卒中专病门诊对提高他汀类药物使用的影响

Objective To describe the impact of stroke clinic on the usage of statins for secondary prevention of ischemic stroke.Methods Data about the demography, social economic status, personal histories, blood lipid profiles, and the status of the usage of statins from 568 serial ischemic stroke patients were retrospectively analysed.Results A total of 51.3% patients followed up in stroke clinic ( 306 patients) and 7.6% patients followed up in general clinic (262 patients) were treated with statins.71.6% patients with and 44.8% patients without hyperlipidemia in stroke clinics were taking statins, which were higher than that patients in the general clinics(27.1% and 2.0% respectively).The patients in the stroke clinics with high LDL-C level ( ＞ 3.4 mmol/L) were more likely to be treated with statins than those with lower level (25.6% vs 14.7%, P = 0.017).Conclusions The rate of statins usage is extremely low in stroke patients followed up in a general clinic, but it can been improved greatly in a stroke clinic.Stroke clinic can narrow the gap between the clinical practice and the guideline for secondary prevention of ischemic stroke.     

The effects of enhanced external counterpulsation on the serum level of C-reactive protein and endothelin-1 in patients with ischemic stroke

<正>Objective To explore the effects of enhanced external counterpulsation(EECP)on the serum level of C-reactive protein and endothelin-1 in patients with cerebral ischemic stroke,to provide clinical evidence for the treatment and secondary prevention of patients with serebral ischemic stroke.Methods Total 187 patients with ischemic stroke and enrolled measure the serum level of     

代谢综合征在缺血性卒中患者心脑血管事件发生中的作用

Objective To explore the association between metabolic syndrome (MS) and risk of cardiovascular disease events (CVD) in patients with ischemic stroke. Method A total of 1087 patients with ischemic stroke were enrolled from 5 community-based medical centres and underwent baseline evaluation on risk factors of stroke during the period of Jar. 2003 to Dec. 2006. After baseline survey, all patients were followed up until Dec 31, 2008 and new CVD events were recorded. MS was defined using CDS criteria. Proportional hazard models were used to assess the HRus and 95% CI of CVD events associated with MS and other components. Results The prevalence of MS was 40. 4% at baseline. During an average follow-up of 3.5 years, 178 patients developed new CVD events. After adjusted for age, gender, smoking,drinking, marriage status, education level, hospitalization, recurrence of stroke, stroke duration,depression, cognition impairment and ADL, MS remains the independent predictor for the risk of CVD events. Compared with patients with non-MS, the risk of CVD events increased by 44% (HR:1.44, 95%CI:1.06-1.95 ). The risk of CVD also increased with the number of MS components. Compared with patients with 1 or less than 1 components of MS, the risk of CVD events increased by 30% (HR:1. 30,95%CI:0.83-2.04) in those with 2 components and by 69% ( HR: 1.69,95% CI: 1.11-2.56) in those with 3or more components of MS. Hypertension and hyperglycemia and impaired fasting glucose also served as independent risk factors for CVD event ( all P ＜ 0. 001 ) . Conclusions MS was independently associated with increased risk of CVD events in patients with ischemic stroke. There was a dose-response relationship between the numbers of MS components and the risk of CVD event.     

Level of systolic blood pressure within the normal range and risk of recurrent stroke

