介入螺旋电吸式祛栓术治疗急性大面积肺梗死

目的 评价用Straub螺旋电吸式祛栓术治疗急性大面积肺梗死的疗效和安全性.方法 5例患者经CT和肺动脉造影确诊为大面积肺血管栓塞.所有患者均有急性肺梗死的症状.采用Staub Rotarex对5例患者进行了经皮机械祛栓,1例使用了辅助局部溶栓.结果 所有患者在技术上和临床症状改善上均取得了成功.机械祛栓后患者的平均肺动脉压从(41.8±7.9)mmHg降低至(30.7±8.5)mmHg(P<0.01),动脉血氧分压(PaO2)从(56.6±9.3)mmHg增加至(85.8±5.0)mmHg(P<0.01).血氧饱和度(SaO2)从(79.0±4.3%)升至术后的(92.8±3.5)%(P<0.01).结论 初步经验显示Straub螺旋电吸式祛栓术在急性大面积肺梗死治疗中具有较好的安全性与疗效.     

急性肺血栓栓塞症的介入综合治疗

目的评价介入综合治疗急性肺血栓栓塞症(PTE)的疗效。方法7例PTE病人,经肺动脉造影进一步明确栓塞部位后,即采用介入综合治疗(经导管碎栓、抽吸取栓、局部溶栓及下腔静脉滤器置入),观察临床症状、肺动脉开通情况、动脉血氧分压(PaO2)、血氧饱和度(SaO2)、肺动脉平均压(PAPm)。结果所有PTE患者临床症状显著改善,肺动脉完全开通率90%以上;PAPm术前平均31 mmHg降至术后25 mmHg;PaO2术前平均54 mmHg升至术后95 mmHg,SaO2术前平均80%升至术后94%,术后未有再发PTE者。结论介入综合治疗急性PTE能够快速改善血液动力学,降低右心室后负荷,预防PTE复发。     

急性大面积肺梗死的介入机械碎栓治疗

目的探讨急性大面积肺梗死介入机械碎栓治疗的可行性和临床疗效。方法对15例急性大面积肺栓塞患者采用碎栓器械行介入治疗,观察临床症状、肺动脉平均压、血氧分压和肺动脉开通情况。结果疗效评价为11例显效,3例好转,1例无效,术后动脉血氧分压明显升高,由(60.6±7.8)mmHg升至(91.0±7.7)mmHg,P=0.00;肺动脉平均压明显降低由(39.7±10.8)mmHg降至(27.3±7.9)mmHg,P=0.000。结论介入机械碎栓治疗急性大面积肺栓塞是一种可行且行之有效、安全的方法。     

单纯经皮机械祛栓治疗急性大面积肺栓塞的临床应用

目的评价单纯介入机械祛栓在治疗急性大面积肺栓塞(PE)方面的临床疗效和安全性。方法回顾性收集2003年1月到2008年1月经皮机械碎栓(PMT)或(和)Straub Rotarex系统祛栓治疗急性大面积PE病例6例。结果6例患者的肺动脉主干血流得以再通且临床症状改善。介入术后,患者SaO2从术前79.5%±5.3%增加至92.8%±3.4%(P<0.01);PaO2从术前从(58.0±9.8)mmHg增加至(88.7±4.1)mmHg(P<0.01);术后患者的平均肺动脉压(PAP)从(40.8±7.8)mmHg降至(29.8±8.0)mmHg(P<0.01);Miller指数从术前的0.54±0.03降至术后的0.18±0.07(P<0.01)。在完成临床随访的4例患者中,1～5年内均未有PE复发。结论初步临床经验显示单纯PMT是治疗急性大面积PE的一种简单、有效、安全的方法,尤其是针对有溶栓禁忌证的患者。     

经导管祛栓术治疗急性肺动脉栓塞

目的：探讨经导管栓子祛除术治疗急性肺动脉栓塞的临床疗效。方法：对24例急性肺动脉栓塞的病人，经肺动脉造影明确诊断，通过旋转猪尾导管碎栓、抽吸导管抽吸和局部溶栓来开通肺动脉。观察临床症状、动脉血氧分压（PaO2)、肺动脉平均压（PAPm）和肺动脉开通情况。结果：术后症状即刻缓解者23例，完全开通者20例，与术前相比PaO2明显升高（P＜0．05），PAPm明显降低（P＜0．05），并发脑出血1例，死亡2例，22例病人存活。结论：经导管栓子祛除术治疗急性肺动脉栓塞是安全有效的方法。     

