Antenatal diagnosis of idiopathic dilatation of pulmonary artery with 3D power doppler imaging

We present a case of antenatal diagnosis of idiopathic dilatation of the pulmonary artery by three‐dimensional power Doppler imaging (HDliveFlow with silhouette mode). Two‐dimensional sonography clearly demonstrated a 10.4‐mm‐diameter fetal pulmonary artery (PA), whereas the aorta (Ao) diameter was 5.04 mm. HDliveFlow clearly demonstrated the spatial relationships and different sizes of PA and Ao. The PA size returned to normal (8.0 mm) on the 11th day after birth (Ao: 9.0 mm). HDliveFlow may be an adjunctive tool to two‐dimensional sonography to diagnose abnormalities of fetal great vessels. © 2016 Wiley Periodicals, Inc. J Clin Ultrasound 45 :121–123, 2017;     

Acute diffuse thyroid swelling: A rare complication of fine‐needle aspiration

We present a case illustrating the rare complication of acute generalized thyroid swelling shortly after sonographic‐guided fine needle aspiration of a thyroid nodule. Ultrasound revealed the presence of characteristic linear hypoechoic avascular areas interspersed throughout the gland suggestive of edema. The patient was treated conservatively, with near complete normalization of the thyroid within 24 hours. Recognition of this potential complication is important, as the rapid onset of diffuse thyroid enlargement is often alarming but typically has a transient and self‐limiting course. © 2017 Wiley Periodicals, Inc. J Clin Ultrasound 45 :426–429, 2017     

Effect of the small molecule plasminogen activator inhibitor‐1 (PAI‐1) inhibitor,PAI‐749, in clinical models of fibrinolysis

Summary. Background: The principal inhibitor of fibrinolysis in vivo is plasminogen activator inhibitor‐1 (PAI‐1). PAI‐749 is a small molecule inhibitor of PAI‐1 with proven antithrombotic efficacy in several preclinical models. Objective: To assess the effect of PAI‐749, by using an established ex vivo clinical model of thrombosis and a range of complementary in vitro human plasma‐based and whole blood‐based models of fibrinolysis. Methods: In a double‐blind, randomized, crossover study, ex vivo thrombus formation was assessed using the Badimon chamber in 12 healthy volunteers during extracorporeal administration of tissue‐type plasminogen activator (t‐PA) in the presence of PAI‐749 or control. t‐PA‐mediated lysis of plasma clots and of whole blood model thrombi were assessed in vitro. The role of vitronectin was examined by assessing lysis of fibrin clots generated from purified plasma proteins. Results: There was a dose‐dependent reduction in ex vivo thrombus formation by t‐PA (P < 0.0001). PAI‐749 had no effect on in vitro or ex vivo thrombus formation or fibrinolysis in the presence or absence of t‐PA. Inhibition of PAI‐1 with a blocking antibody enhanced fibrinolysis in vitro (P < 0.05). Conclusions: Despite its efficacy in a purified human system and in preclinical models of thrombosis, the current study suggests that PAI‐749 does not affect thrombus formation or fibrinolysis in a range of established human plasma and whole blood‐based systems.     

In vivo migration of endogenous brain progenitor cells guided by an injectable peptide amphiphile biomaterial

Biomaterials hold great promise in helping the adult brain regenerate and rebuild after trauma. Peptide amphiphiles (PAs) are highly versatile biomaterials, gelling and forming macromolecular structures when exposed to physiological levels of electrolytes. We are here reporting on the first ever in vivo use of self‐assembling PA carrying a Tenascin‐C signal (E₂Ten‐C PA) for the redirection of endogenous neuroblasts in the rodent brain. The PA forms highly aligned nanofibers, displaying the migratory sequence of Tenascin‐C glycoprotein as epitope. In this in vivo work, we have formed in situ a gel of aligned PA nanofibers presenting a migratory Tenascin‐C signal sequence in the ventral horn of the rostral migratory stream, creating a track reaching the neocortex. Seven days posttransplant, doublecortin positive cells were observed migrating inside and alongside the injected biomaterial, reaching the cortex. We observed a 24‐fold increase in number of redirected neuroblasts for the E₂Ten‐C PA–injected animals compared to control. We also found injecting the E₂Ten‐C PA to cause minimal neuroinflammatory response. Analysing GFAP⁺ astrocytes and Iba1⁺ microglia activation, the PA does not elicit a stronger neuroinflammatory response than would be expected from a small needle stab wound. Redirecting endogenous neuroblasts and increasing the number of cells reaching a site of injury using PAs may open up new avenues for utilizing the pool of neuroblasts and neural stem cells within the adult brain for regenerating damaged brain tissue and replacing neurons lost to injury.     

