主动脉夹层并发急性心肌梗死3例

主动脉夹层最主要的临床表现是胸背部剧痛和主动脉各分支受累的症状。其发病急骤、病情笃重，易与急性心肌梗死混淆，夹层血肿累及冠状动脉可并发急性心肌梗死。我院收治3例。     

尿免疫球蛋白和补体C3测定的临床意义

自1987年8月以来,我们对40例肾脏病患者测定尿免疫球蛋白和C_3,并与10例健康者对照,以探讨其判断肾小球病损程度和激素治疗效果的价值。1.病例选择:肾脏病患者40例中,男37例,女3例,年龄为12～70岁。其中急性肾炎4例,慢性肾炎普通型2例,高血压型2例,肾病综合征Ⅰ型18例,Ⅱ型11例,狼疮性肾炎2例,肾结核1例。本组18例作肾活     

急性主动脉夹层分离患者急性期护理

主动脉夹层分离是临床非常凶险的急症之一，为了最大限度地减少急性期的病死率和并发症，探讨其针对性的监护方法显得尤为重要。我科2000年6月至2005年4月收治动脉夹层分离患者26例，无1例发生死亡，现报告监护要点如下。     

补体5a受体在阿霉素致急性心力衰竭心肌损伤的早期研究

目的:探讨补体系统补体5a受体(complement 5a receptor,C5aR)在急性心力衰竭(心衰)早期,对心脏功能影响以及对心肌损伤的作用。方法:选择12 w龄C57BL/6J野生型及C5aR敲除小鼠各12只,分别随机分为野生小鼠对照组、野生小鼠心衰组、C5aR敲除小鼠对照组和C5aR敲除小鼠心衰组等共4组,每组6只。采用单次腹腔注射阿霉素20 mg/kg建立小鼠急性心衰模型,对照组采用同计量0.9%氯化钠液注射;阿霉素注射3d后显微超声检测小鼠心室射血分数和短轴缩短率,处死后测量体质量以及心脏质量;运用半定量PCR、蛋白印迹技术Western Blotting、免疫荧光等实验方法观察C5aR在野生小鼠心脏中的表达。C5aR敲除小鼠心脏组织采用HE染色观察心肌形态、Masson染色观察心肌纤维化程度,WGA染色观察心肌横截面大小,免疫组化染色观察转化生长因子-β(TGF-β)及α-平滑肌肌动蛋白(α-SMA)在心脏中表达。结果:与野生小鼠对照组相比,野生小鼠心衰组中C5aR的mRNA及蛋白表达均显著上调(P<0.05);与野生小鼠心衰组相比,C5aR敲除小鼠心衰组体质量及血压均显著升高(均为P<0.05),心室射血分数和短轴缩短率均显著升高(均为P<0.05),C5aR敲除小鼠心衰组胶原沉积及α-SMA表达均显著降低(均为P<0.05),TGF-β表达显著降低(P<0.01)。结论:C5aR在阿霉素诱导心衰模型中表达上调、加重了心肌损伤且促进了心脏纤维化,而C5aR敲除保护小鼠心功能并抑制纤维化,提示C5aR在小鼠急性心衰早期具有促进心脏纤维化作用。     

Stanford A型主动脉夹层患者血浆骨桥蛋白的表达及临床意义

目的探讨Stanford A型主动脉夹层患者血浆骨桥蛋白(OPN)表达水平及其临床意义。方法入选51例Stanford A型主动脉夹层患者(其中合并高血压29例,未合并高血压22例),同时选取14例单纯高血压患者及11名健康者作为对照。ELISA法检测血浆OPN水平。结果与健康对照者相比,主动脉夹层患者的血浆OPN水平显著升高[(234.9±20.5)pg/ml比(26.0±25.9)pg/ml,P<0.001]。与单纯高血压组[(24.6±21.9)pg/ml]及健康对照组[(26.0±25.9)pg/ml]相比,合并[(274.4±164.6)pg/ml]及未合并高血压的主动脉夹层患者[(182.8±99.5)pg/ml]的血浆OPN水平均显著升高(均为P<0.05)。Spearman相关性分析发现,主动脉夹层患者的血浆OPN水平与炎症指标C反应蛋白之间无显著相关性(r~2=0.06,P=0.09)。结论 OPN可能参与Stanford A型主动脉夹层的发生发展,但与血清C反应蛋白水平无相关性,其深入机制有待进一步研究。     