静脉溶栓联合导管碎栓和切栓治疗急性大面积肺栓塞

目的评价静脉溶栓联合导管碎栓和切栓治疗急性大面积肺栓塞的临床疗效和安全性。方法对19例急性大面积肺栓塞患者，采用下腔静脉滤器置入、肺动脉导管碎栓和静脉溶栓加低分子肝素抗凝治疗，19例中4例加用了Straub Rotarex导管血栓旋切术。结果19例共行21次治疗。18例经介入治疗后胸闷、紫绀症状均明显改善，肺动脉中央分支血流恢复通畅，血氧饱和度由术前平均86％（74％～96％）上升到治疗后的平均97％（94％～100％）。肺动脉压力从术前的（334-5）mmHg（1mmHg=0．133kPa）下降到术后的（254-5）mmHg（t=13．2，P〈0．01）。l例双侧肺动脉主干大块血栓栓塞的患者，介入治疗无效，后经胸外科手术取栓未能成功，患者死亡。4例成功地采用了Straub Rotarex旋切治疗肺动脉血栓，未出现并发症。结论采用导管碎栓和血栓旋切等介入技术联合静脉溶栓抗凝治疗，是治疗急性大面积肺动脉栓塞的有效而且安全的方法。     

创伤后急性大面积肺栓塞的切开取栓治疗

目的 探讨肺动脉切开取栓治疗创伤后急性大面积肺栓塞的方法、围术期处理及外科治疗的安全性.方法 回顾总结自2001年3月至2007年2月采用肺动脉切开取栓治疗的7例急性大面积肺栓塞资料.7例患者在病史中均有近期手术或外伤史,其中男性5例,女性2例,年龄(45±7)岁.所有患者术前均采用CT或肺动脉造影确诊,手术在中低温体外循环辅助下完成.患者出院后随访3～12 个月.结果 8例患者术后即刻肺动脉压下降20～30 mm Hg(1 mm Hg=0.133 kPa),血氧饱和度恢复至100%.体外循环转流时间(67±11) min,失血量(870±34) ml,术后呼吸机辅助时间(161±13) h.1例偏瘫患者术后5个月死于肺部真菌感染,其余6例患者均康复出院.所有患者均未放置下肢静脉滤网,采用华法林钠抗凝,维持国际凝血比值(INR) 2～3.随访复查CT与肺通气-灌注扫描可见肺血管显影良好,无肺动脉高压形成. 结论早期行肺动脉切开取栓是治疗创伤后急性大面积肺栓塞的有效方式,并且可防止慢性肺动脉高压的形成.     

血管内介入治疗急性肺栓塞疗效观察

目的:研究经皮血管内介入治疗肺栓塞的临床价值。方法:21例临床疑诊病例,经多层螺旋CT或心脏彩超诊断为大面积或次大面积肺栓塞后,立即接受经皮肺动脉内导管碎栓及溶栓治疗。观察肺循环和临床症状改善情况。18例同时合并有下肢深静脉血栓患者,溶栓治疗后放置下腔静脉滤器。结果:20例患者临床症状明显改善。1例改善不明显。治疗前平均肺动脉压(36±5)mmHg、动脉血氧分压(32±6)mmHg,溶栓治疗后分别为(20±3)mmHg、(66±4)mmHg,前后比较有统计学意义(P<0.05)。结论:血管内介入治疗急性大面积或次大面积肺栓塞安全、有效。     

