230例急性肺动脉血栓栓塞症患者对症治疗、抗凝治疗和溶栓治疗的住院转归

目的:介绍对症治疗、抗凝治疗和溶栓治疗3种治疗方法治疗急性肺动脉血栓栓塞症或慢性肺动脉血栓栓塞症急性再发患者的住院转归。方法:回顾性分析1974-2002年的28年来我院住院收治的230例急性肺动脉血栓栓塞症或慢性肺动脉血栓栓塞症急性再发患者经对症治疗、抗凝治疗和溶栓治疗3种治疗方法的住院有效率、显效率和病死率。结果:对症治疗、单纯抗凝和溶栓+抗凝治疗的住院总有效率分别为60．0％、91．5％和96．6％;其中住院显效率分别为0、0．9％和42．7％;住院病死率分别为17．1％、4．7％和3．4％。结论:通过回顾性临床分析表明,对症治疗、抗凝治疗和溶栓治疗对急性肺动脉血栓栓塞症或慢性肺动脉血栓栓塞症急性再发患者均有效。由于患者治疗方法的选择受历史等因素的影响,对3种治疗方法的临床疗效不能进行比较。     

慢性栓塞性肺动脉高压的外科治疗

一、背景慢性栓塞性肺动脉高压 (ｃｈｒｏｎｉｃｔｈｒｏｍｂｏｅｍｂｏｌｉｃｐｕｌｍｏｎａｒｙｈｙｐｅｒｔｅｎｓｉｏｎ ,ＣＴＥ ＰＨ )是由于肺动脉内反复栓塞和血栓形成而造成的肺动脉高压。既可由急性肺动脉栓塞演变而来 ,也可因下肢静脉血栓等反复栓塞肺动脉所致。慢性栓塞性肺动脉高压呈渐进性 ,最终造成右心衰竭和呼吸衰竭死亡。其自然预后与肺平均动脉压 (ｍＰＡＰ)有关。ｍＰＡＰ >30ｍｍＨｇ(1ｍｍＨｇ =0 .133ｋＰａ) ,5年生存率为 30 % ;ｍＰＡＰ >50ｍｍＨｇ ,5年生存率为 10 % [1] 。内科对慢性栓塞性肺动脉高压的治疗多是…     

肺栓塞的药物治疗

肺栓塞的药物治疗主要包括溶栓和抗凝,目的是缩小或消除深静脉和肺动脉血栓,控制栓塞所致心肺功能紊乱,防治复发及慢性血栓栓塞性肺动脉高压发生。     

如何在实践中理解及运用肺栓塞指南中危肺动脉血栓栓塞症患者的溶栓治疗

中危组肺动脉血栓栓塞症的患者溶栓治疗已经争论很多年,尤其是溶栓治疗为患者带来益处/风险比得到重视,慢性血栓栓塞性肺动脉高压是决定肺动脉血栓栓塞患者预后的重要因素,所以残余血栓的研究对慢性血栓栓塞性肺动脉高压的影响更值得关注.     

反复血栓栓塞性肺动脉高压误诊分析

尽管急性肺栓塞已有溶栓、抗凝等有效治疗,但由于误诊、漏诊、治疗不当或反复栓塞,部分患者可遗留或发展成慢性栓塞性肺动脉高压(CTEPH)。当前,肺动脉血栓内膜切除术已成功地用于该病的治疗,因此如何提高CTEPH诊断水平显得非常重要。本文回顾本院近3年诊治的CTEPH7例患者的临床资料,旨在提高对CTEPH的认识。1临床资料经UCG根据三尖瓣反流压差估测肺动脉压增高的患者共7例,其中经放射性核素灌注扫描6例,经肺动脉造影1例,证实有肺段以上多发性肺栓塞。7例中男5例,女2例;年龄34～51(平均42.9)岁;病程24～72(平均42)个月。并发高血压…     

慢性血栓栓塞性肺动脉高压新治疗方法的进展

慢性血栓栓塞性肺动脉高压是由于肺动脉血栓未完全溶解导致的一类毛细血管前性肺动脉高压.肺动脉内膜剥脱术是目前慢性血栓栓塞性肺动脉高压的首选治疗方案.但很多患者因远端血管病变或严重合并症而无法手术,或手术后有持续性肺动脉高压,球囊肺血管成形术和靶向药物的发展为这些患者的治疗带来了新的希望.现就慢性血栓栓塞性肺动脉高压新疗法...     