鼻息肉组织中补体C3、C4、C1q的表达及意义

采用免疫组化SABC法检测补体C3、C4和C1q在30例鼻息肉（NP）和14例正常下鼻甲组织中的表达,对C3、C4和C1q。表达阳性细胞的类型、分布进行分析。结果显示,C3、C4和C1q。在NP组织中的阳性表达率分别为76．67％、66．67％、63．33％,在下鼻甲组织中分别为21．43％、21．43％、14．29％,两者相比,P均〈0．01;C3、C4和C1q。主要表达于NP的上皮细胞及炎性细胞中。认为补体C3、C4和C1q。在NP的发生、发展中起着重要作用。     

急性主动脉夹层198例患者临床特征及两型比较

目的 分析急性主动脉夹层(acute aortic dissection,AAD)患者的危险因素、临床表现、并发症、诊断、治疗及结局。方法 回顾性分析198例AAD患者的临床资料,并比较A型AAD（type A AAD,A-AAD）和B型AAD（type B AAD,B-AAD）患者的临床特征。结果 AAD患者男女比例为3.5∶1。71.7%的AAD患者既往有高血压病史。81.3%的AAD患者发病时会出现胸痛。A-AAD患者并发急性心肌梗死的比例显著高于B-AAD患者（35% vs. 12%,P<0.01）。经胸心脏超声对A-AAD的筛检价值要高于B-AAD（36% vs. 8%,P<0.01）。A-AAD患者的院内总病死率显著高于B-AAD患者（20% vs. 1%,P<0.01）。结论 AAD患者男性明显多于女性,发病年龄呈正态分布。高血压病是其最常见的危险因素。AAD临床表现复杂多样,以胸痛最为常见。A-AAD患者更易并发急性心肌梗死。经胸心脏超声可作为A-AAD急诊筛查的首选方法。A-AAD和B-AAD患者的治疗和结局有所差异。     

老年急性脑梗死患者血清超敏C反应蛋白、补体3水平变化及临床意义

目的动态观察老年急性脑梗死(ACI)患者入院2 w内血清超敏C反应蛋白(hs-CRP)、补体3(C3)水平变化及临床意义。方法检测60例老年ACI患者入院1、3、7、14 d的血清hs-CRP和C3水平,并选取50例健康体检者作为对照。比较不同梗死面积、不同神经功能缺损程度ACI患者的血清hs-CRP和C3水平变化。结果 ACI组在入院1 d hs-CRP水平高于对照组(P<0.01),而C3水平低于对照组(P<0.01),在入院3、7 d时血清hs-CRP、C3水平均高于对照组(P<0.01),14 d时两组比较无明显差异(P=0.62)。ACI组中,不同病灶体积患者入院1、3、7 d的血清hs-CRP水平及入院3、7 d的补体C3水平差异有统计学意义,随着病灶体积的增大,血清hs-CRP及C3水平呈上升趋势(P<0.01)。不同神经功能缺损程度患者入院1、3、7 d的血清hs-CRP水平及入院3、7 d的补体C3水平差异有统计学意义,神经缺损程度越重,血清hs-CRP、C3水平越高(P<0.01)。结论 hs-CRP及C3与ACI的发生、发展、严重程度有关,有脑血管病危险因素者及ACI患者应常规检测血清hs-CRP及C3水平。     

主动脉夹层合并急性心肌梗死1例

<正>急性心肌梗死是我国常见急症,主要是由于冠脉病变后,发生冠脉血供减少或者中断,使相应的心肌严重而持久的缺血所致的部分心肌急性坏死,临床表现为胸痛,急性循环功能障碍,出现心电图(ECG)动态演变及心肌损伤标志物的升高。临床上其他肺动脉粥样硬化的原因如冠状动脉栓塞、主动脉夹层     

Analysis of complement C3 activation products in human atherosclerotic lesions.

Cleavage of the complement C3 protein is essential for complement activation. Saline extracts of human atherosclerotic lesions were examined by various techniques for the presence of C3 cleavage fragments. Crossed intermediate gel immunoelectrophoresis revealed that native C3 was the predominate C3 protein in extracts and that the C3dg fragment was also detected. SDS-PAGE/Western blot analyses of lesion extracts employing monoclonal antibodies directed at C3c and C3dg fragment determinants demonstrated molecular weight bands corresponding to the known molecular weights of all the physiologic C3 cleavage fragments, except C3b which is known to have a short half-life. After C3, the two most common fragments observed were C3c and C3dg. No bands other than those corresponding to known C3 cleavage fragments were observed and control antibody stains were always negative. In some blots bands with a greater molecular mass than C3 were evident, indicating that some of the C3 in lesions may be covalently bound to an activator. We have previously identified a large (100-500 nm) nonapoprotein containing lipid particle (LCA) as a major complement activating structure in human atherosclerotic lesions. Fractionation of lesion extracts by molecular sieve chromatography and sucrose density gradient centrifugation failed to reveal a concordance between LCA and C3 antigens. The results indicate that complement activation, i.e. C3 convertase formation, takes place in human atherosclerotic lesions and that activated C3 is degraded according to normal complement regulatory mechanisms.     