经导管封堵治疗合并肺动脉高压的老年继发孔房间隔缺损

目的评估经导管封堵治疗合并肺动脉高压的老年继发孔房间隔缺损(房缺)的疗效和安全性。方法2002年1月-2006年12月于我院行房缺封堵术的34例患者入选本研究,其中15例老年合并肺动脉高压的继发孔房缺患者作为肺动脉高压组。全部患者均在术前、术后1d、1、3、6和12个月行经胸心动超声图和12导联心电图检查。在透视及经胸心动超声图引导下经导管植入Amplatzer封堵器闭合房缺。结果所有患者封堵器植入均获成功,术中和术后均无并发症发生。肺动脉高压组与非肺动脉高压组年龄分别为(67±5)岁和(24±9)岁,(P<0.01),心功能分级分别为2.8±0.7和1.7±0.7,(P<0.01),房缺直径分别为(30.5±3.2)mm和(14.2±4.0)mm(P<0.01),封堵器直径分别为(35.3±4.5)mm和(18.2±4.4)mm(P<0.01),肺动脉收缩压分别为(65.2±11.2)mmHg和(29.5±3.3)mmHg(P<0.01)肺动脉平均压分别为(31.0±4.4)mmHg和(17.9±1.1)mmHg(P<0.01),封堵后,肺动脉高压组患者的肺动脉收缩压为(36.6±11.4)mmHg,肺动脉平均压为(21.6±4.3)mmHg,均有明显下降,两者与术前比较P均<0.01,心功能有明显提高(从术前2.8±0.7增加到1.8±0.8,P<0.01)。结论经导管封堵治疗合并肺动脉高压的老年继发孔房缺安全、有效。     

高危肺动脉栓塞介入治疗的疗效评价

目的:探讨高危肺动脉栓塞进行肺动脉内介入治疗的疗效及安全性。方法:危险分层为高危肺动脉栓塞患者26例,经肺动脉内导管碎栓和局部灌注瑞替普酶溶栓的综合介入治疗,观察处理前后肺循环改善情况,分析心肺血流动力学的改变。结果:26例术前平均肺动脉压、动脉血氧分压和血压分别为(63.78±6.89)、(73.23±11.51)和(87.35±10.92)mmHg。术后分别为(26.23±10.27)、(93.48±6.17)和(127.14±13.15)mmHg,与治疗前比较均有统计学意义(P<0.01)。随访6~36个月,25例疗效持续,1例复发。结论:肺动脉内导管碎栓联合局部灌注瑞替普酶溶栓的介入治疗方法能迅速改善高危肺栓塞患者肺循环梗阻状况和临床症状,无明显并发症,对维持血流动力学稳定有很好作用。     

Right ventricular dysfunction secondary to acute massive pulmonary embolism detected by helical computed tomography pulmonary angiography

OBJECTIVE: Acute massive pulmonary embolism causes abrupt pulmonary arterial hypertension and right ventricular dysfunction (RVD). Patients with RVD have a worse prognosis than those with normal right ventricular function. Consequently, recognizing the RVD at the time of pulmonary embolism is useful for risk stratification and enables more aggressive therapy. The study compared the accuracy of helical computed tomographic (CT) scans with echocardiography in the detecting of RVD in patients with acute massive pulmonary embolism. MATERIALS AND METHODS: Specifically, this work reviewed the CT pulmonary angiograms of 14 patients who were positive for acute massive pulmonary embolism during a 52-month period. CT scans were reviewed for findings indicating RVD. Scans were considered positive for RVD if the right ventricle was dilated or there was leftward shift of the interventricular septum. Echocardiographic reports serving as the reference standard for the diagnosis of RVD were also reviewed. CT study results were then correlated with echocardiography results. RESULTS: Among 14 patients with massive pulmonary embolism, echocardiography identified 12 patients having RVD, whereas the remaining two patients were negative for RVD. Meanwhile, CT correctly identified 11 of 12 patients as having RVD, and was negative for RVD in the remaining 3 patients. Correlated with echocardiography, CT scan for RVD detection had a sensitivity of 91.6% and a specificity of 100%. CONCLUSIONS: CT can accurately detect RVD in patients with acute massive pulmonary embolism. However, this result requires confirmation using a larger prospective cohort study.     

