CHA2DS2-VASc评分与非瓣膜性心房颤动并缺血性脑卒中患者预后的关系

目的:探讨非瓣膜病房颤卒中风险评分(CHA2DS2-VASc)与老年非瓣膜性心房颤动(NVAF)合并缺血性脑卒中(ICS)患者短期预后的关系。方法:入选我院2011年6月到2013年8月住院的206例老年NVAF合并ICS患者,应用CHA2DS2-VASc进行评分,分为低危组(24例,0分)、中危组(78例,1分)和高危组(104例,2~9分)。在发病后3个月时,采用改良Rankin量表(mRS)评定患者的预后,根据mRS得分将患者分为预后良好组(89例,0~2分)和预后不佳组(117例,3~6分)。分析患者3个月预后不佳的独立预测因素。结果:中危和高危组在年龄、高血压、糖尿病、心力衰竭、卒中、血管疾病史比例和美国国立卫生研究院卒中量表(NIHSS)评分显著高于低危组(P0.05或0.01)。与预后良好组比较,预后不佳组年龄[(72.81±7.68)岁比(81.56±8.03)岁]、高血压(58.4%比71.8%)、卒中史比例(9.0%比29.9%)、NIHSS评分[(2.97±1.42)分比(7.67±3.92)分]和CHA2DS2-VASc评分[(1.70±1.63)分比(4.03±2.53)分]显著升高,P0.05或0.01。多因素Logistic回归分析显示NIHSS评分(高危:OR=1.78,95%CI:1.27~2.56,P=0.001)、CHA2DS2-VASc评分(高危:OR=3.24,95%CI:1.32~6.98,P=0.001)和年龄(高危:OR=1.23,95%CI:1.07~1.54,P=0.01)是老年NVAF合并ICS患者3个月预后不佳的独立预测因素。结论:CHA2DS2-VASc评分与NVAF合并ICS早期病情改善有关,年龄、NIHSS评分和CHA2DS2-VASc评分是短期预后不佳的独立预测因素。     

CHA_2DS_2-VASc评分结合左心房内径在预测非瓣膜性心房颤动患者脑卒中风险评估中的应用

目的探讨CHA2DS2-VASc评分结合左房内径(LAD)对非瓣膜性房颤(NVAF)患者卒中风险的预测价值。方法对北京市应急总医院干部医疗科、心内科和首都医科大学附属北京市朝阳医院综合科于2012年1月至2014年12月收治的首次诊断为非瓣膜病心房颤动的患者共1216例进行同群队列研究,分为两组,一组为脑卒中组(366例),另一组为非脑卒中组(850例),收集相关资料,以缺血性脑卒中为终点事件,平均随访时间为(30±6)月,分析两组患者的CHA2DS2-VASc评分、左心房内径及二者联合在非瓣膜性房颤患者发生脑卒中风险评估中的ROC曲线下面积。结果脑卒中组患者的CHA2DS2-VASc评分(5.23±1.58分)显著高于非脑卒中组(2.96±1.52)分(P0.01)。脑卒中组患者的左心房内径(42.39±5.79)mm与非脑卒中组(42.12±6.85)mm相比,无显著差异(P0.05)。非瓣膜性房颤患者发生脑卒中风险评估中CHA2DS2-VASc评分、左心房内径、CHA2DS2-VASc评分+左心房内径的ROC曲线下面积分别为0.854、0.524、0.856,95%CI分别为0.83～0.88、0.49～0.56、0.83～0.88。CHA2DS2-VASc评分+LAD二者联合ROC曲线下面积较CHA2DS2-VASc评分相比无显著差异(P0.05)。结论 CHA2DS2-VASc评分对我国NVAF患者卒中风险的预测价值良好;LAD对NVAF患者卒中风险预测有诊断价值,但较CHA2DS2-VASc评分相比,诊断价值不高;CHA2DS2-VASc评分联合LAD对预测NVAF患者卒中风险价值较单独应用CHA2DS2-VASc评分无明显优势。     

