肺动脉造影与核素肺灌注/通气扫描在肺栓塞诊断价值相关性研究

目的 :探讨选择性肺动脉造影与核素肺灌注 通气扫描在肺栓塞诊断的相关性。方法 :回顾性分析 2 3例肺栓塞选择性肺动脉造影与核素肺灌注 通气扫描显像。结果 :2 3例选择性肺动脉造影与核素肺灌注 通气扫描显像结果比较 ,肺血管堵塞≥ 8支以上者 ,二者相关性达 10 0 % ;<8支者二者相关性为 90 5 %。 7例冠状动脉造影阴性患者 ,经肺动脉造影证实为肺栓塞。结论 :选择性肺动脉造影是临床肺栓塞诊断和病变定位的可靠依据 ,而核素肺灌注 通气扫描显像检查则是目前临床诊断肺栓塞的有价值的无创性诊断方法之一。     

肺灌注/通气显像在肺动脉栓塞诊断中的价值

目的:评价核素肺通气/灌注(V/Q)显像在肺动脉栓塞(PE)诊断中的价值。方法:回顾总结40例核素肺灌注/通气显像与肺动脉造影(CPA)诊断PE的对照研究。结果:31例患者V/Q显像示不相匹配的肺叶、肺段或多发亚肺段的放射性分布稀疏或缺损,提示为PE,其中肺动脉造影证实30例为PE,1例多发大动脉炎;9例患者的V/Q显像为相匹配的肺叶、肺段或多发亚肺段的稀疏或缺损,提示不是PE,与肺动脉造影结果一致。核素V/Q显像诊断PE的灵敏度为100%(30/30例),特异性为90.0%(9/10例),准确性为97.5%(39/40例)。结论:多数PE患者通过核素肺V/Q显像可以作出明确诊断,少数肺V/Q显像与临床表现不符的患者需行肺动脉造影。     

超声心动图诊断急性肺动脉栓塞的价值

目的 :分析评价床旁超声心动图 (ECHO)在急性肺动脉栓塞 (APE)诊断中的实用价值。方法 :采用经胸ECHO对临床怀疑APE的 5 8例患者在 4～ 6h内行床旁ECHO检查。结果 :超声直接检出主肺动脉及左右肺动脉主干近端血栓者 4例 ,均被外科手术或肺动脉造影证实。本组具有典型右心负荷过重超声征象者 15例 (其中包括具有超声直接征象的 4例 ) ,核素肺灌注 通气扫描提示为双肺多发性大面积栓塞。仅右房、右室轻度增大或肺动脉轻度增宽者 19例 ,ECHO无改变者 2 4例 ,但核素肺灌注 通气扫描均提示为肺段或亚段栓塞。结论 :ECHO能够发现主肺动脉、左右肺动脉干内附壁血栓直接提示肺动脉栓塞 ,或根据右室负荷过重表现间接提示肺栓塞的可能 ,但对肺段或亚段栓塞者超声不能作出或排除诊断。     

肺血栓栓塞症的诊断研究进展

近年来,肺血栓栓塞症的诊断研究进展主要包括以下几个方面:①就多种临床症状评分对肺血栓栓塞症的诊断价值进行了大量研究;②通过前瞻性大规模临床试验对肺通气/灌注扫描、螺旋CT肺动脉造影/螺旋CT静脉造影等检查手段的诊断价值进行了评价,③制定了一些肺血栓栓塞症诊断流程.     

16层螺旋CT肺动脉造影对肺栓塞诊断的应用价值

目的探讨16层螺旋CT在肺动脉栓塞中临床应用价值。方法选择肺动脉栓塞患者36例,所有患者均接受胸部CT及肺动脉造影检查,分析16排螺旋CT对肺动脉显影及肺栓塞显示情况,观察肺动脉栓子的类型、分布和数量。结果1.16排螺旋CT共显示肺动脉干、左/右肺动脉、肺叶、段、亚段及以下动脉1787支,肺动脉栓塞429支,栓塞率为24.01%,其中肺叶动脉比例最高,为38.79%,肺动脉干比例最低,为7.50%。在肺动脉栓塞栓子类型方面,Ⅱ型栓子数量最多,为202处,其次为Ⅳ型,共118处,Ⅲ型数量最少,为31处。其直接征象为充盈缺损,间接征象包括肺纹理稀疏、肺梗死、westemark征及肺动脉高压、胸腔积液、心包积液及胸膜增厚等。结论 16排螺旋CT能够清晰显示肺动脉栓塞的特点,在其诊断和鉴别诊断中具有较高的应用价值。     