Pilomatricoma: An unusual cause of lump in a male breast

We present the case of a 48‐year‐old man who presented with a painless, progressively increasing lump in the left breast. The mammographic and sonographic appearance of the lesion was suspicious for malignancy. Fine needle aspiration cytology and histopathologic examination confirmed the diagnosis of pilomatricoma. © 2017 Wiley Periodicals, Inc. J Clin Ultrasound 46 :209–211, 2018     

Retinoids and activation of PKC induce tissue‐type plasminogen activator expression and storage in human astrocytes

Summary. Background: Emerging data demonstrate important roles for tissue‐type plasminogen activator (t‐PA) in the central nervous system (CNS). In contrast to endothelial cells, little is known about the regulation of t‐PA gene expression and secretion in astrocytes. Objectives: The aims of the present study were to investigate whether t‐PA gene expression is regulated by retinoids and the protein kinase C (PKC) activator phorbol 12‐myristate 13‐acetate (PMA) in human astrocytes, and to study whether t‐PA is stored and subject to regulated release from these cells, as with endothelial cells. Methods: Native human astrocytes were treated with RA and/or PMA. mRNA was quantified by real‐time RT‐PCR and protein secretion determined by ELISA. Intracellular t‐PA immunoreactivity in astrocytes was examined by immunocyto‐ and histochemistry. Results: RA and/or PMA induced a time‐dependent increase in t‐PA mRNA and protein levels in astrocytes, reaching 10‐fold after combined treatment. This was associated with increased amounts of t‐PA storage in intracellular granular structures. Both forskolin and histamine induced regulated release of t‐PA. The presence of t‐PA in reactive astrocytes was confirmed in human brain tissue. Conclusions: These data show that RA and PKC activation induce a strong up‐regulation of t‐PA expression in astrocytes, and increased intracellular storage pools. Moreover, a regulated release of t‐PA can be induced from these cells. This raises the possibility that astrocytes contribute to the regulation of extracellular t‐PA levels in the CNS.     

The spatial dynamics of fibrin clot dissolution catalyzed by erythrocyte‐bound vs. free fibrinolytics

Summary. Background: Coupling fibrinolytic plasminogen activators to red blood cells (RBCs) has been proposed as an effective, yet safe method of thromboprophylaxis, because of increased circulation lifetime and reduced propensity to induce hemorrhage by selectivity for nascent thrombi rather than pre‐formed hemostatic clots. Objectives and methods: We used confocal microscopy of fluorescently labeled fibrin and erythrocytes in plasma‐derived clots to study the spatial dynamics of lysis catalyzed by RBC‐coupled vs. free plasminogen activators (RBC‐PA vs. PA). Results: Clot lysis catalyzed by free PA progressed gradually and uniformly. In contrast, distinct holes formed surrounding RBC‐PA while the rest of the clot remained intact until these holes enlarged sufficiently to merge, causing sudden clot dissolution. Compared with naïve RBCs within clots lysed by free PA, RBC‐PA moved faster inside the fibrin network prior to clot dissolution, providing a potential mechanism for spatial propagation of RBC‐PA induced lysis. We also showed the focal nature of fibrinolysis by RBC‐PA as dense loading of PA onto RBCs initiates more efficient lysis than equal amounts of PA spread sparsely over more RBCs. In an in vitro model of clots exposed to buffer flow, incorporated RBC‐PA increased permeability and formed channels eventually triggering clot dissolution, whereas clots containing free PA remained intact. Conclusions: Clot lysis by RBC‐PA begins focally, has a longer lag phase when measured by residual mass than homogeneous lysis by PA, is propagated by RBC‐PA motility and provides more effective clot reperfusion than free PA, making RBC‐PA attractive for short‐term thromboprophylaxis.     