非瓣膜性心房颤动患者红细胞分布宽度与CHADS2、CHA2DS2-VASc评分的关系

目的:探讨非瓣膜性心房颤动(房颤)患者红细胞分布宽度(RDW)与评估房颤患者发生血栓栓塞风险的CHADS2和CHA2DS2-VASc评分的关系。方法:连续入选非瓣膜性房颤患者99例(其中阵发房颤68例,持续房颤31例),每例患者均进行CHADS2和CHA2DS2-VASc评分,同时记录年龄、性别、伴发疾病、实验室指标及超声心动图结果。根据CHADS2及CHA2DS2-VASc评分将房颤患者发生血栓栓塞的风险分为低中危组和高危组,比较房颤患者发生血栓栓塞风险的低中危组与高危组各项指标的差异,同时探讨房颤患者RDW与CHADS2、CHA2DS2-VASc评分的关系。结果:无论何种分组方式,两组间年龄、高血压史、糖尿病史、冠心病史、脑卒中史有统计学差异(P0.05)。与低中危组相比,高危组患者年龄增加,RDW、血肌酐升高,左房直径增加,左室射血分数下降(P0.05)。多变量Logistic回归分析显示,RDW是房颤患者CHADS2、CHA2DS2-VASc评分的独立预测因素(OR值分别是2.184、3.815,均P0.05)。预测CHADS2高分的RDW的ROC曲线下面积为0.690(95%CI:0.583~0.797,P0.05),预测CHA2DS2-VASc高分的RDW的ROC曲线下面积为0.735(95%CI:0.634~0.836,P0.05)。结论:非瓣膜性房颤患者RDW与CHADS2和CHA2DS2-VASc评分呈正相关,而且是CHADS2、CHA2DS2-VASc评分的独立预测因素。     

CHADS2评分与CHA2DS2-VASc评分在非瓣膜病房颤患者左房血栓风险评估中的对比分析

目的探讨CHADS2评分及CHA2DS2-VASc评分在非瓣膜病心房颤动(AF)患者左房血栓风险评估中的作用。方法 2011年6月至2015年6月选择该院收治的非瓣膜病AF患者423例,根据其左房是否发生血栓分为左房血栓组和未发生左房血栓组;采用CHADS2评分系统和CHA2DS2-VASc评分系统对非瓣膜病AF患者发生血栓事件的风险进行危险分层,收集患者一般临床资料,采用Logistics回归对左房血栓发生的危险因素进行分析。结果 423例非瓣膜病AF患者进行食道心脏超声检查发现65例(15.36%)发生左房血栓;患者CHADS2评分显著低于CHA2DS2-VASc评分(P0.05);秩和检验显示CHA2DS2-VASc评分系统对患者危险分层的严重程度显著高于CHADS2评分系统(P0.05);随着CHADS2评分系统和CHA2DS2-VASc评分系统危险的增加患者发生左房血栓的比例逐渐升高(P0.05);单因素分析显示年龄≥65岁、左房内径≥38 mm及射血分数≤40%是非瓣膜病AF患者发生左房血栓的危险因素(P0.05);多因素Logistics回归显示CHA2DS2-VASc评分是导致非瓣膜病AF患者发生左房血栓的危险因素。结论 CHA2DS2-VASc评分能够预测非瓣膜病AF患者左房血栓的发生,其预估价值明显优于CHADS2评分。     

CHADS2及CHA2DS2-VASc评分在冠心病外科治疗中的应用

目的：评价CHADS2及CHA2DS2-VASc评分系统在冠心病外科治疗中的意义。 方法：选择2006年1月至2010年1月行不停跳冠状动脉旁路移植术的768个病人,术后新发房颤患者97例,回顾病人的围术期及随访资料,应用CHADS2及CHA2DS2-VASc评分系统,进行分析。 结果：分为术后新发房颤组与非房颤组。术后新发房颤发生率12.6%。平均年龄70.74±8.21岁和65.90±9.83岁,围术期脑卒中8例和9例,CHADS2评分值分别为3.2±1.26和2.13±0.94,CHA2DS2-VASc评分值分别为4.2±1.50和3.23±1.07,CHADS2和CHA2DS2-VASc评分是术后新发房颤的预测因素,与围术期脑卒中显著相关,P < 0.01。 结论：冠心病外科治疗中应用CHADS2及CHA2DS2-VASc评分系统可预测术后新发房颤及围术期脑卒中,对冠心病术后新发房颤的抗凝及抗血小板治疗决策提供了依据,对卒中风险及预后有一定的评估价值。     

