辛伐他汀治疗COPD合并肺动脉高压的临床研究

目的 探讨辛伐他汀治疗慢性阻塞性肺疾病(COPD)合并肺动脉高压(PH)患者肺动脉压、动脉血气、肺功能以及对血浆内皮素-1 (ET-1)、脑钠肽(BNP)的影响.方法 选择稳定期COPD合并PH患者36名,随机分成治疗组和对照组,两组患者均按COPD常规治疗,治疗组加用辛伐他汀40 mg/d,于治疗前及治疗三月后检测肺动脉压、动脉血气、肺功能以及血浆ET-1、BNP水平.结果 治疗组和对照组临床疗效分别66.7％和50.0％.治疗组优于对照组;两组肺动脉平均压治疗后均降低(P＜0.05),治疗组较对照组降低更显著(P＜0.05);治疗组肺功能改善较对照组更明显(P＜0.05);治疗组治疗3个月时ET-1和BNP的水平与对照组比较明显下降(P＜0.05,P ＜0.05).结论 辛伐他汀治疗COPD合并PH,可降低BNP的水平,降低肺动脉平均压及改善肺功能;并能降低ET-1改善内皮功能.     

阿托伐他汀对慢性阻塞性肺疾病合并肺动脉高压患者慢性炎症反应的影响

目的 探讨阿托伐他汀对慢性阻塞性肺疾病(COPD)合并肺动脉高压(PH)患者慢性炎症反应的影响及其安全性.方法 选择COPD合并PH患者78例,随机分为阿托伐他汀组和常规组,两组各39例.常规组采用常规治疗措施治疗,阿托伐他汀组在常规组基础上加用阿托伐他汀.比较两组患者治疗前、治疗后3个月时炎性因子、一氧化氮(NO)、内皮素-1(ET-1)、肺动脉平均压(PAPm)、肺动脉收缩压(PAPs)及肺功能指标变化情况.结果 两组患者治疗后白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α、C反应蛋白(CRP)、ET-1、肺动脉平均压(PAPm)、肺动脉收缩压(PAPs)水平均较治疗前明显降低(P＜0.05),但阿托伐他汀组降低程度更明显(P ＜0.05);NO、FEV1％、FVC较治疗前明显升高(P＜0.05),而阿托伐他汀组升高程度更明显(P＜0.05).阿托伐他汀组服药期间无明显不良反应发生.结论 阿托伐他汀可降低COPD合并PH患者的各种细胞炎性因子,减轻炎症反应,调节NO与ET-1的平衡,降低PH,同时减少肺损伤,改善肺功能,疗效安全可靠,可作为治疗COPD合并PH的有效药物.     

慢性阻塞性肺疾病合并不成比例肺动脉高压患者血浆D-二聚体水平测定及分析

目的 探讨慢性阻塞性肺疾病(COPD)合并不成比例肺动脉高压患者血液是否呈高凝状态.方法 选择稳定期COPD合并肺动脉高压(PH)患者46例,其中COPD合并不成比例PH患者9例(A组),其余COPD合并PH患者37例(B组),具有可比条件的正常中老年人20例为正常对照组(C组),分别检测三组受检查血浆D-二聚体水平.结果 A组血浆D-二聚体水平显著高于B组(P＜0.05),也显著高于C组(正常对照组)(P＜0.05);B组血浆D-二.聚体水平与C组无明显差异(P＞0.05).COPD合并不成比例PH组患者平均肺动脉压与血浆D-二聚体水平有显著相关性(r=0.86,P＜0.01).结论 COPD合并不成比例PH患者血液呈高凝状态,理论上可行抗凝治疗.     

慢性阻塞性肺疾病合并肺动脉高压诊断和治疗的新认识

肺动脉高压(pulmonary hypertension,PH)是慢性阻塞性肺疾病(chronic obstructivepulmonary disease,COPD)的一个重要合并症.COPD患者出现PH时临床上并无特异症状.目前,右心导管检查仍是诊断PH的金标准,多普勒超声心动图则为无创性诊断PH的最佳方法,核磁共振在诊断COPD合并PH中的作用仍需进行研究.长期氧疗是目前惟一证明能稳定、减轻PH进展的方法,但肺动脉压罕见恢复正常,肺血管结构的改变也依然存在.不建议使用传统的血管扩张剂,如钙离子拮抗剂、血管紧张素Ⅱ拮抗剂来治疗COPD相关的PH.新型血管扩张剂,如前列环素、磷酸二酯酶5抑制剂、内皮素受体拮抗剂在COPD相关PH中的作用缺乏大规模的随机对照研究,目前的少量研究结果令人失望.     