Acute endothelial tissue plasminogen activator release in pregnancy

Summary. Objective: Pregnancy is associated with marked changes in vascular physiology and an increased risk of thrombosis. The aim of the study was to assess the effect of pregnancy on the acute release of tissue plasminogen activator (t‐PA) from the endothelium. Methods and results: Ten primigravida pregnant women were recruited in the third trimester of pregnancy (week 36 ± 1) and compared with 20 age‐matched non‐pregnant women (day 9.8 ± 0.3 of menstrual cycle). Blood flow and plasma fibrinolytic factors were measured in both forearms by venous occlusion plethysmography and blood sampling, respectively, during unilateral brachial artery infusions of bradykinin (100–1000 pmol min^?1). Pregnant women had higher plasma plasminogen activator inhibitor type 1 (PAI‐1) antigen concentrations (77.1 ± 12.4 vs. 21.5 ± 9.8 ng mL^?1; P = 0.004) that resulted in lower basal t‐PA/PAI‐1 ratios (0.2 ± 0.1 vs. 0.6 ± 0.1; P = 0.02) and plasma t‐PA activity concentrations (0.17 ± 0.02 vs. 0.58 ± 0.06 IU mL^?1; P < 0.0004). In both groups, bradykinin caused dose‐dependent increases in blood flow and local release of plasma t‐PA antigen and activity (P < 0.005 for all). Both the plasma t‐PA/PAI‐1 ratios and the net release of active t‐PA were markedly reduced in pregnant women (P < 0.05 for both). Area under the curve for net active t‐PA release was reduced by 36%. Conclusions: Pregnancy is associated with major perturbations of endogenous fibrinolytic capacity with an overwhelming increase in plasma PAI‐1 concentrations and an inadequate release of active t‐PA. These prothrombotic effects may, in part, explain the increased risk of arterial and venous thrombosis in pregnant women.     

Activation of single‐chain urokinase‐type plasminogen activator by platelet‐associated plasminogen: a mechanism for stimulation of fibrinolysis by platelets

Summary. Background and Objective: Platelets are essential for hemostasis, and they cause resistance to fibrinolysis by tissue‐type plasminogen activator. In contrast, platelets enhance fibrinolysis mediated by single‐chain urokinase‐type plasminogen activator (scu‐PA). This study investigated the mechanism behind this profibrinolytic role of platelets. Methods and Results: Platelets enhanced scu‐PA activity, but not urokinase‐type plasminogen activator (u‐PA) activity, in plasma clot lysis and chromogenic assays. We established, using the non‐cleavable scu‐PA mutant (Lys158→Glu) and protease inhibitors, that platelets increased activation to u‐PA by a serine protease. Activation of scu‐PA was platelet‐dependent, even in plasma. It occurred in platelet‐rich but not in platelet‐poor plasma, as assessed by sodium dodecylsulfate polyacrylamide gel electrophoresis and zymography after addition of plasminogen activator inhibitor‐1. Candidate proteases that are known to activate scu‐PA and are present in platelet preparations were investigated. Factor VII activating protease was detected in platelet preparations by western blotting, but its inhibition by antibodies did not inhibit activation of scu‐PA by platelets. Plasmin and plasma kallikrein both mimicked the platelet effect, but were distinguished by their responses to a range of inhibitors. Analysis of platelet‐associated protease activity and the time course of scu‐PA activation pointed towards plasminogen, and the data were consistent with a mechanism of reciprocal activation. The essential role of plasminogen was revealed using platelets from plasminogen‐deficient mice, which could not activate scu‐PA. Local plasminogen on platelet membranes was markedly more effective than solution‐phase plasminogen in activation of scu‐PA. Conclusions: Platelets enhance fibrinolysis by scu‐PA through reciprocal activation of scu‐PA and platelet‐associated plasminogen, a system that is potentially important in the lysis of platelet‐rich thrombi.     

The role of thrombin activatable fibrinolysis inhibitor and factor XI in platelet‐mediated fibrinolysis resistance: a thromboelastographic study in whole blood