老年非瓣膜性心房颤动患者发生缺血性脑卒中的危险因素分析

目的:分析老年非瓣膜性心房颤动(房颤)患者发生缺血性脑卒中的危险因素。方法:回顾性分析我院2010-01至2014-12期间收入院的180例房颤患者的临床资料。根据计算机断层摄影术(CT)和(或)核磁共振成像(MRI)检查确诊缺血性脑卒中,分为房颤合并缺血性脑卒中组(n=120例)和单纯房颤组(n=60例),分别评估两组患者CHA2DS2-VASc评分、CHADS2评分、同型半胱氨酸(HCY)、纤维蛋白原(FIB)、左心房内径(LAD)、血脂水平和肾功能等之间的差异。结果:房颤合并缺血性脑卒中组和单纯房颤组患者在CHA2DS2-VASc评分、CHADS2评分、HCY、FIB、LAD之间差异存在统计学意义(P0.05)。Logistic回归分析显示CHA2DS2-VASc评分、CHADS2评分、HCY、FIB、LAD是房颤患者发生缺血性脑卒中的独立危险因素。CHA2DS2-VASc评分用于卒中危险分层与CHADS2评分比较有差异。结论:影响老年房颤患者发生缺血性脑卒中的因素除CHA2DS2-VASc评分、CHADS2评分系统外,联合测定HCY、FIB和LAD预测房颤患者发生缺血性脑卒中具有重要的临床价值,可使筛查非瓣膜性房颤患者发生缺血性脑卒中高危人群的工作操作更加方便、客观。CHA2DS2-VASc适宜筛查低危人群,CHADS2适宜筛查高危人群。     

比较CHADS2和CHA2DS2-VASc评分对非瓣膜性心房颤动卒中和血栓栓塞发生风险的预测价值——Meta分析

目的:比较CHADS2和CHA2DS2-VASc评分对非瓣膜性心房颤动(NVAF)患者卒中和血栓栓塞发生风险的预测价值。方法:系统性检索Cochrane图书馆,EMBASE、EBSCO和PubMed数据库中有关CHADS2和CHA2DS2-VASc评分预测NVAF患者卒中和血栓栓塞发生风险的英文文献。采用STATA 12.0软件进行统计分析。结果:本研究共纳入11篇文献。当C-统计量作为连续型变量分析时,CHADS2评分C-统计量分布从0.650到0.717,中位数0.660;CHA2DS2-VASc评分C-统计量分布从0.637到0.724,中位数0.697,合并后C-统计量分别为0.66(0.66~0.67)和0.67(0.66~0.68)。当C-统计量作为分类型变量分析时,CHADS2评分C-统计量分布从0.586到0.722,中位数0.630;CHA2DS2-VASc评分C-统计量分布从0.521到0.850,中位数0.606,合并后C-统计量分别为0.65(0.62~0.67)和0.63(0.59~0.68),但存在高异质性,结果需慎重分析。CHA2DS2-VASc评分低危组的不良事件发生率明显比CHADS2评分低(0.54%:1.40%,P0.05),且将更多的患者划分到高危组(81.0%:46.0%,P0.05)。结论:CHADS2和CHA2DS2-VASc评分对NVAF患者卒中和血栓栓塞发生风险的预测价值相类似。但CHA2DS2-VASc评分更容易发现真正"低危"患者,且将更多的患者纳入高危组,有利于指导临床上预防性治疗。     

CHA 2DS 2_VASc 评分与射频消融术前心房颤动患者左心房／左心耳血栓形成的关系

目的探讨CHA2DS2-VASc评分与射频消融术前心房颤动患者左心房（left atrium ,LA）/左心耳（left atrial ap-pendage ,LAA ）发生血栓事件的关系。方法根据术前食管超声心动图检查结果,将接受射频消融术的心房颤动患者分为LA/LAA血栓形成组（n＝21）与血栓未形成组（n＝21）,对照分析CHA2 DS2-VASc及CHADS2评分对血栓事件的预测价值。结果血栓形成组21例（3.8％）患者血栓均位于LAA ,低危组（0分）、中危组（1分）、高危组（≥2分）间,LA/LAA血栓事件发生率无统计学意义（ P＞0.05）,但≥3分患者血栓形成明显多于＜2分（ P＜0.01）。血栓形成组CHA2 DS2-VASc评分、CHADS2评分、左心房内径（LAD ）显著高于血栓未形成组外,其余临床因素间比较均无统计学意义。多元Logistic回归分析显示：LAD、CHA2 DS2-VASc评分是LA/LAA血栓形成的独立危险因素（OR＝0.81、0.89,P＜0.05）。结论无论CHA2 DS2-VASc评分的高低,所有房颤患者射频消融术前均需接受食管超声心动图探查,LAD越大、CHA2 DS2-VASc评分越高,LA/LAA血栓事件发生可能性越高。     