Methods and Results Recurrent stroke prevention guidelines suggest that larger reductions in systolic blood pressure (SBP) are positively associated with a greater reduction in the risk of recurrent stroke and define an SBP level of less than 120 mm Hg as normal. However, the association of SBP maintained at such levels with risk of vascular events after a recent ischemic stroke is unclear. To assess the association of maintaining low-normal vs high-normal SBP levels with risk of recurrent stroke. Post hoc observational analysis of a multicenter trial involving 20,330 patients (age ≥50 years) with recent non-cardioembolic ischemic stroke; patients were recruited from 695 centers in 35 countries from September 2003 through July 2006 and followed up for 2.5 years (follow-up ended on February 8, 2008). Patients were categorized based on their mean SBP level: very low-normal ( < 120 mmHg), low-normal (120 ≤ 130 mmHg), high-normal (130 ≤ 140 mmHg), high (140 ≤ 150 mmHg), and very high (≥150 mmHg). The primary outcome was first recurrence of stroke of any type and the secondary outcome was a composite of stroke, myocardial infarction, or death from vascular causes. The recurrent stroke rates were 8.0% (95% CI, 6.8%-9.2%) for the very low-normal SBP level group, 7.2% (95% CI, 6.4%-8.0%) for the low-normal SBP group, 6.8% (95% CI, 6.1%-7.4%) for the high-normal SBP group, 8.7% (95% CI, 7.9%-9.5%) for the high SBP group, and 14.1% (95% CI, 13.0%-15.2%) for the very high SBP group. Compared with patients in the high-normal SBP group, the risk of the primary outcome was higher for patients in the very low-normal SBP group (adjusted hazard ratio [AHR], 1.29; 95% CI, 1.07 - 1.56), in the high SBP group (AHR, 1.23; 95% CI, 1.07-1.41), and in the very high SBP group (AHR, 2.08; 95% CI, 1.83-2.37). Compared with patients in the high-normal SBP group, the risk of secondary outcome was higher for patients in the very low-normal SBP group (AHR, 1.31; 95% CI, 1.13-1.52), in the low-normal SBP group (AHR, 1.16; 95% CI, 1.03-1.31), in the high SBP group (AHR, 1.24; 95% CI, 1.11- 1.39), and in the very high SBP group (AHR, 1.94; 95% CI, 1.74-2.16). Conslusions Among patients with recent non-cardioembolic ischemic stroke, SBP levels during follow-up in the very low-normal ( < 120 mmHg), high (140 ≤ 150 mmHg), or very high (≥150 mmHg) range were associated with increased risk of recurrent stroke.     

代谢综合征在缺血性卒中患者心脑血管事件发生中的作用

Objective To explore the association between metabolic syndrome (MS) and risk of cardiovascular disease events (CVD) in patients with ischemic stroke. Method A total of 1087 patients with ischemic stroke were enrolled from 5 community-based medical centres and underwent baseline evaluation on risk factors of stroke during the period of Jar. 2003 to Dec. 2006. After baseline survey, all patients were followed up until Dec 31, 2008 and new CVD events were recorded. MS was defined using CDS criteria. Proportional hazard models were used to assess the HRus and 95% CI of CVD events associated with MS and other components. Results The prevalence of MS was 40. 4% at baseline. During an average follow-up of 3.5 years, 178 patients developed new CVD events. After adjusted for age, gender, smoking,drinking, marriage status, education level, hospitalization, recurrence of stroke, stroke duration,depression, cognition impairment and ADL, MS remains the independent predictor for the risk of CVD events. Compared with patients with non-MS, the risk of CVD events increased by 44% (HR:1.44, 95%CI:1.06-1.95 ). The risk of CVD also increased with the number of MS components. Compared with patients with 1 or less than 1 components of MS, the risk of CVD events increased by 30% (HR:1. 30,95%CI:0.83-2.04) in those with 2 components and by 69% ( HR: 1.69,95% CI: 1.11-2.56) in those with 3or more components of MS. Hypertension and hyperglycemia and impaired fasting glucose also served as independent risk factors for CVD event ( all P ＜ 0. 001 ) . Conclusions MS was independently associated with increased risk of CVD events in patients with ischemic stroke. There was a dose-response relationship between the numbers of MS components and the risk of CVD event.     