Summary. Background: The resistance of platelet‐rich thrombi to fibrinolysis is generally attributed to clot retraction and platelet PAI‐1 release. The role of TAFI in platelet‐mediated resistance to lysis is unclear. Objective: We investigated the contribution of TAFI to the antifibrinolytic effect of platelets in whole blood by thromboelastography. Methods: Platelet‐poor (PP‐WB, < 40 × 10³ μL^?1) and platelet‐rich (PR‐WB, > 400 × 10³ μL^?1) blood samples were obtained from normal human blood (N‐WB, 150–220 × 10³ μL^?1). Clot lysis time was measured by thromboelastography in recalcified blood supplemented with t‐PA (100 ng mL^?1) and tissue factor (1:1000 Recombiplastin). Results: t‐PA‐induced lysis time increased in parallel with platelet concentration (up to 3‐fold). Neutralization of TAFI, but not of PAI‐1, shortened the lysis time by ～ 50% in PR‐WB and by < 10% in PP‐WB. Accordingly, prothrombin F1+2 and TAFIa accumulation was greater in PR‐WB than in PP‐WB. A similar TAFI‐dependent inhibition of fibrinolysis was observed when clot retraction was prevented by cytochalasin D or abciximab, or when platelet membranes were tested. Moreover, in blood with an intact contact system, platelet‐mediated fibrinolysis resistance was attenuated by an anti‐FXI but not by an anti F‐XII antibody. Finally, platelets made the clots resistant to the profibrinolytic effect of heparin concentrations displaying a strong anticoagulant activity. Conclusions: Our data indicate that TAFI activation is one major mechanism whereby platelets make clots resistant to fibrinolysis and underscore the importance of TAFI inhibitors as new antithrombotic agents.     

Portal systemic shunt between the hepatic portal vein and right renal vein in a patient with multifocal hepatocellular carcinoma: Case report

Portal hypertension is a clinical syndrome characterized by the development of collateral circulation and portosystemic shunts, as well as ascites and hepatic encephalopathy. We present the case of a large portosystemic shunt between the hepatic portal vein and aneurysmal right renal vein in a cirrhotic 64‐year‐old man with thrombosis of the portal vein and hepatocellular carcinoma. This is a very rare clinical manifestation which, to our knowledge, has been described only once previously in the literature. © 2017 Wiley Periodicals, Inc. J Clin Ultrasound 45 :524–527, 2017     

Sex differences in the relationship between inflammatory and hemostatic biomarkers and metabolic syndrome: British 1958 Birth Cohort

Summary. Background: Circulating levels of C‐reactive protein (CRP), fibrinogen, fibrin D‐dimer, tissue plasminogen activator antigen (t‐PA) and von Willebrand factor (VWF) are associated with incident coronary heart disease (CHD). However, their associations with metabolic syndrome and its components in large populations of men and women have not been well defined. Objectives: We compare the sex associations of these biomarkers with established CHD risk factors, metabolic syndrome and its components in a large cohort. Patients and Methods: 8302 men and women aged 45 years from the British 1958 birth cohort provided a blood sample. Analyses were restricted to 3457 men and 3464 women with complete data on all risk factors and no history of cardiovascular disease. Multiple regression analyses adjusted for smoking, social class, alcohol consumption and variables related to biomarker measurement error. Results: Adjusted sex differences in levels of all biomarkers (except VWF) varied according to presence/absence of metabolic syndrome, its components and obesity (BMI ≥30 kg m^?2). Associations in women were up to twice as strong for CRP, fibrinogen and t‐PA with markers of obesity (body mass index, waist circumference), blood pressure, blood lipids and metabolic syndrome. D‐dimer showed weaker associations and less heterogeneity by sex. There was no evidence of sex interaction in associations with VWF. Conclusions: Associations between CRP, fibrinogen and t‐PA and metabolic syndrome and its components were stronger in women than in men. Understanding the reasons for these differences across sex will be important in understanding the pathophysiology of cardiovascular and metabolic disease in men and women.     

Predicting physical activity among urban adolescent girls: A test of the health promotion model

The purpose of this study was to test hypothesized relationships of the health promotion model (HPM) as a means of predicting moderate‐to‐vigorous physical activity (MVPA) among urban, adolescent girls. A secondary analysis of baseline data from a group randomized controlled trial was conducted. The study involved eight urban schools in the Midwestern United States. The sample included girls (N = 517) in the 5th–8th grades. Data were collected on age, body mass index, pubertal status, enjoyment, self‐efficacy, social support, options for physical activity (PA), and commitment to PA. MVPA was measured via accelerometers worn by the girls for 7 days. Structural equation modeling was used to analyze study aims. Mean age of the sample was 11.8 years (standard deviation [SD] = 1.0). Girls attained an average of 3.0 (SD = 1.2) minutes per hour of MVPA. Self‐efficacy had a positive direct (β = .337; p < .001) and total effect (β = .310; p < .001) on MVPA. Social support and options for PA were not significant predictors of commitment to PA or MVPA. Commitment to PA had a negative but nonsignificant effect (β = ?.056; p = .357) on MVPA. The model predicted 10.1% of the variance in MVPA with 9.6% of the variance predicted by self‐efficacy. Limitations include lack of longitudinal analysis and inability to generalize the results to other populations such as boys. PA self‐efficacy continues to emerge as a significant predictor of MVPA in the HPM. Continued theory testing is needed to better understand the correlates and determinants of PA among adolescent girls before designing theory‐based interventions to promote PA.     