CHADS2和CHA2DS2-VASc对病窦综合征患者起搏器置入术后脑卒中风险的评估

目的:探讨CHADS2和CHA2DS2-VASc对病窦综合征患者起搏器置入术后脑卒中风险的评估作用。方法:分别采用CHADS2和CHA2DS2-VASc评分标准对病窦综合征起搏器置入术后患者进行评分,并随访5年观察脑梗死的发生率。结果:CHADS2和CHA2DS2-VASc评分法预测病窦综合征起搏器置入术后患者5年内脑梗死风险,受试者工作曲线下面积(AUCROC)分别为(0.59,95%CI:0.49~0.70)和(0.72,95%CI:0.63~0.80)。CHA2DS2-VASc评分低危组14例患者均未并发脑梗死,中危组33例患者中1例(3.6%)并发脑梗死,高危组167例患者中13例(7.78%)并发脑梗死;三组间脑梗死发生率比较,差异有统计学意义(均P0.05)。线性回归分析显示,CHA2DS2-VASc评分与病窦综合征起搏器置入术后患者并发脑梗死呈正相关(r=0.851,P=0.007)。CHA2DS2-VASc评分标准中,病窦综合征起搏器置入术后患者并发脑梗死的各项,差异均有统计学意义(均P0.05)。结论:CHA2DS2-VASc评分法可有效评估病窦综合征起搏器置入术后患者并发脑梗死的风险。     

老年非瓣膜性心房颤动合并缺血性脑血管病住院患者抗凝治疗研究

目的:本研究回顾性调查老年非瓣膜性心房颤动(NVAF)合并缺血性脑血管病[缺血性脑卒中和短暂性脑缺血发作(TIA)]的住院患者抗凝治疗实际应用情况。方法:选择出院诊断为NVAF合并缺血性脑卒中/TIA的老年住院患者626例,应用CHA2DS2-VASc评分评估脑卒中危险,结合CHA2DS2-VASc评分调查各分层的住院期间抗凝治疗情况,并按年龄分为非高龄组(65~74岁,n=316)和高龄组(≥75岁,n=310),比较两组的抗凝治疗情况。结果:626例老年NVAF合并缺血性脑卒中/TIA患者CHA2DS2-VASc评分均>2分,平均(5.48±1.27)分,其中仅35.3%使用口服抗凝药物治疗,而51.6%使用抗血小板治疗,13.1%未使用上述两种药物治疗,高龄组的患者抗凝比例明显小于非高龄组的患者(28.4%vs.42.1%,P<0.001)。结论:本研究结果提示老年NVAF合并缺血性脑卒中/TIA住院患者抗凝治疗比例偏低,应使用指南推荐的CHA2DS2-VASc评分制定抗凝策略以提高抗凝比例。     

Classification and characterization of hereditary types 2A, 2B, 2C, 2D, 2E, 2M, 2N, and 2U (unclassifiable) von Willebrand disease.

All variants of type 2 von Willebrand disease (VWD) patients, except 2N, show a defective von Willebrand factor (VWF) protein (on cross immunoelectrophoresis or multimeric analysis), decreased ratios for VWF:RCo/Ag and VWF:CB/Ag and prolonged bleeding time. The bleeding time is normal and FVIII:C levels are clearly lower than VWF:Ag in type 2N VWD. High resolution multimeric analysis of VWF in plasma demonstrates that proteolysis of VWF is increased in type 2A and 2B VWD with increased triplet structure of each visuable band (not present in types 2M and 2U), and that proteolysis of VWF is minimal in type 2C, 2D, and 2E variants that show aberrant multimeric structure of individual oligomers. VWD 2B differs from 2A by normal VWF in platelets, and increased ristocetine-induced platelet aggregation (RIPA). RIPA, which very likely reflects the VWF content of platelets, is normal in mild, decreased in moderate, and absent in severe type 2A VWD. RIPA is decreased or absent in 2M, 2U, 2C, and 2D, variable in 2E, and normal in 2N. VWD 2M is usually mild and characterized by decreased VWF:RCo and RIPA, a normal or near normal VWF multimeric pattern in a low resolution agarose gel. VWD 2A-like or unclassifiable (2U) is distinct from 2A and 2B and typically featured by low VWF:RCo and RIPA with the relative lack of high large VWF multimers. VWD type 2C is recessive and shows a characteristic multimeric pattern with a lack of high molecular weight multimers, the presence of one single-banded multimers instead of triplets caused by homozygosity or double hereozygosity for a mutation in the multimerization part of VWF gene. Autosomal dominant type 2D is rare and characterized by the lack of high molecular weight multimers and the presence of a characteristic intervening subband between individual oligimers due to mutation in the dimerization part of the VWF gene. In VWD type 2E, the large VWF multimers are missing and the pattern of the individual multimers shows only one clearly identifiable band, and there is no intervening band and no marked increase in the smallest oligomer. 2E appears to be less well defined, is usually autosomal dominant, and accounts for about one third of patients with 2A in a large cohort of VWD patients.     