256层螺旋CT肺动脉造影在老年肺动脉栓塞诊断中的价值

目的 探讨256层螺旋CT肺动脉造影应用于老年肺动脉栓塞诊断的临床价值.方法 2011年2月至2012年2月对可疑肺动脉栓塞而进行螺旋CT肺动脉造影检查的老年患者分别采用256层螺旋CT及64排CT肺动脉造影进行诊断,并比较两种诊断方法图像质量、图像信噪比(SNR)、对比噪声比(CNR)、平均扫描时间、肺动脉平均CT值及造影剂使用剂量等.结果 两种检查设备对老年肺动脉栓塞的显示率均为100.00％;其中39例患者为多发栓塞,包括双侧多发29例,右侧多发6例,左侧多发4例.两组均获得了满意的影像,256层螺旋CT扫描时间和平均造影剂使用剂量均明显低于64排CT(P＜0.05).结论 在肺动脉栓塞的检查中,与64排螺旋CT肺动脉造影相比较,256层螺旋CT肺动脉造影在没有降低图像质量的情况下,能够明显缩短扫描时间,减少患者屏气时间,降低放射剂剂量,具有一定的优势.     

320层CT单容积肺动脉成像诊断老年肺动脉血栓栓塞的临床应用

目的探讨320层CT单容积肺动脉成像诊断肺动脉血栓栓塞(肺栓塞)的临床应用价值。方法应用320层CT单容积扫描模式对75例年龄60岁临床怀疑肺栓塞患者行肺动脉CT成像,采用容积再现技术、多平面重建及曲面重建等方法分析扫描数据。结果本组75例患者均成功完成扫描,图像质量均可满足诊断,41例诊断为肺栓塞,其中段级肺栓塞12例,余34例除外肺栓塞。全部病例最终诊断均经核素肺通气灌注扫描及临床溶栓治疗有效所证实。应用320层CT单容积肺动脉成像扫描时间1 s,平均射线剂量为(2.73±0.47)mSv,造影剂总量45 ml。结论 320层CT单容积肺动脉成像诊断肺栓塞是一种有效的无创检查手段,其具有低射线损伤、低对比剂用量、成像速度快等优势,尤其适用于临床急重症及老年患者。     

320排动态容积CT对冠状动脉狭窄的诊断价值

目的探讨320排动态容积CT冠状动脉成像对冠状动脉狭窄的诊断价值。方法 2011年6月至2011年9月我院收治拟诊冠心病患者40例,先后行320排动态容积CT冠状动脉成像和冠状动脉造影检查。以冠状动脉造影为诊断冠心病金标准,评价320排动态容积CT冠状动脉成像诊断冠心病的临床应用价值。结果 40例患者320排动态容积CT冠状动脉成像检测出≥50%狭窄91处,冠状动脉造影检测出67处。320排动态容积CT冠状动脉成像诊断冠心病(狭窄≥50%)的敏感度为93%(95%CI:84%～97%),特异度为95%(95%CI:93%～97%),阳性预测值为74%(95%CI:6%～82%),阴性预测值为99%(95%CI:98%～100%)。诊断试验的ROC曲线下面积为0.98(95%CI:0.97～0.99)。结论 320排动态容积CT评价冠状动脉狭窄的可靠性较高,是一种较为理想的冠心病无创诊断方法。     

64排与256层螺旋CT肺动脉造影诊断老年肺动脉栓塞的对比研究

目的 比较64排与256层螺旋CT肺动脉造影诊断老年肺动脉栓塞的临床应用价值.方法 选择2009年12月至2010年12月于我院CT室检查的肺动脉栓塞患者30例,所有患者均于发病3d内行256层螺旋CT及64排CT肺动脉造影检查.比较两种检查设备对肺动脉栓塞的检出率、图像质量、扫描时间及造影剂剂量.结果 30例患者中,两种检查设备对肺动脉栓塞的显示率均为100％.其中,23例患者为多发栓塞,包括双侧多发16例,右侧多发4例,左侧多发3例.256层CT图像信噪比及图像噪声比与64排CT图像相比无统计学差异(P＞0.05).256层CT平均有效射线剂量为(4.86±1.74) mSv,平均扫描时间为(3.35±1.56)s,均明显低于64排CT,均有统计学差异(P＜0.05).结论 在肺动脉栓塞的检查中,256层螺旋CT与64排螺旋CT相比,能够显著缩短扫描时间,降低放射剂量,具有一定的优势.     