慢性血栓栓塞性肺动脉高压治疗现状

正慢性血栓栓塞性肺动脉高压(CTEPH)是以反复性、未溶解肺动脉栓子和/或进行性肺动脉血栓形成,以及肺动脉重塑导致肺血管阻力增高,肺动脉压力进行性增高的致命性疾病。以上改变可使患者发生呼吸困难、右心衰竭,最终导致死亡。其诊断条件需满足以下2点:1肺栓塞患者需充分抗凝至少3个月;2肺动脉平均压≥25 mm Hg(1mm Hg=0.133k Pa)、肺毛细血管压力≤15 mm Hg。其发病机     

急性肺血栓栓塞症患者溶栓治疗后的远期预后分析

目的　分析急性大面积肺血栓栓塞症 (PTE)患者溶栓治疗后的远期预后。方法　对2 60例急性PTE患者进行溶栓治疗并随访 ,分析其临床资料及引起远期临床事件 [死亡、再发深静脉血栓形成、再发PTE、慢性血栓栓塞性肺动脉高压和 (或 )右心衰竭、抗凝治疗出现大出血、依赖家庭氧疗 ]的危险因素。结果　 2 60例PTE患者在住院期间死亡 2 2例 (8 5 % ) ,其中 1 5例 (62 8% )死于PTE。随访 2 2 7例患者 ,为期 3 9～ 8 4年 ,死亡 72例 (31 7% ) ,其中有 2 1例患者死于再发PTE。对随访资料完整的 1 65例患者进行远期临床事件的危险因素分析 ,单因素分析显示 ,既往有血栓栓塞病史、抗凝治疗不足 6个月、植入下腔静脉滤器、溶栓后超声心动图仍显示右室功能障碍和 (或 )扩大、溶栓后超声多普勒仍测得肺动脉收缩压 >50mmHg、出院前核素肺通气 /灌注扫描显示肺血管床阻塞 >30 %与远期临床事件的发生相关 ;多变量分析显示 ,溶栓后超声心动图仍显示右室功能障碍和 (或 )扩大、溶栓后超声多普勒仍测得肺动脉收缩压 >50mmHg、出院前核素肺通气 /灌注扫描显示肺血管床阻塞 >30 %是PTE远期预后的独立危险因素。结论　通过高危因素的确立 ,可予患者更积极的治疗 ,改善患者的预后     

应用波生坦治疗肺动脉高压

本试验是研究肺功能Ⅳ级 (ＷＨＯ分级 )肺动脉高压患者用波生坦 (Ｂｏｓｅｎｔａｎ)对运动能力的影响 ,并比较 1 2 5及 2 50ｍｇ每日 2次给药的疗效。方法　应用抗凝药物、血管扩张剂、利尿剂等仍有症状的肺功能Ⅲ或Ⅳ级重度肺动脉高压(原发性或伴有结缔组织疾病如硬皮病或系统性红斑狼疮 )患者进入本研究。入选标准 :基线6ｍｉｎ行走距离 1 50～ 450米 ,静止平均肺动脉压 >2 5ｍｍＨｇ( 1ｍｍＨｇ =0 1 3 3ｋＰａ) ,肺毛细管楔压 <1 5ｍｍＨｇ,肺血管阻力 >2 40ｄｙｎ·ｓｅｃ 1 ·ｃｍ 5。采用双盲随机安慰剂对照试验 ,分配患者接受安慰…     