Combined therapy with PJ34, a poly(ADP‐ribose)polymerase inhibitor,reduces tissue plasminogen activator‐induced hemorrhagic transformations in cerebral ischemia in mice

Recombinant tissue‐type plasminogen activator (rt‐PA) is presently the only pharmacological treatment approved for thrombolysis in patients suffering from ischemic stroke. Although reperfusion of ischemic tissue is essential, the use of rt‐PA is limited due to its narrow therapeutic window and risk of hemorrhagic transformations. Recent studies have shown that rt‐PA amplifies the post‐ischemic activation of the nuclear enzyme poly(ADP‐ribose)polymerase (PARP). This enzyme has been shown to contribute to both the breakdown of the blood brain barrier and spontaneous hemorrhagic transformations after ischemia. We therefore examined the capacity of PJ34 (N‐(6‐oxo‐5,6‐dihydrophenanthridin‐2‐yl)‐2‐(N,N‐dimethylamino) acetamide hydrochloride), a potent inhibitor of PARP, to reduce the hemorrhagic transformations that occur after rt‐PA in mice with permanent focal cerebral ischemia. Ischemia was produced by intraluminal occlusion of the left middle cerebral artery and treated with vehicle, rt‐PA (10 mg/kg, i.v., 6 h after occlusion) or rt‐PA plus PJ34 (3, 6 or 12 mg/kg, i.p., at ischemia onset and 4 h later). Hemorrhagic transformations, neurological examination, and infarct volumes were evaluated 48 h after the onset of ischemia. Delayed administration of rt‐PA resulted in increased hemorrhagic transformations and aggravated the neurological deficit. Giving PJ34 (3 mg/kg) markedly reduced the hemorrhagic transformations, an effect not owing to a modification of matrix metalloprotease activity. Furthermore, PJ34 improved the neurological functions of rt‐PA‐treated ischemic mice. To conclude, the PARP inhibitor PJ34 makes rt‐PA safer in experimental ischemic stroke.     

Type 3 takayasu arteritis diagnosed by parvus‐tardus renal Doppler signal modulation

Takayasu's arteritis is known to cover the youngest age group in the etiology of secondary hypertension. The type 3 pattern is rare and involves the thoraco‐abdominal aorta and its main abdominal branches. Here, we present the imaging results of a patient who had been followed up for systemic arterial hypertension and was diagnosed with Takayasu's arteritis type 3 by CT and MR angiography following bilateral detection of a parvus‐tardus Doppler signal modulation in the renal arteries. We discuss the differential diagnoses that should be considered when observing a tardus‐parvus Doppler signal. © 2017 Wiley Periodicals, Inc. J Clin Ultrasound 45 :612–615, 2017     

组合式输尿管软镜联合超声引导下可视穿刺治疗肾下盏结石的临床疗效观察

目的观察铂立组合式输尿管软镜联合超声引导下可视穿刺系统治疗肾下盏结石的临床疗效。方法采用输尿管软镜联合超声引导下可视穿刺系统治疗,回顾性分析2016年1月-2017年1月该院63例肾下盏结石患者(多发结石16例,单发下盏结石47例)的临床资料,包括手术时间、出血量、结石清除率和术后并发症发生率等,评估该手术方式的安全性及有效性。结果该组患者手术时间30~60 min,平均45 min,术后并发症发热3例,疼痛2例;无需输血患者;2例因视野模糊术中改行经皮肾镜手术。术后住院时间2或3 d,平均2 d,术后复查结石残留3例,2周后行体外碎石治疗,术后1个月复查患者结石清除率100.0%。结论逆行组合式输尿管软镜联合超声引导下可视穿刺治疗肾下盏结石安全、有效,可行。     

A synthetic peptide derived from staphylokinase enhances plasminogen activation by tissue‐type plasminogen activator