Relationship between polymorphism of angiotensin-converting enzyme 2 gene and the risk factor of essential hypertension with complicated stroke

Background Essential hypertension (EH) is considered to be one of the most important risk factor of ischemic stroke. Studies about risk factors in the patients are meaningful in early forecast and effective prevention of the onset of stroke. Renin-angiotensin-aldosterone system plays an important role in the regulation of blood pressure and the development of stroke, while recent studies have found that the angiotensin-converting enzyme 2 (ACE2) may be a reversal agent for the development and progression of ischemic stroke. Methods The ACE2 gene was measured in 139 EH patients with ischemic stroke using polymerase chain reaction (PCR) and restriction fragment length polymorphism (PCR-RFLP) tests. Detailed and complete clinical and biochemical data were collected, including pulse pressure, hsCRP, IMT, HDL-C and uric acid levels. Study the correlation between angiotensin-converting enzyme 2 gene and the risk factor for onset of ischemic stroke in EH patients. Results Pulse pressure, hsCRP, IMT and uric acid levels had a positive correlation with on- set of ischemic stroke in EH patients. Among male patients , pulse pressure, hsCRP, IMT and HDL-C were higher in patients carrying A allele than B allele (P < 0.05). While these factors were different in female pa- tients carrying different genotypes in which AA allele were highest. Patients with various genotypes showed different uric acid levels but showed no significant difference. Conclusion Among EH patients with complicated ischemic stroke, those carrying the A / AA allele show high level of risk factors and is likely to have the susceptibility of recurrence of stroke.     

Correlation between blood glucose variability and TOAST type of patients with acute ischemic stroke

<正>Objective To study the correlation between blood glucose variability and TOAST type of patients with acute ischemic stroke and provide new evidence which can improve the prognosis of ischemic stroke.Methods One hundred and forty-three hospitalized patients with acute ischemic stroke from August 2013 to August 2014 were included.All patients were estimated the general state of     

Carvedilol vs endoscopic variceal ligation for primary and secondary prevention of variceal bleeding: Systematic review and metaanalysis

BACKGROUND Variceal hemorrhage is associated with high mortality and is the cause of death for 20–30% of patients with cirrhosis. Nonselective β blockers(NSBBs) or endoscopic variceal ligation(EVL) are recommended for primary prevention of variceal bleeding in patients with medium to large esophageal varices.Meanwhile, combination of EVL and NSBBs is the recommended approach for the secondary prevention. Carvedilol has greater efficacy than other NSBBs as it decreases intrahepatic resistance. We hypothesized that there was no difference between carvedilol and EVL intervention for primary and secondary prevention of variceal bleeding in cirrhosis patients.AIM To evaluate the efficacy of carvedilol compared to EVL for primary and secondary prevention of variceal bleeding in cirrhotic patients METHODS We searched relevant literatures in major journal databases(CENTRAL,MEDLINE, and EMBASE) from March to August 2018. Patients with cirrhosis and portal hypertension, regardless of aetiology and severity, with or without a history of variceal bleeding, and aged ≥ 18 years old were included in this review.Only randomized controlled trials(RCTs) that compared the efficacy of carvedilol and that of EVL for primary and secondary prevention of variceal bleeding and mortality in patients with cirrhosis and portal hypertension were considered, irrespective of publication status, year of publication, and language.RESULTS Seven RCTs were included. In four trials assessing the primary prevention, no significant difference was found on the events of variceal bleeding(RR: 0.74,95%CI: 0.37-1.49), all-cause mortality(RR: 1.10, 95%CI: 0.76-1.58), and bleedingrelated mortality(RR: 1.02, 95%CI: 0.34-3.10) in patients who were treated with carvedilol compared to EVL. In three trials assessing secondary prevention, there was no difference between two interventions for the incidence of rebleeding(RR:1.10, 95%CI: 0.75-1.61). The fixed-effect model showed that, compared to EVL,carvedilol decreased all-cause mortality by 49%(RR: 0.51, 95%CI: 0.33-0.79), with little or no evidence of heterogeneity.CONCLUSION Carvedilol had similar efficacy to EVL in preventing the first variceal bleeding in cirrhosis patients with esophageal varices. It was superior to EVL alone for secondary prevention of variceal bleeding in regard to all-cause mortality reduction.     

