artery in two groups. RESULTS： All 102 patients with cerebral infarction and 96 healthy subjects were involved in the final analysis. ①Comparisons of level of high-sensitivity C-reactive protein： Level of high-sensitivity C-reactive protein in normal tunica media was higher in the cerebral infarction group [（4.66±1.55） mg/L] than the control group [（3.49±1.24） mg/L, t =2.541, P 〈 0.05]. In addition, level of high-sensitivity C-reactive protein in patients with thickening tunica media and plaque was not significantly different between the cerebral infarction group and the control group （P 〉 0.05）. ② Correlation between various degrees of vascular lesion and level of high-sensitivity C-reactive protein in the cerebral infarction group： Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with thickening tunica media [（8.16±2.42） mg/L] than patients with normal tunica media [（4.66±1.55） mg/L, t =4.132, P 〈 0.01]. In addition, level of high-sensitivity C-reactive protein was statistically significantly higher in patients with carotid plaque [（12.08±3.85） mg/L] than patients with normal tunica media （t =5.994, P 〈 0.01） and thickening tunica media （t =4.197, P 〈 0.01）. ③ Levels of high-sensitivity C-reactive protein in patients with various kinds of carotid plaque： Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with unsteady carotid plaque [（13.54±2.62） mg/L] than patients with steady carotid plaque [（8.61±3.71） mg/L, t =2.002, P 〈 0.05]. That was to say level of serum high-sensitivity C-reactive protein in patients who suffered acute cerebral infarction combined with carotid atherosclerosis especially carotid plaque was higher than that in those patients who did not have carotid lesions. This suggested that serum high-sensitivity C-reactive protein had a certain correlation with onset of carotid atherosclerosis in patients with acute cerebral infarction. CONCLUSION： Serum high-sensitivity C-reactive protein certainly correlates with onset of carotid atherosclerosis in patients with acute cerebral infarction, while inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.展开更多
Background Radiofrequency catheter ablation （RFCA） for atrial fibrillation （AF） has developed rapidly,and is a commonly performed ablation in many major hospitals throughout the world,due to its satisfactory resul...Background Radiofrequency catheter ablation （RFCA） for atrial fibrillation （AF） has developed rapidly,and is a commonly performed ablation in many major hospitals throughout the world,due to its satisfactory results.The aim of this study was to detect the effect of RFCA on C-reactive protein （CRP）,brain natriuretic peptide （BNP）,and echocardiograph in patients with persistent and permanent AF.Methods A total of 120 patients （71 males,mean age （50.8＆#177;12.0） years） with persistent and permanent AF undergoing RFCA under guidance of the Carto merge technique were studied.Left atrial diameter （LAD）,right atrial diameter （RAD）,left ventricular ejection fraction （LVEF）,CRP,and BNP were observed 3,6 and 12 months after RFCA and compared with results before RFCA.The recurrence of atrial arrhythmias was observed 3 and 12 months after the procedure.Results Compared with that before RFCA,LAD and RAD decreased and LVEF increased significantly after RFCA.Meanwhile,the levels of CRP and BNP were reduced significantly at 3,6,and 12 months after RFCA （P〈0.05）.In the non-recurrent patients,LVEF was increased significantly compared with the recurrent patients at 3,6,and 12 months after RFCA （P〈0.05）.CRP and BNP levels were decreased significantly in the non-recurrent patients compared with the recurrent patients at 3,6,and 12 months after RFCA （P〈0.05）.After one or two applications of RFCA,during a follow-up of 12 months,12 patients （10.0%） had AF,10 patients （8.3%） had atrial flutter,and 5 patients had atrial tachycardia （4.2%）.Conclusions Conversion of AF to sinus rhythm by RFCA,has been shown to reduce LA size and improve LVEF.It can also significantly decrease the levels of CRP and BNP in patients with persistent and permanent AF and reduce the risk of inflammation and developing heart failure.展开更多
Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the –607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, ...Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the –607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, we recruited 291 patients with ischemic cerebrovascular disease from the Affiliated Hospital of Qingdao University Medical College, China, and 226 healthy controls. Both patients and controls were from the Han population in northern China. Immunoresonance scattering assays detected increased serum amyloid A protein, C-reactive protein, and interleukin-18 levels in ischemic cerebrovascular disease patients compared with healthy controls. Analysis of the –607C/A （rs1946518） polymorphism in the interleukin-18 gene promoter showed ischemic cerebrovascular disease patients exhibited increased frequencies of the CC genotype and C alleles than healthy controls. Genotype and allele frequencies of the interleukin-18 –137G/C （rs187238） polymorphism and the –13T/C （rs11024595） polymorphism in the 5＇-flanking region of serum amyloid A, showed no significant difference between the two groups. Multivariate logistic regression analysis on the interleukin-18 promoter A/C genetic locus, for correction of age, gender, history of smoking, hypertension, diabetes mellitus, hypercholesteremia, and an ischemic stroke family history, showed ischemic cerebrovascular disease risk in individuals without the A allele （C homozygotes） was 2.2-fold greater than in A allele carriers. Overall, our findings suggest that the –13T/C （rs11024595） polymorphism in the 5′-flanking region of serum amyloid A has no correlation with ischemic cerebrovascular disease, but the C allele of the –607C/A （rs1946518） polymorphism in the interleukin-18 promoter is a high-risk factor for ischemic cerebrovascular disease in the Han population of northern China. In addition, the A allele is likely a protective gene for ischemic cerebrovascular disease.展开更多
文摘BACKGROUND： Some reports indicate that electric and/or chemical stimulation at various brain sites of experimental animals can raise regional cerebral blood flow and improve cerebral circulation; however, its mechanism is still unclear.OBJECTIVE： To observe the effects of electric stimulation at cerebellar fastigial nucleus on serum C-reactive protein of patients with acute cerebral infarction.DESIGN： Non-randomized synchronized contrast study.SETTING： The Second People＇s Hospital of Xinxiang City.PARTICIPANTS： A total of 54 patients with acute cerebral infarction were selected from the Department of Neurology, the Second People＇s Hospital of Xinxiang from December 2005 to December 2006. There were 31 males and 23 females, and their ages ranged from 56 to 80 years. All patients met the diagnostic criteria of the Fourth National Cerebrovascular Academic Meeting, were finally diagnosed by using CT examination,and provided the confirmed consent. Based on therapeutic demands, patients were divided into electric stimulation group and routine treatment group with 27 cases in each group. In addition, 21 healthy subjects,including 11 males and 10 females and aging 53 - 78 years, were selected as the control group. All the subjects in the control group did not have any histories of cerebrovascular diseases and severe body diseases.METHODS： Based on routine drug therapy, patients in the electric stimulation group were also treated by using CVFT-010M cerebral circulation function therapeutic device （made in Shanghai）. Electrode was fixed at bilateral mastoid in the first group and at extensible sides of upper limbs in the second group. Electric stimulation was given twice a day and lasted for 30 minutes each time. Ten days were regarded as a course.Parameters of device： mode Ⅲ, frequency 198%, and intensity 90% - 110% （bionic current）. Patients in the routine treatment group received the routine drug treatment. Content of serum C-reactive protein was measured in both electric stimulation group and routine treatment group before treatment and at 20 days after treatment, while in the control group on the exact day of health examination by using immunization.MAIN OUTCOME MEASURES： Level of serum C-reactive protein in the three groups.RESULTS： All 54 patients with acute cerebral infarction and 21 healthy subjects were involved in the final analysis. Level of serum C-reactive protein was higher in both electric stimulation group and routine treatment group than that in the control group before treatment （P 〈 0.01）. While, level of serum C-reactive protein was lower in the electric stimulation group than that in the routine treatment group after electric stimulation at cerebellar fastigial nucleus （P 〈 0.01）.CONCLUSION： Electric stimulation at cerebellar fastigial nucleus can decrease level of serum C-reactive protein in patients with acute cerebral infarction, and this may be one of the therapeutic mechanisms for curing acute cerebral infarction.