暂时介入性肺切除治疗急性大面积肺栓塞的实验研究

目的 尝试应用经气道球囊导管栓塞术稳定大面积肺栓塞动物模型的生命体征.方法 健康绵羊27只,应用自体血凝块或自制可脱落球囊栓塞右肺动脉建立肺栓塞动物模型.18只动物模型当SaO_2较栓塞前下降≥25%时,于相应的右主支气管放置球囊干预,5只制作肺栓塞动物模型成功后对照观察,4只制作肺栓塞动物模型后未达到干预指标.有创监测肺动脉压、外周动脉压、中心静脉压、心率、SaO_2、PaO_2、PaCO_2等.结果 23只动物成功建立了急性肺栓塞模型,心率、呼吸加快,SaO_2平均在30 min之内下降≥25%,肺动脉压升高.18例实验组进行干预,肺动脉压下降、SaO_2和PaO_2升高,与对照组比较有统计学意义(P<0.05).结论 动物实验证实球囊阻塞气道可作为大面积肺栓塞急救,为其后的溶栓等治疗争取时间.     

犬急性大块肺动脉栓塞动物模型的建立

目的制作一种适合器械祛栓试验使用的犬急性大块肺栓塞动物模型。方法7只杂种犬,体外制作动物自体血栓,采用经皮股静脉穿刺置入导管,选择性插入一侧肺动脉中央分支动脉后注入制作好的自体血凝块,栓塞一侧肺动脉中央分支动脉,栓塞前后检测血气、肺动脉压及肺动脉造影。实验存活动物于12h后处死,取两侧肺组织进行病理检查。结果1只注射血栓时造成两侧肺栓塞死亡,1只在栓塞12h后肺动脉有部分再通;其余各只均成功栓塞至靶肺动脉的中央分支动脉。结论该方法制作急性大块肺栓塞的动物模型是可行和可重复的,可以为相关试验提供急性大块肺动脉栓塞动物模型。     

CT angiography findings of the left atrium and right ventricle in patients with massive pulmonary embolism

OBJECTIVE: The purpose of this study was to show the imaging findings of the left atrium and right ventricle on CT angiography in patients with massive pulmonary embolism. CONCLUSION: Massive pulmonary embolism can cause abrupt acute pulmonary arterial hypertension, right ventricular dysfunction, and decrease in left ventricular preload. Patients with these findings on CT angiography can have a poorer prognosis than those without these imaging findings. Consequently, recognizing anatomic changes such as right ventricular dilation or septal bowing, decrease in size of left atrium and pulmonary veins (a manifestation of decreased pulmonary venous return) would be useful for risk stratification at the time of massive pulmonary embolism.     

Detection of central pulmonary embolism on computed tomography densitometry images before computed tomography pulmonary angiography

OBJECTIVE: The purpose of this article is to describe the imaging findings of acute central pulmonary embolism on computed tomography (CT) densitometry images performed before contrast-enhanced CT pulmonary angiography. METHODS: A retrospective review was conducted of reports from all CT pulmonary angiograms performed at our institution, and cases of acute central pulmonary embolism, defined as those with clot in the main, left, or right pulmonary arteries, were identified. Images of positive studies were reviewed on a picture archiving and communications system (PACS) workstation. RESULTS: A total of 1282 CT pulmonary angiograms were obtained for evaluation of possible acute pulmonary embolism, and 1 combined CT aortogram and pulmonary angiogram was performed for aortic dissection and acute pulmonary embolism. Two hundred fourteen (16.7%) examinations positive for acute pulmonary embolism were identified, 26 (12.1%, 2.0% of total examinations) of which had central clots. Of the 26 patients with central acute pulmonary embolism, 12 (46.1%, 5.6% of all positive studies and 0.9% of all CT pulmonary angiograms) had clots that were visible on the densitometry images. CONCLUSION: Although an uncommon finding, acute central pulmonary embolism can be detected on CT densitometry performed to optimize opacification of the pulmonary arteries for CT pulmonary angiography and may prove useful in selected clinical situations.     