Structure-function of Hb Marseille-Long Island [alpha 2 beta 2 N-methionyl-2(NA2) His----Pro

Suspensions of red cells containing Hb Marseille-Long Island showed decreased oxygen affinity and low interaction with 2,3-diphosphoglycerate. Oxygen equilibrium studies of the purified component confirmed these abnormalities. Oxidation rate measurements of carbonmonoxy-Hb Marseille and carbonmonoxy-Hb A by ferricyanide showed an increased rate for the former, suggesting an increased dissociation constant for carbon monoxide. Nuclear Magnetic Resonance spectra in the high field region revealed small changes in the proximal region of the heme pocket. These results indicated that the mutation causes a perturbation at a distance from the mutation site.     

Different RBC aggregating properties of the Aalpha2Bbeta2gammaA2 and Aalpha2Bbeta2gammaAgamma' subpopulations of human fibrinogen

Human fibrinogen (TF) has been separated into two fractions: F1 - homodimers with respect to the gamma chain, and F2 - heterodimers composed of gammaA and gamma' polypeptides. Their rouleaux-inducing properties were as follows: (1) both, at the same concentration of 0.8%, were less effective than TF; (2) F1 produced larger rouleaux even under static conditions of a hemocytometer where F2 was silent; (3) F2 induced the process when a suspension was gently sheared between microscopic slides. Since the synthetic peptide gamma'(414-427) inhibited the rouleau formation in a mixture with F2, the C-terminal amino acids of the gamma' polypeptide probably bind the molecule to the cell. The inhibition was feebly visible in the native ratio of F1/F2, implicating a compensatory effect of F1.     

Identification of SH2B2beta as an inhibitor for SH2B1- and SH2B2alpha-promoted Janus kinase-2 activation and insulin signaling

The SH2B family has three members (SH2B1, SH2B2, and SH2B3) that contain conserved dimerization (DD), pleckstrin homology, and SH2 domains. The DD domain mediates the formation of homo- and heterodimers between members of the SH2B family. The SH2 domain of SH2B1 (previously named SH2-B) or SH2B2 (previously named APS) binds to phosphorylated tyrosines in a variety of tyrosine kinases, including Janus kinase-2 (JAK2) and the insulin receptor, thereby promoting the activation of JAK2 or the insulin receptor, respectively. JAK2 binds to various members of the cytokine receptor family, including receptors for GH and leptin, to mediate cytokine responses. In mice, SH2B1 regulates energy and glucose homeostasis by enhancing leptin and insulin sensitivity. In this work, we identify SH2B2beta as a new isoform of SH2B2 (designated as SH2B2alpha) derived from the SH2B2 gene by alternative mRNA splicing. SH2B2beta has a DD and pleckstrin homology domain but lacks a SH2 domain. SH2B2beta bound to both SH2B1 and SH2B2alpha, as demonstrated by both the interaction of glutathione S-transferase-SH2B2beta fusion protein with SH2B1 or SH2B2alpha in vitro and coimmunoprecipitation of SH2B2beta with SH2B1 or SH2B2alpha in intact cells. SH2B2beta markedly attenuated the ability of SH2B1 to promote JAK2 activation and subsequent tyrosine phosphorylation of insulin receptor substrate-1 by JAK2. SH2B2beta also significantly inhibited SH2B1- or SH2B2alpha-promoted insulin signaling, including insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1. These data suggest that SH2B2beta is an endogenous inhibitor of SH2B1 and/or SH2B2alpha, negatively regulating insulin signaling and/or JAK2-mediated cellular responses.