Surgical pathology of pulmonary thromboendarterectomy: a study of 54 cases from 1990 to 2001

Thromboendarterectomy is performed to treat chronic thromboembolic pulmonary hypertension with obstruction of main, lobar, or segmental pulmonary arteries. The present study evaluated surgical specimens removed between 1990 and 2001. Medical histories and microscopic slides were reviewed in each case. Study slides were stained with hematoxylin and eosin and Verhoeff-van Gieson and evaluated for thrombus, collagen, elastin, atherosclerosis, hemosiderin, calcification, and inflammation. The study group comprised 54 patients (30 women and 24 men), ranging in age from 33 to 77 years (mean, 58 years). Clinically, 28 (52%) had a history of deep leg vein thrombosis and 42 (78%) had a history of pulmonary embolism; 24 (44%) had both events. Coagulation abnormalities were documented in 15 (28%); autoimmune or hematologic disorders, in 8 (15%). Pulmonary thromboendarterectomy was bilateral in 52 patients (96%) and right-sided in 2. Six patients also had obstructions resected from the main pulmonary arteries. Obstruction limited to segmental arteries occurred only in women. Grossly, right-sided specimens were larger than left-sided ones (P = 0.003). Microscopically, ages of thrombi were uniform in 72% and variable in 28%. Intima was thickened in all patients and consisted of collagen (100%), elastin (67%), hemosiderin (56%), inflammation (53%), atherosclerosis (32%), and calcification (15%). We determined that pulmonary thromboendarterectomy was performed most often in middle-aged and elderly patients with a history of deep venous thrombosis or pulmonary embolism. Less than 50% of the patients had an identifiable coagulation, autoimmune, or hematologic abnormality. Most patients had bilateral disease and resections. Right-sided specimens were significantly larger than left-sided specimens, and lower lobe involvement was more common than involvement elsewhere. Resected tissues most commonly exhibited old organized thrombus.     

Pulmonary circulation in embolic pulmonary edema

Laboratory of Pathophysiology of Respiration and Bioengineering Laboratory, Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Department of Pathological Physiology, Yaroslavl' Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR B. I. Tkachenko.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 107, No. 2, pp. 157–161, February, 1989.     

Dual endothelin receptor blockade with tezosentan markedly attenuates hypoxia-induced pulmonary vasoconstriction in a porcine model

Aim: Our aim was to test the hypothesis that dual endothelin receptor blockade with tezosentan attenuates hypoxia‐induced pulmonary vasoconstriction. Methods: Fourteen anaesthetized, ventilated pigs, with a mean ± SEM weight of 30.5 ± 0.6 kg, were studied, in normoxia (FiO₂ 0.21) and with tezosentan (5 mg kg^?1) infusion during (n = 7) or before (n = 7) hypoxia (FiO₂ 0.10). Results: Compared to normoxia, hypoxia increased (P < 0.05) pulmonary vascular resistance (PVR) by 3.4 ± 0.7 WU, mean pulmonary artery pressure by 13.7 ± 1.3 mmHg, mean right atrial pressure by 1.9 ± 0.4 mmHg and decreased (P < 0.02) systemic vascular resistance (SVR) by 5.2 ± 2.1 WU. Pulmonary capillary wedge pressure (PCWP), mean aortic blood pressure, heart rate, cardiac output, stroke volume and blood‐O₂‐consumption were unaltered (P = ns). Tezosentan infused during hypoxia, normalized PVR, decreased (P < 0.05) maximally mean pulmonary artery pressure by 7.5 ± 0.8 mmHg, SVR by 5.8 ± 0.7 WU, mean aortic blood pressure by 10.8 ± 3.0 mmHg and increased (P < 0.04) stroke volume by 8.5 ± 1.8 mL. Mean right atrial pressure, PCWP, heart rate, cardiac output and blood‐O₂‐consumption were unaltered (P = ns). Tezosentan infused before hypoxia additionally attenuated approx. 70% of the initial mean pulmonary artery pressure increase and abolished the PVR increase, without additionally affecting the other parameters. Conclusion: Dual endothelin receptor blockade during hypoxia attenuates the ‘sustained’ acute pulmonary vasoconstrictor response by reducing the mean pulmonary artery pressure increase by approx. 62% and by normalizing PVR. Pre‐treatment with tezosentan before hypoxia, additionally attenuates the initial hypoxia‐induced mean pulmonary artery pressure rise by approx. 70% and abolishes the PVR increase, during stable circulatory conditions, without affecting oxygenation.     

A practical approach to vascular pathology in pulmonary hypertension

Pulmonary hypertension (PH) is the common physiological denominator in an otherwise heterogeneous disease. While pulmonary hypertension itself is not a pathologists' diagnosis, various patterns of pulmonary vasculopathy may be recognized in pulmonary hypertension. These patterns of vasculopathy are at the basis of classification, as they point towards (groups of) risk factors and aetiology. However, as surgical lung biopsy is a high risk procedure in PH, the role for histopathological evaluation is now mainly in retrospective evaluation on explanted lung or tissue obtained at autopsy, taking clinical work-up, including haemodynamic parameters and HRCT imaging, into account. Such multidisciplinary evaluation and classification may help assess the prognosis, including risk of recurrence in a transplant, and possible risk of PH in family members. More generally, systematic evaluation may identify clues as to pathogenesis and may help to fill the knowledge gap between histopathology and non-invasive diagnostic procedures such as imaging. This will hopefully eventually lead to a patho-physiologic rationale for classification, and to improved treatment strategies. This review aims to offer some practical guidelines for pathologists, pointing out pitfalls along the way.     