Bronchial artery dilatation on MDCT scans of patients with acute pulmonary embolism: comparison with chronic or recurrent pulmonary embolism

OBJECTIVE: The purpose of our study was to compare the bronchial arteries of patients with acute pulmonary embolism with those of patients with chronic or recurrent pulmonary embolism. MATERIALS AND METHODS: Twenty-seven patients with acute pulmonary embolism and 14 patients with chronic or recurrent pulmonary embolism were retrospectively identified from 700 consecutive patients with suspected pulmonary embolism. The case data for the patients were assessed by two thoracic radiologists whose final judgments were reached by consensus. On the MDCT pulmonary angiograms obtained in these patients, the bronchial arteries were assessed by finding enhancing, small, round or curvilinear structures within the mediastinum and tracing their paths along the bilateral main bronchi. Bronchial arteries with a diameter greater than 1.5 mm were considered to be dilated. RESULTS: The diameters of the bronchial arteries in the group with chronic or recurrent pulmonary embolism were significantly larger than diameters of the bronchial arteries in the group with acute pulmonary embolism (p = 0.0002). Dilatation of bronchial arteries was observed in two of the 27 patients with acute pulmonary embolism and in seven of 14 patients with chronic or recurrent pulmonary embolism. This difference was statistically significant (p = 0.004). No dilated bronchial arteries were seen in patients who had acute pulmonary embolism but had no a history of deep venous thrombosis. CONCLUSION: Acute pulmonary embolism did not appear to cause dilatation of bronchial arteries, whereas chronic or recurrent pulmonary embolism was frequently associated with dilated bronchial arteries. In patients in whom the distinction between acute and chronic or recurrent pulmonary embolism on MDCT pulmonary angiography is clinically unclear and in whom the bronchial arteries are dilated, a diagnosis of chronic or recurrent pulmonary embolism should be favored.     

Endovascular therapy for acute pulmonary embolism

Acute pulmonary embolism (PE) is the third most common cause of death among hospitalized patients. Treatment escalation beyond anticoagulation therapy is necessary in patients with massive PE (defined by hemodynamic shock) as well as in many patients with submassive PE (defined by right ventricular strain). The best current evidence suggests that modern catheter-directed therapy to achieve rapid central clot debulking should be considered as an early or first-line treatment option for patients with acute massive PE; and emerging evidence suggests a catheter-directed thrombolytic infusion should be considered as adjunctive therapy for many patients with acute submassive PE. This article reviews the current approach to endovascular therapy for acute PE in the context of appropriate diagnosis, risk stratification, and management of acute massive and acute submassive PE.     

Panvenography and pulmonary angiography in the diagnosis of deep venous thrombosis and pulmonary thromboembolism

In summary, high-quality pulmonary angiography remains the most accurate and reliable means of diagnosing pulmonary embolism. It can be performed with relative safety, and the inherent mortality risks with pulmonary angiography (in the range of 0.2 to 0.5 per cent in active angiography laboratories) must be weighed against the significant risks incurred with inaccurate diagnosis obtained without pulmonary arteriography. Pulmonary arteriography and transvenous catheter embolectomy can be of great benefit in sudden cardiovascular collapse due to massive pulmonary embolism. Transvenous catheter embolectomy has survival rates at least as good as those of open embolectomy, and it has the advantage that it can be performed in any hospital with angiographic facilities and trained personnel, thus allowing more expeditious management of massive pulmonary embolism in hospitals that do not have cardiopulmonary bypass capabilities.     

Severity assessment of acute pulmonary embolism: role of CT angiography

Helical CT has gained wide acceptance in the noninvasive diagnosis of acute pulmonary embolism (APE) and has therefore largely replaced conventional pulmonary angiography as well as ventilation perfusion scan in the work-up of patients suspected of nonsevere pulmonary embolism (PE). Massive PE is life-threatening; its occurrence may require aggressive treatment such as thrombolysis or embolectomy. Identification of patients suffering from major thromboembolic events based solely on clinical grounds may, however, be difficult. Acute right heart failure is the principal cause of circulatory collapse and death for patients with massive PE, and rapid and specific diagnosis and therapy are required in such patients. Bedside echocardiography, a commonly performed first-line examination, demonstrates signs of cor pulmonale, if present, and can identify large central thrombi. However, echocardiography has limitations. In this review, our goal is to discuss the potential role of CT in assessing patients with severe APE. CT evaluation is based on the direct quantification of pulmonary arterial bed obstruction using various scores and the evaluation of morphological heart changes indicating acute cor pulmonale.