文摘BACKGROUND： Some researches demonstrate that high-sensitivity C-reactive protein may be a risk factor to cause carotid atherosclerosis in patients with cerebral infarction. Inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction. OBJECTIVE： To investigate the correlation between levels of serum high-sensitivity C-reactive protein and carotid atherosclerosis in patients with acute cerebral infarction accompanied with carotid atherosclerosis. DESIGN： Contrast observation between two groups. SETTING： Department of Neurology, Zhenzhou Hospital, Shenyang Medical College. PARTICIPANTS： A total of 102 patients with acute cerebral infarction regarded as cerebral infarction group were selected from Department of Neurology, Shenzhou Hospital Affiliated to Shenyang Medical College from February 2005 to September 2006. There were 55 males and 47 females and their ages ranged from 55 to 86 years. All patients met the variously diagnostic points of cerebral infarction established by the Fourth National Cerebrovascular Disease Academic Meeting and were finally diagnosed with CT or MRI examination. Illness course was in an acute phase. A total of 96 healthy subjects were regarded as control group, including 51 males and 45 females aged from 48 to 78 years. All accepted subjects provided the confirmed consent. METHODS： ① Patients in the cerebral infarction group received carotid ultrasound Doppler examination and serum high-sensitivity C-reactive protein detection within 72 hours after onset. IMMAGE immune biochemical system and latex reinforcement particle-enhanced nephelometric ilnmunoassay （PENIA） were used for quantitative detection of serum high-sensitivity C-reactive protein. ② Healthy subjects in the control group received the same detection. SEQUOIA512 color Doppler ultrasound （Siemens Company, USA） was used to detect carotid artery of all subjects so as to observe intima media thickness of artery and formation of artery atherosclerostic plaques. If artery atherosclerostic plaques were formed, their properties and amounts were determined based on the characteristics of light-echo signals. Evaluating criteria： Intima media thickness of artery was the vertical dimension from crossed face between lumen and tunica intima to crossed face between tunica media and tunica adventitia. Intima media thickness ≤ 0.9 into was regarded as normal; 0.9 inm 〈 intima media thickness ≤ 1.2 inm was regarded as thickening; when local eminence thickening was processed towards to lumen, the intima media thickness was more than 1.2 into and plaque of tunica intima was formed at the same time. Properties of plaque were classified into 4 types： steady low-echo lipid malacoplakia, equal-echo fiber plaque, strong-echo or sound-imaging calcification hard plaque and unsteady-echo ulcer mixed plaque. Fiber plaque and calcification hard plaque were steady but malacoplakia and mixed plaque were unsteady. MAIN OUTCOME MEASURES： Thickness of tunica media, characteristics of plaque and level of serum high-sensitivity C-reactive protein in carotid artery in two groups. RESULTS： All 102 patients with cerebral infarction and 96 healthy subjects were involved in the final analysis. ①Comparisons of level of high-sensitivity C-reactive protein： Level of high-sensitivity C-reactive protein in normal tunica media was higher in the cerebral infarction group [（4.66±1.55） mg/L] than the control group [（3.49±1.24） mg/L, t =2.541, P 〈 0.05]. In addition, level of high-sensitivity C-reactive protein in patients with thickening tunica media and plaque was not significantly different between the cerebral infarction group and the control group （P 〉 0.05）. ② Correlation between various degrees of vascular lesion and level of high-sensitivity C-reactive protein in the cerebral infarction group： Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with thickening tunica media [（8.16±2.42） mg/L] than patients with normal tunica media [（4.66±1.55） mg/L, t =4.132, P 〈 0.01]. In addition, level of high-sensitivity C-reactive protein was statistically significantly higher in patients with carotid plaque [（12.08±3.85） mg/L] than patients with normal tunica media （t =5.994, P 〈 0.01） and thickening tunica media （t =4.197, P 〈 0.01）. ③ Levels of high-sensitivity C-reactive protein in patients with various kinds of carotid plaque： Level of high-sensitivity C-reactive protein was statistically significantly higher in patients with unsteady carotid plaque [（13.54±2.62） mg/L] than patients with steady carotid plaque [（8.61±3.71） mg/L, t =2.002, P 〈 0.05]. That was to say level of serum high-sensitivity C-reactive protein in patients who suffered acute cerebral infarction combined with carotid atherosclerosis especially carotid plaque was higher than that in those patients who did not have carotid lesions. This suggested that serum high-sensitivity C-reactive protein had a certain correlation with onset of carotid atherosclerosis in patients with acute cerebral infarction. CONCLUSION： Serum high-sensitivity C-reactive protein certainly correlates with onset of carotid atherosclerosis in patients with acute cerebral infarction, while inflammatory reaction may participate in formation of carotid atherosclerosis in patients with acute cerebral infarction.