Effect of ezetimibe on the prevalence of cholelithiasis

AIM:To investigate the prevalence of cholelithiasis among patients treated with ezetimibe.METHODS:A retrospective,case-control study based on computerized medical records from patients of the Clalit Health Services,Sharon-Shomron region,from 2000 to 2009.Patients 20-85 years of age,who had been treated with ezetimibe and statins or statins only for at least 6 mo,and who had an abdominal ultrasound were included in the study.Collected data included age,gender,ezetimibe treatment duration,presence of hypothyroidism or diabetes,and existence of cholelithiasis as determined by ultrasound.Excluded were subjects after gallbladder resection,with hemolysis,myeloproliferative or inflammatory bowel diseases,and those treated with ursodeoxycholic acid and fibrates.Patients treated with statins and ezetimibe(study group) were compared to patients treated with statins only(control group).RESULTS:The study group included 25 patients and the control group 168.All patients in the study were treated with statins.The study group included 13 males(52%) and 12 females(48%),the control group 76 males(45%) and 92(55%) females(P = 0.544).The groups did not differ in age(mean age:68 ± 8 years,range 53-85 years vs mean age:71 ± 8 years,range 51-85 years;P = 0.153) or in the rate of diabetic and hypothyroid patients [11(44%) vs 57(33%),P = 0.347 in the study group and 5(20%) vs 23(14%),P = 0.449 in the control group,respectively].Patients in the study group were treated with ezetimibe for an average of 798 ± 379 d.Cholelithiasis was found in 4(16%) patients in the study group and in 33(20%) patients in the control group(P = 0.666).CONCLUSION:Ezetimibe does not appear to influence the prevalence of gallstones.     

Long-term effects of simvastatin on protection against atrial fibrillation in patients with acute myocardial infarction

Objective To investigate the impact of simvastatin on blood lipid and the incidence of atrial fibrillation and ischemic-related events in patients with acute myocardial infarction accompanied by paroxysmal atrial fibrillation. Methods One hundred and three patients with acute myocardial infarction and paroxysmal atrial fibrillation were selected as subjects,and were divided into a simvastatin group and a control group. Forty-five patients were in the simvastatin group,who took simvastatin 20mg/d orally for 18 months;fifty-eight patients were in the control group,and received conventional therapy except for statins. All patients were followed up for 18 months. The level of blood lipid,recurrence rate of paroxysmal atrial fibrillation,incidence rate of persistent or permanent atrial fibrillation,and the ischemic-related events were investigated and compared between the two groups. Results ① The levels of blood lipids did not change significantly in the control group(P>0.05) ;concentrations of total cholesterol(TC) and low density lipoprotein cholesterol(LDL-C) decreased significantly after treatment of simvastatin(P<0.05) . ② Recurrence of atrial fibrillation was observed in five patients during 18 months follow-up in the simvastatin group(11.1%) ,whereas it occurred in 14 patients of the control group(24. 1%,P<0.05) ;the occurrence rate of persistent or permanent atrial fibrillation in the simvastatin group was 4.4%,which was lower than that of control(12.1%,P<0.05) . ③ Nine patients had ischemic-related events in the simvastatin group(20.0%) ,with three heart failures(6.6%) ,two rehospitalizations for deterioration of coronary heart diseases(4.4%) ,three cardiac deaths(6.6%) ,and one cerebral stroke(2.2%) ,which was lower evidently than in the control group(41.4%,P<0.05) . Conclusions Simvastatin can not only decrease the levels of serum TC and LDL-C but also prevent the occurrence of atrial fibrillation and ischemic-related events.     