Differential expression of microRNAs in aortic tissue and plasma in patients with acute aortic dissection

Background Biomarker-assisted diagnosis of acute aortic dissection (AAD) is important for diagnosis and treatment. However, identification of biomarkers for AAD in blood is a challenging task. The aim of this study is to search for new potentially microRNA (miRNAs) biomarkers in AAD. Methods The miRNAs expression profiles in ascending aortic tissue and plasma were examined by microarray analysis in two sets or groups. The tissue group was composed of four patients with AAD and four controls of healthy male organ donors. The plasma group included 20 patients with AAD and 20 controls without cardiovascular disease. Bioinformatics was used to analyze the potential targets of the differentially expressed miRNAs. Results Our study revealed that in AAD patients, the aortic tissue had 30 differentially expressed miRNAs with 13 up-regulated and 17 down-regulated, and plasma had 93 differentially expressed miRNAs, of which 33 were up-regulated and 60 were down-regulated. Four miRNAs were found to be up-regulated in both aortic tissue and plasma in AAD patients. The predicted miRNA targets indicated the four dysregulated miRNAs mainly targeted genes that were associated with cell-cell adhesion, extracellular matrix metabolism, cytoskeleton organization, inflammation, and multiple signaling pathways related to cellular cycles. Conclusions Four miRNAs, which are up-regulated both in aortic tissue and in plasma in AAD patients, have been identified in this study. These miRNAs might be potential diagnostic biomarkers for AAD. Larger sample investigations are needed for further verification.     

C3bi receptor (complement receptor type 3) recognizes a region of complement protein C3 containing the sequence Arg-Gly-Asp.

Human phagocytes express a receptor termed complement receptor type 3 (CR3) that recognizes the complement protein fragment C3bi. We show here that CR3 recognizes a region of C3 that contains the sequence Arg-Gly-Asp (RGD). CR3 is down-modulated upon spreading of macrophages on surfaces coated with a synthetic 21-residue peptide from C3 (residues 1383-1403). This peptide was also attached to erythrocytes by coupling myristic acid to its amino terminus and allowing the myristoylated peptide to bind to erythrocytes through hydrophobic interactions. Erythrocytes coated with this RGD-containing segment of C3 were bound by macrophages, and binding could be blocked by specific monoclonal antibodies against CR3. Since CR3 recognizes a peptide sequence that contains the RGD triplet, it appears to be a member of a larger family of adhesion-promoting receptors that recognize RGD-containing proteins. However, since CR3 does not recognize a hexapeptide containing RGD, we presume that residues beyond the RGD triplet contribute to binding. We have compared the RGD-containing region of fibronectin and vitronectin, proteins known to be recognized by means of their RGD-containing regions, with those in human and murine C3. A striking homology is observed over an approximately equal to 50 amino acid sequence present in all four proteins. We suggest that this extended region of homology contains a structure recognized by adhesion-promoting receptors.     

D-dimer in acute aortic dissection

STUDY OBJECTIVE: Laboratory testing plays a minor role in the assessment of aortic dissection. Its main value is in the exclusion of other diseases. Following an incidental observation, we systematically investigated the relationship between elevated d-dimer levels and acute aortic dissection. DESIGN: We prospectively tested d-dimer levels in patients with suspected acute aortic dissection (10 patients). In addition, we investigated 14 patients who had received a confirmed diagnosis of thoracic aortic dissection during the previous 5 years, in whom d-dimer testing had been performed for differential diagnosis. Thirty-five patients with acute chest pain of other origin served as a control group. SETTING: Tertiary referral hospital. PATIENTS: Twelve patients had type A dissection (Stanford classification), and 12 patients had type B. MEASUREMENTS AND RESULTS: A d-dimer analysis was performed (Tina-quant assay; Roche Diagnostics; Mannheim, Germany) [normal limit of the assay, 0.5 micro g/mL]. The result of the d-dimer test was positive (ie, > 0.5 micro g/mL) in all patients (sensitivity of the test, 100%) with a mean value of 9.4 micro g/mL and a range of 0.63 to 54.7 micro g/mL. The degree of the elevation was correlated to the delay from the onset of symptoms to laboratory testing (mean, 12.6 h; range, 1 to 120 h) and showed a trend to the extent of the dissection, but not to the outcome (14 patients could be discharged; 10 patients died). CONCLUSIONS: Based on our observation, we suggest that testing for d-dimer should be part of the initial assessment of patients with chest pain, especially if aortic dissection is suspected. A negative test result makes the presence of the disease unlikely.     