文摘Background Radiofrequency catheter ablation （RFCA） for atrial fibrillation （AF） has developed rapidly,and is a commonly performed ablation in many major hospitals throughout the world,due to its satisfactory results.The aim of this study was to detect the effect of RFCA on C-reactive protein （CRP）,brain natriuretic peptide （BNP）,and echocardiograph in patients with persistent and permanent AF.Methods A total of 120 patients （71 males,mean age （50.8＆#177;12.0） years） with persistent and permanent AF undergoing RFCA under guidance of the Carto merge technique were studied.Left atrial diameter （LAD）,right atrial diameter （RAD）,left ventricular ejection fraction （LVEF）,CRP,and BNP were observed 3,6 and 12 months after RFCA and compared with results before RFCA.The recurrence of atrial arrhythmias was observed 3 and 12 months after the procedure.Results Compared with that before RFCA,LAD and RAD decreased and LVEF increased significantly after RFCA.Meanwhile,the levels of CRP and BNP were reduced significantly at 3,6,and 12 months after RFCA （P〈0.05）.In the non-recurrent patients,LVEF was increased significantly compared with the recurrent patients at 3,6,and 12 months after RFCA （P〈0.05）.CRP and BNP levels were decreased significantly in the non-recurrent patients compared with the recurrent patients at 3,6,and 12 months after RFCA （P〈0.05）.After one or two applications of RFCA,during a follow-up of 12 months,12 patients （10.0%） had AF,10 patients （8.3%） had atrial flutter,and 5 patients had atrial tachycardia （4.2%）.Conclusions Conversion of AF to sinus rhythm by RFCA,has been shown to reduce LA size and improve LVEF.It can also significantly decrease the levels of CRP and BNP in patients with persistent and permanent AF and reduce the risk of inflammation and developing heart failure.
文摘Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the –607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, we recruited 291 patients with ischemic cerebrovascular disease from the Affiliated Hospital of Qingdao University Medical College, China, and 226 healthy controls. Both patients and controls were from the Han population in northern China. Immunoresonance scattering assays detected increased serum amyloid A protein, C-reactive protein, and interleukin-18 levels in ischemic cerebrovascular disease patients compared with healthy controls. Analysis of the –607C/A （rs1946518） polymorphism in the interleukin-18 gene promoter showed ischemic cerebrovascular disease patients exhibited increased frequencies of the CC genotype and C alleles than healthy controls. Genotype and allele frequencies of the interleukin-18 –137G/C （rs187238） polymorphism and the –13T/C （rs11024595） polymorphism in the 5＇-flanking region of serum amyloid A, showed no significant difference between the two groups. Multivariate logistic regression analysis on the interleukin-18 promoter A/C genetic locus, for correction of age, gender, history of smoking, hypertension, diabetes mellitus, hypercholesteremia, and an ischemic stroke family history, showed ischemic cerebrovascular disease risk in individuals without the A allele （C homozygotes） was 2.2-fold greater than in A allele carriers. Overall, our findings suggest that the –13T/C （rs11024595） polymorphism in the 5′-flanking region of serum amyloid A has no correlation with ischemic cerebrovascular disease, but the C allele of the –607C/A （rs1946518） polymorphism in the interleukin-18 promoter is a high-risk factor for ischemic cerebrovascular disease in the Han population of northern China. In addition, the A allele is likely a protective gene for ischemic cerebrovascular disease.