书讯

<正>由首都医科大学附属北京安贞医院心脏外科中心,甘辉立教授主编的《肺动脉栓塞学》一书,已由人民军医出版社出版,其ISBN 978-7-5091-8006-8,有感兴趣者可在各大书店订购。全书原价为98元人民币。该书为中文著作,全书310页,附图60余帧,为有关急性肺动脉栓塞和慢性血栓栓塞性肺动脉高压内科治疗及外科治疗的专著。急性肺动脉栓塞和慢性血栓栓塞性肺动脉高压是严重威胁健康的疾病,死亡率和病残率都很高。抗凝治疗和溶栓治疗、肺动脉取栓术和肺动脉血栓内膜剥脱术治疗,分别是治疗急性肺动脉栓塞和慢性血栓栓塞性肺动脉高压的有效治疗方法,可     

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.     

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.     

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.     

Reperfusion pulmonary edema after pulmonary artery thromboendarterectomy

Pulmonary artery thromboendarterectomy (PAT) is a potentially curative procedure in chronic, major vessel thromboembolic pulmonary hypertension. However, postoperative reperfusion pulmonary edema (RPE) has been a serious complication, often requiring prolonged mechanical ventilation. This entity has been described only anecdotally in the past. To characterize it more fully, we retrospectively analyzed the course and potential determinants of RPE after thromboendarterectomy in 22 patients who had PAT at our institution from 1969 through 1984. Particular attention was directed to clinical data, thrombus location, areas operated, postoperative roentgenograms, and preoperative and postoperative hemodynamic data. In all patients but 1, RPE developed within 72 h after surgery, corresponding to anatomic locations distal to vessels subjected to PAT. Regions of lung not reperfused at surgery were uniformly spared. Pulmonary capillary wedge and/or left atrial pressures preoperatively and postoperatively were not elevated. None of the preoperative data predicted which patients would develop more persistent RPE. These observations suggest that the phenomenon of RPE is a peculiar, focal form of pulmonary edema, the basis for which remains to be defined.     

Nitroglycerin-responsive pulmonary hypertension in idiopathic pulmonary hemosiderosis

Idiopathic pulmonary hemosiderosis (IPH) is an uncommon disease found predominantly in pediatric patients. It can produce severe chronic pulmonary injury that results in chronic hypoxemia, pulmonary insufficiency, and progressive pulmonary fibrosis, leading to irreversible pulmonary hypertension and death. We studied the pulmonary hemodynamics in an 9-yr-old boy with IPH to determine if pulmonary hypertension contributed to exacerbations of this disease. Our results showed that this patient demonstrated pulmonary hypertension during acute exacerbations. Initially, the elevated pulmonary artery pressure responded both to oxygen and to a pulmonary vasodilator in the form of nitroglycerin. However, this improvement was not sustained. We conclude that pulmonary hypertension is probably a result of chronic hypoxemia experienced by patients with pulmonary hemosiderosis. Further investigation is warranted to assess whether or not intervention aimed at reducing pulmonary artery pressure in IPH improves outcome.     

Primary pulmonary artery sarcoma mimicking pulmonary thromboembolism

A 69-year-old woman presenting with dyspnea had a pericardial window created for fibrinous pericarditis. The patient subsequently developed pulmonary hypertension and a ventilation perfusion scan was compatible with pulmonary thromboembolism. A primary tumour of the pulmonary artery was suggested by angiography, computerized axial tomography and magnetic resonance imaging. Pathology confirmed a spindle cell pulmonary artery sarcoma.     

Ruptured pulmonary artery aneurysm mimicking pulmonary embolism

Aneurysms of the pulmonary artery are very rare pathological vascular conditions. Peripheral pulmonary aneurysms have been reported only in a few cases. The causes of these aneurysms include extensive degenerative changes, traumas, infection and congenital malformations. Because of the imminent danger of rupture, surgical treatment should always be preferred. The following case report demonstrates one of a multitude of possible misdiagnoses for rupture of a pulmonary aneurysm.