Biomarkers in acute aortic dissection and other aortic syndromes

Acute aortic syndromes have an incidence of >30 per million per annum and a high mortality without definitive treatment. Survival may relate to the speed of diagnosis. Although pain is the most common symptom, there is a large fraction of patients in whom the diagnosis may be mistaken or overlooked. Currently, a high index of clinical suspicion is the chief prompt that diverts a patient into a definitive algorithm of imaging investigations. Although there is no point-of-care biochemical test that can be reliably used to positively identify dissection, biomarkers are available that could accelerate the diagnostic pathway and thereby expedite treatment.     

Autoantibody-mediated complement c3a receptor activation contributes to the pathogenesis of preeclampsia

Preeclampsia (PE) is a prevalent life-threatening hypertensive disorder of pregnancy associated with increased complement activation. However, the causative factors and pathogenic role of increased complement activation in PE are largely unidentified. Here we report that a circulating maternal autoantibody, the angiotensin II type 1 receptor agonistic autoantibody, which emerged recently as a potential pathogenic contributor to PE, stimulates deposition of complement C3 in placentas and kidneys of pregnant mice via angiotensin II type 1 receptor activation. Next, we provide in vivo evidence that selectively interfering with C3a signaling by a complement C3a receptor-specific antagonist significantly reduces hypertension from 167±7 to 143±5 mm Hg and proteinuria from 223.5±7.5 to 78.8±14.0 μg of albumin per milligram creatinine (both P<0.05) in angiotensin II type 1 receptor agonistic autoantibody-injected pregnant mice. In addition, we demonstrated that complement C3a receptor antagonist significantly inhibited autoantibody-induced circulating soluble fms-like tyrosine kinase 1, a known antiangiogenic protein associated with PE, and reduced small placental size with impaired angiogenesis and intrauterine growth restriction. Similarly, in humans, we demonstrate that C3 deposition is significantly elevated in the placentas of preeclamptic patients compared with normotensive controls. Lastly, we show that complement C3a receptor activation is a key mechanism underlying autoantibody-induced soluble fms-like tyrosine kinase 1 secretion and decreased angiogenesis in cultured human villous explants. Overall, we provide mouse and human evidence that angiotensin II type 1 receptor agonistic autoantibody-mediated activation contributes to elevated C3 and that complement C3a receptor signaling is a key mechanism underlying the pathogenesis of the disease. These studies are the first to link angiotensin II type 1 receptor agonistic autoantibody with complement activation and to provide important new opportunities for therapeutic intervention in PE.     

Optimal management of acute aortic dissection

Opinion statement  Acute aortic syndrome (AAS) encompasses a group of life-threatening aortic disorders that are increasing in prevalence. It classically presents with abrupt-onset chest pain that is of maximum intensity at onset. The syndrome requires prompt recognition and efficient treatment to optimize outcome. Contrast-enhanced CT is most commonly used as the definitive diagnostic imaging modality. Patients must be expeditiously transferred to institutions with case experience and medical, surgical, and endovascular expertise. Stanford type A dissections involve the ascending aorta and require emergent surgical consideration, unless underlying comorbidities make surgical risk prohibitive. Patients with Stanford type B, or descending, aortic dissection are less prone to rupture, shock, and cardiac complications. These patients are initially medically managed with targeted blood pressure and heart rate control. Surgical management is reserved for patients with intractable or recurrent pain, aortic expansion, end-organ ischemia, or progression of dissection. The feasibility of endovascular treatment is established, and its role in management continues to expand. Long-term follow-up with medical treatment and serial imaging of AAS patients is critical. Future directions in the diagnosis and treatment of AAS include using biomarkers to aid in diagnosis and prognosis, enhanced imaging with better resolution and reduced radiation exposure, and definition of the role of endovascular methods in acute and chronic settings.