慢性阻塞性肺疾病相关肺动脉高压的影像学评估及研究进展

随着临床诊疗水平的提高,慢性阻塞性肺疾病(COPD)患者的预后得以提升,但其并发症成为了影响患者生存质量的主要原因.肺动脉高压(PH)是其重要并发症之一,是指静息状态下肺动脉压力升高,同时合并有不同程度的右心功能衰竭.2018年中国肺动脉高压诊断和治疗指南将肺高血压分为五大类[1]:①动脉性肺动脉高压;②左心疾病所致肺...     

慢性阻塞性肺疾病相关性肺动脉高压的研究进展

正慢性阻塞性肺疾病(COPD)是一种严重危害人类健康的常见病、多发病。至2020年,COPD将位居世界疾病经济负担的第5位,全球死亡原因的第3位。肺动脉高压(pulmonary hypertension,PH)是COPD患者的常见并发症,COPD合并PH是影响预后的独立危险因素~([1]),增加患者病死率~([2])。近几年来,关于特发性肺动脉高压(IPAH)的治疗取得了较大     

慢性阻塞性肺疾病并发肺动脉高压的相关基因多态性的研究

肺动脉高压(pulmonary hypertension,PH)是慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)的重要合并症,影响COPD患者的预后.长期慢性缺氧是主要的发病机制.近几年,文献报道某些基因多态性与PH关系的研究,发现某些基因多态性的等位点是COPD患者合并PH易感因素.本文对COPD并发PH的相关基因多态性的研究作一综述.     

CT测量肺动脉直径对COPD肺动脉高压的诊断价值

目的探讨胸部CT测量肺动脉直径在慢性阻塞性肺疾病(COPD)肺动脉高压(PH)诊断中的价值。方法回顾性分析92例COPD患者。所有患者接受胸部CT、肺功能及超声心动图检查。通过CT测量肺动脉(PA)和升主动脉(A)直径。计算PA及PA:A比值在诊断PH中的不同临界值。结果 92例COPD患者中,包括PH 43例,非PH 49例。PH组、非PH组主肺动脉直径分别为(30. 83±3. 82) mm、(25. 66±2. 54) mm,肺动脉与升主动脉直径比分别为(0. 99±0. 12)、(0. 84±0. 10),两者差异有统计学意义(P 0. 05)。PA:A≥1的阴性预测值78%,阳性预测值为94%。PA直径≥30mm的阴性预测值为77%,阳性预测值为64%。PA和PA:A比值与肺动脉收缩压(PASP)之间呈显著正相关(r=0. 73、0. 54,P 0. 01)。结论 PA及PA:A比值可作为筛查PH的指标。     

西地那非治疗慢性阻塞性肺疾病相关肺动脉高压的疗效

目的探讨西地那非对慢性阻塞性肺疾病(COPD)相关肺动脉高压(PH)患者的治疗作用及其对血浆一氧化氮(NO)及内皮型一氧化氮合酶(eNOS)水平的影响。方法将56例COPD合并PH住院患者,随机分为常规治疗组(吸氧、抗感染、利尿、强心等常规治疗)和西地那非组(常规治疗+口服枸橼酸西地那非25mg,2次/d),分别观察两组治疗前、治疗4w后肺动脉收缩压(PASP),6 min步行距离,血浆NO及eNOS的变化。结果常规治疗组及西地那非组治疗后PASP均明显低于治疗前,6min步行距离较治疗前明显增加(P0.001);且西地那非组更为明显(P0.05)。常规治疗组及西地那非组治疗后血浆NO和eNOS明显高于治疗前(P0.001)。西地那非组治疗后血浆NO和eNOS明显高于常规治疗组(P0.05)。结论西地那非联合常规治疗比单用常规治疗更有效。西地那非可能通过上调NO含量和eNOS活性来抑制血管重建和血管收缩,降低肺动脉压力,改善运动耐量,从而治疗COPD相关pH。     

Tei指数对慢性阻塞性肺病肺动脉高压患者的右心功能评价

目的:应用Tei指数评价慢性阻塞性肺病（chronic obstructive pulmonary disease,COPD）伴肺动脉高压(pulmonary hypertension,PH)患者的右心功能。方法: 临床确诊的慢性阻塞性肺病伴肺动脉高压(COPD+PH)患者68例,另30例正常人作为对照组。根据三尖瓣反流压差,超声估测肺动脉收缩压,并按其分别判定为重度PH组、中度PH组和轻度PH组。超声常规测量参数包括右心室前后径、右心房横径、肺动脉主干内径,并计算右心室Tei指数。结果: 68例COPD+PH患者中,重度PH组22例,中度PH组30例,轻度PH组16例;与对照组相比,重度PH组和中度PH组右心大小、Tei指数均有统计学差异,轻度PH组无明显右心形态改变,Tei指数无统计学差异。结论: 右心室Tei指数可作为COPD伴中重度PH患者右心功能评价的参考指标。     

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.     

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.