Pathology of stroke

Large cerebral infarctions were caused by atherosclerosis with or without thrombosis in the proximal circumflex (cortical) cerebral arteries. Hypertension, hypercholesterolemia, hypoxidosis, and vasospasm were considered to induce endothelial cell injuries, which might be the primary events not only in atherosclerosis, but also in arteriosclerosis and arteriosis formation. Morphogenesis of atherosclerosis and causes of associated thrombosis were also discussed. Small cerebral infarcts were produced not only by arteriosclerosis, arteriosis, and atherosclerosis, but also by arterionecrosis-derived microaneurysms occluded by thrombi in the distal penetrating (perforating) cerebral arteries. Pathogenesis and morphogenesis of the arterial lesions were discussed. Recent increase of the arterionecrosis occluded by thrombosis in the pathogenesis of small infarcts (lacunes) was noted. The direct cause of hypertensive cerebral hemorrhage was the rupture of arterionecrosis-derived microaneurysms in the distal penetrating cerebral arteries. The primary change of the arterionecrosis was the medial muscle cell necrosis, the causes of which were considered to be hypertension, aging, poor diet low in cholesterol, vasospasm, and the congenitally poor wall structure of the arteries. The development and healing of experimental arterionecrosis in hypertensive rats were also reported.     

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中国人群脑卒中的发病率呈上升趋势,脑卒中康复治疗是降低致残率最有效的方法。中国脑卒中康复治疗指南的出版,为脑卒中康复治疗的实施和评价提供了一个科学的证据基础。文章从脑卒中的康复管理及康复治疗两个方面,即卒中单元及三级康复管理,和有关脑卒中运动功能障碍的康复治疗方面进行阐述。     

Epidemiology of stroke

Stroke is the most common neurologic disease and the leading cause of adult disability in Western countries. The number of patients affected by stroke will increase by the effect of aging. Mainly due to increased life expectancy, the proportion of individuals over 65 years in the L'Aquila district showed an increase of 18.3% in a 10 years period (1981-1991). Among the resident population, in a five-year period (1994-1998) we collected all the patients with a first-ever stroke, and we found high crude and standardized (European population 1996) incidence rates. There was a significant correlation between crude and standardized incidence rates and proportion of individuals aged 65 and over, suggesting that the high incidence was due to an increased stroke risk linked to aging. As a cosequence, the number of subjects with atherosclerotic comorbidity will increase and the quality of life will worsen.     

Psychopathology of stroke

The psychopathology of stroke encompasses several psychiatric and behavioral disorders that have high prevalence in the geriatric population, reduce the patient autonomy and increase the caregiver's burden. These disorders are usually associated with other cognitive and neurological deficits, and are labelled as neuropsychiatric when the whole clinical picture is consistent with the specific dysfunction of a neural system or brain region. Thus the neuropsychiatry of stroke comprises disorders of the perception/identification of the self and the environment (anosognosia of hemiplegia, misidentification syndromes, confabulations, visual hallucinations, delirium and acute confusional state), amotivational syndromes (apathy and athymhormia), disorders of emotional reactivity (blunted affect, emotional incontinence, irritability, catastrophic reactions), poor impulse or ideation control (mania) and personality changes. The clinical profile of the subcortical vascular dementia also points to specific brain dysfunction (frontal-subcortical pathways) that manifests with behavioral (depression, emotionalism, irritability) and cognitive symptoms (psychomotor retardation, attention, executive and memory deficits). However, post-stroke depression and anxiety, which have a more variable clinical presentation and might be assimilated, for several aspects, to post-traumatic or adaptive disorders, are disorders less characterized in their neural correlates.     

Genetics of stroke

Stroke is the third leading cause of death and the leading cause of severe long-term disability in developed countries. Despite significant progress in understanding the risk factors conferring disease predisposition, the genetic and molecular basis of stroke remains poorly understood. Recent advances in the identification and characterization of patterns of DNA sequence variation in human populations hold the promise that stroke genomics will offer significant insights into disease pathophysiology and open new avenues for the development of novel therapeutic modalities. However, beyond single nucleotide polymorphisms, the emergence of additional sources of genomic variability as major factors in disease etiology is likely to transform our DNA-centric approaches toward more integrative and comprehensive strategies. This review provides an overview of the current progress and future prospects of the application of genomic sciences to stroke research.