Summary. Background: A synthetic nonadecapeptide (SP; GPYLMVNVTGVDGKGNELL) previously enhanced the activation of plasminogen by the SAK/plasmin complex. Objectives: To identify the binding site for SP on plasminogen and elucidate the effects of SP on plasminogen activation by the tissue‐type plasminogen activator (t‐PA). Methods: The effects of SP on plasminogen activation were estimated using a chromogenic substrate and from the cleavage of plasmin on SDS‐PAGE under reduced conditions. The binding to SP of various peptides derived from the amino acid sequence of plasminogen was analyzed with an IAsys biosensor. The SP‐mediated structural change to plasminogen was analyzed by circular dichroism (CD) spectroscopy. The thrombolytic effects of SP were examined using a mouse model of thrombosis. Results: SP enhanced the activation of plasminogen by t‐PA. The catalytic efficiency (k_cat/K_m) of Glu‐plasminogen activation by t‐PA was 11.4‐fold higher in the presence than absence of SP. The binding of SP to plasminogen was greatly inhibited by a synthetic peptide, FEKDKYILQGVTSWGLG, located close to the C‐terminal of the plasminogen B region. Near‐ultraviolet CD spectra of the complex between SP and Glu‐plasminogen significantly differed from those of Glu‐plasminogen. When SP was administered in a mouse model of thrombosis, early recanalization was observed in a dose‐dependent manner. However, SP did not cause recanalization in t‐PA gene‐deficient mice. Conclusions: SP bound to the B region and promoted the activation of plasminogen by t‐PA, and then induced effective thrombolysis.     

Characterization of putative haematopoietic cells from bovine yolk sac

The yolk sac is an extra‐embryonic membrane that plays an important role in early embryonic survival. It is the production site for blood cells during embryonic mammalian development and is a likely source of stem cells. The aim of this study was to identify and characterize the putative haematopoietic cells from the yolk sac of bovine embryos at different stages of gestation. The yolk sac regresses according to gestational age and embryos are characterized into groups (I–V) according to the crown–rump measurement. Groups I–III survived in culture longer and exhibited the formation of cell clusters, whereas groups IV and V could not be maintained in culture for an extended period of time. Flow‐cytometry analysis revealed that groups I–III had similar characteristics, including high expression levels of the haematopoietic markers CD34, CD90 and CD117. In groups IV and V, decreases were observed in the expression levels of CD117 and CD34. Cells were found to be capable of survival post‐cryopreservation and exhibited varying abilities to form colonies in a methylcellulose matrix, depending on gestational age. Cytological analysis revealed the presence of blood cells (lymphocytes and monocytes). Quantitative PCR analysis demonstrated the presence of the haematopoietic progenitor genes GATA3 and LMO2, but not RUNX1. Thus, we have successfully isolated and characterized haematopoietic cells from the bovine embryo yolk sac at varying gestational ages. This study is crucial for the understanding of the development of the haematopoietic system and the embryonic function of this organ. Copyright © 2015 John Wiley & Sons, Ltd.     

超声鉴别诊断瘢痕妊娠与宫腔下段非瘢痕妊娠

目的 观察二维及三维超声诊断剖宫产瘢痕妊娠（CSP）与宫腔下段非瘢痕妊娠的价值。方法 收集67例CSP患者（CSP组）和29例宫腔下段非瘢痕妊娠患者（宫腔下段非瘢痕妊娠组）,以二维及三维超声观察孕囊种植部位、与剖宫产瘢痕关系和滋养血流主要来源部位,并测量剖宫产瘢痕处残余肌层厚度;建立Logistic回归模型,以ROC曲线评价其诊断效能。结果 CSP组与宫腔下段非瘢痕组间孕囊与瘢痕关系、滋养血流来源部位及瘢痕处残余肌层厚度差异均有统计学意义（P均<0.001）。Logistic回归模型显示ROC曲线下面积为0.878（P<0.001）。以预测概率=0.680为临界值,该模型预测CSP的准确率为86.46%,敏感度为89.55%,特异度为79.31%。以孕囊植入瘢痕和滋养血流来源于子宫前壁下段为诊断CSP的标准,二维与三维超声诊断CSP和宫腔下段非瘢痕妊娠的Kappa值分别为0.699和0.711。结论 通过Logistic回归模型综合分析孕囊与瘢痕关系、滋养血流来源部位和瘢痕处残余肌层厚度,可提高对CSP与宫腔下段非瘢痕妊娠的鉴别效能。