螺旋CT在肺动脉高压疾病中的应用

目的 探讨螺旋CT在肺动脉高压疾病中的应用价值。方法 回顾分析了31例肺动脉高压的临床和螺旋CT资料，其中慢性血栓栓塞性肺动脉高压18例，原发性肺动脉高压2例，结缔组织病4例，肝肺综合征2例，纵隔纤维化1例，Takayasu动脉炎1例，房间隔缺损2例，肺淋巴管肌瘤病1例。CT普通扫描结合CT肺动脉造影观察肺窗和纵隔窗以分别显示肺实质、肺血管、肺门及纵隔结构。结果 CT肺动脉造影诊断了96．77％待查肺动脉高压，同时对肺动脉高压原因做了有益的分析。结论 CT普通扫描结合CT肺动脉造影能准确诊断肺动脉高压，为明确病因或倾向性病因诊断提供有用信息。     

肺动脉血栓内膜剥脱术后再灌注肺水肿的进展

肺血栓栓塞症是一种常见、多发且病死率和致残率高的疾病。大多数急性肺动脉血栓栓塞经及时的溶栓抗凝等治疗和 (或 )自身的纤溶系统能将血栓不同程度地溶解 ,另有0 1%～ 0 2 %的患者因血栓在急性期未能溶解或栓塞反复发生进而发展成慢性栓塞性肺动脉高压。慢性栓塞性肺动脉高压溶栓无效 ,抗凝、扩血管治疗效果不佳 ,其病理过程多呈进行性加重或稳定一段时间后再次加重 ,自然预后差。肺动脉平均压 >3 0ｍｍＨｇ(1ｍｍＨｇ =0 13 3ｋＰａ)的慢性栓塞性肺动脉高压患者 5年生存率为 3 0 % ,肺动脉平均压 >5 0ｍｍＨｇ者仅为 10 %。肺动脉血…     

Chronic pulmonary embolism and pulmonary hypertension

Incomplete resolution of acute pulmonary embolism (PE) is frequently observed after acute PE and may rarely result in chronic thromboembolic pulmonary hypertension (CTEPH). The underlying pathophysiological mechanism is largely unknown. Evidence underlines the concept of a dual pulmonary vascular compartment model consisting of increased pulmonary vascular resistance by both large vessel obstruction and distal small vessel obliteration, the latter initiated by pathological vascular remodeling. Up to 40% of patients with established CTEPH have no prior history of symptomatic venous thromboembolism. CTEPH is associated with a poor prognosis if left untreated. Therefore, the diagnostic approach of CTEPH aims at assessing the location and extent of the embolic obstruction, establishing the operability and prognosis of the patients and ruling out other variations of pulmonary hypertension with distinct indicated treatment. Heart catheterization for invasive pressure measurements and pulmonary catheter angiography is obligatory for the final diagnosis. Pulmonary thromboendarterectomy is the treatment of choice. In certain patients with persistent or recurrent pulmonary hypertension after surgery or with inoperable disease, pharmacotherapy might be beneficial.     

Retrograde pulmonary perfusion improves results in pulmonary embolectomy for massive pulmonary embolism

Mortality rates for pulmonary embolectomy in patients with acute massive pulmonary embolism have decreased in recent years. However, they still range from 30% to 45% when the surgery is performed on critically ill patients, and the rates reach 60% in patients who have experienced cardiac arrest before the procedure. The causes of death in these patients are generally attributed to right heart failure due to persistent pulmonary hypertension, intractable pulmonary edema, and massive parenchymal and intrabronchial hemorrhage. Clinical and experimental findings indicate that venous air embolism causes severe or even lethal damage to the pulmonary microvasculature and the lung parenchyma consequent to the release of endothelium-derived cytokines. These findings are similar to those observed when severely compromised patients undergo pulmonary embolectomy-air entrapped in the pulmonary artery during embolectomy can lead to fatal outcomes.Besides enabling the removal of residual thrombotic material from the peripheral branches of the pulmonary artery, retrograde pulmonary perfusion fills the pulmonary artery with blood and prevents pulmonary air embolism. In this retrospective study, we analyzed a series of 21 consecutive critically ill patients in whom we applied retrograde pulmonary perfusion while performing standard pulmonary embolectomy. No patient died or experienced major postoperative complications. We believe that the use of retrograde pulmonary perfusion decreases morbidity and mortality rates associated with pulmonary embolectomy in critically ill patients.     

Cavitating pulmonary infarcts revealing thromboembolic pulmonary hypertension

Several etiologies are involved in the pathogenesis of cavitating pulmonary disease including neoplastic, infectious or inflammatory processes. Another is pulmonary infarction associated with venous thromboembolism. The lung cavities tend to be located peripherally and are the result of pulmonary embolism. We report the case of a woman with chronic thromboembolic pulmonary hypertension (CTEPH), associated with familial thrombophilia, revealed by cavitating pulmonary infarcts. CTEPH is sometimes diagnosed during an episode of recurrent pulmonary embolism following previously unnoticed lesions. Thrombophilias such as isolated elevated factor VIII are risk factors for CTEPH.     

Residual pulmonary thromboemboli after acute pulmonary embolism

BackgroundAfter an acute pulmonary embolism (PE), the complete resolution of thromboemboli may not be routinely achieved. The rate of persistence may depend on the time and the diagnostic technique used for evaluation.Patients and methodsPatients were diagnosed with acute PE by means of computed tomography angiography (CTA). While they were receiving anticoagulant therapy, a second CTA was used to explore the rate of persistence of residual thromboemboli. During the initial episode, the plasma levels of Troponin I and natriuretic peptide, patient demographics, and hemodynamic and gas exchange data were evaluated as risk factors for persistence of pulmonary thromboemboli.ResultsIn this study 166 patients were diagnosed. A second CTA was not made in 46 (28%) patients for different reasons. In 120 (72%) patients a second CTA was made 4.5 [SD2.34] months after the initial episode (range 2–12 months). Complete clearance of thrombi occurred in 89 (74%, 95% CI 65–81) patients. Residual thrombi remained in 31 (26%, 95% CI 18–34) patients. In 6%, 13% and 81% of the patients the size of the residual thrombi was greater, similar to and smaller than initially diagnosed, respectively.The risk factors for residual thrombi included the thrombotic burden (OR 1.95), the alveolar to arterial difference of oxygen (OR 1.64), and the clinical antecedents of venous thromboembolic disease (OR 0.65).ConclusionsAfter 4.5 months of anticoagulant therapy, residual pulmonary thromboemboli persisted in 26% of the patients. The risk factors for residual thromboemboli include a greater initial thrombotic burden, a deeper gas exchange disturbation and a history of previous venous thromboembolism.     

Chronic solitary pulmonary nodule due to unsuspected pulmonary infarction from silent pulmonary embolism

Abstract A case of pulmonary embolism showing a longstanding solitary pulmonary nodule is presented. An asymptomatic 57 year-old man with a solitary nodule in the right lower lobe was referred to our hospital. A pulmonary perfusion-ventilation scan following a sudden onset of dyspnoea established the diagnosis of recurrent pulmonary embolism. The nodule gradually disappeared after anticoagulant treatment, indicating that the nodule was pulmonary infarction from silent pulmonary embolism. Although the incidence of pulmonary infarction is low in Japan, this case suggests that pulmonary infarction from silent pulmonary embolism should be considered as one important cause of a solitary pulmonary nodule.     

Acute pulmonary embolism and pulmonary infarction]

32 cases of pulmonary embolism were reported, 18 cases had been autopsied (massive pulmonary embolism 9 cases. moderate pulmonary embolism 23 cases). The incidence risk factors pathogenesis, clinical manifestations of pulmonary embolism were presented. The relation between pulmonary embolism and pulmonary infarction and treatment of massive pulmonary infarction were discussed.