Ultrastructure of early plexogenic pulmonary arteriopathy

A lung biopsy specimen from a young woman with the clinical features of primary pulmonary hypertension showed grade 2 plexogenic pulmonary arteriopathy. Electron microscopy revealed 'dark', electron-dense smooth muscle cells in the inner part of the media of muscular pulmonary arteries. Many of these transformed myocytes had migrated into the lumens of pulmonary arteries and arterioles which they occluded. This migration of smooth muscle cells was associated with a substantial increase in the number of pulmonary endocrine cells in the bronchioles containing bombesin and calcitonin.     

亚段及单一段肺栓塞临床特点分析

目的 探讨亚段及单一段肺栓塞的临床特征、高危因素、治疗及预后。方法 分析我院收治的60例累及亚段及单一段肺栓塞患者的危险因素、临床表现、动脉血气分析、D-二聚体、栓塞部位,比较单一段及亚段肺栓塞的临床特征及预后。结果 60例患者中累及单一段36例,累及亚段24例。累及亚段或单一段的肺栓塞患者临床表现不典型,主要包括呼吸困难、心绞痛样胸痛、心悸、胸膜炎样胸痛、咳嗽,其中8.33%无临床症状。单一段组呼吸困难发生率为80.56%,高于亚段组的45.83%（P＜0.05）。栓塞部位累及右肺多见。60例患者中合并高血压病（48.33%）,糖尿病（18.33%）,COPD（6.67%）,脑卒中（10.00%）,肿瘤（8.33%）,心衰（11.67%）,房颤（13.33%）,高脂血症（38.33%）,冠心病（23.33%）,感染性疾病（3.33%）,手术、外伤、骨折（11.67%）,下肢静脉曲张（5.00%）,合并DVT（16.67%）。单一段组肺泡动脉氧分压差、D-二聚体阳性率均高于亚段组（P＜0.05）。结论 累及亚段或单一段的肺栓塞临床表现多样,血浆D-二聚体敏感性不高,抗凝治疗总体预后良好。     

肺部超声对重症肺部感染患者肺通气的评估价值

目的:探讨肺部超声评价重症肺部感染患者通气情况的应用价值。方法:选取88例重症肺部感染患者,采用半定量方法对肺部超声征象进行评分,以CT检查结果为金标准,分析肺部超声评分与患者肺通气的关系;同时分析存活和死亡患者临床资料、肺部超声评分的差异,以及肺部超声评分预测患者死亡的价值。结果:88例患者全肺超声评分平均为（18.50±2.12）分,全肺CT值平均为（-620.50±88.13） HU,不通气/低通气肺组织比例平均为（10.41±3.35）%,正常通气肺组织比例平均为（71.54±6.69）%,过度通气肺组织比例平均为（17.65±4.11）%;患者肺部超声评分与全肺CT值、不通气/低通气肺组织比例呈正相关（r=0.775、0.648, P<0.05）,与正常通气肺组织比例、过度通气肺组织比例无明显相关性（r=-0.170、0.046, P>0.05）;死亡组患者年龄、糖尿病比例、APACHEⅡ评分、肺泡-动脉氧分压差、机械通气治疗和肺部超声评分分别为（59.28±8.12）岁、44.83%、（22.19±2.40）分、（344.40±82.29） mmHg、72.41%和（20.20±1.72）分,明显高于存活组（P<0.05）,而氧合指数为（104.42±21.18）,明显低于存活组（P<0.05）;Logistic回归分析结果显示:年龄、APACHEⅡ、肺部超声评分是重症肺部感染患者死亡的影响因素（OR=1.758、2.841、2.440, P<0.05）;肺部超声评分预测重症肺部感染患者死亡的ROC曲线下面积为0.901（95%CI:0.836~0.966）,截断值为20分,灵敏性和特异性分别为82.80%和84.70%。结论:肺部超声可以作为重症肺部感染患者肺通气的评估指标,同时其在预测患者预后方面有一定应用价值。     

Choriocarcinoma-associated pulmonary thromboembolism and pulmonary hypertension: a case report

Cases of pulmonary embolism and pulmonary artery hypertension caused by choriocarcinoma represent a rare clinical emergency. We report a case of a 25-year-old woman who presented with pulmonary embolism and hypertension and died soon after complete pulmonary embolectomy. A related literature review revealed that almost all of these patients had previously experienced a spontaneous abortion (average, 6 months) and were not pregnant.     

Effect of BQ123 on vasoconstriction as a result of either hypoxia or endothelin-1 in perfused rat lungs

A possible role of endothelin (ET)-1 in mediating hypoxic pulmonary vasoconstriction (HPV) was examined by comparing haemodynamic differences between ET-1-induced vasoconstriction and HPV in isolated perfused rat lungs. An ET_A receptor antagonist (BQ123) was also employed to assess the effects of ET-1. The pulmonary arterial pressure (Ppa) was significantly increased by alveolar hypoxia (3% O₂) and by ET-1 (5 nM). The pulmonary microvascular pressure was not changed by hypoxia, but increased more than two-fold by ET-1 (P < 0.01). Hypoxia significantly increased pulmonary arterial resistance (P < 0.01) while ET-1 significantly increased pulmonary venous resistance (P < 0.01), and slightly increased arterial resistance. Lung weight was increased by ET-1 and decreased by hypoxia, accompanied by similar Ppa responses in both cases. BQ123 (10^-6 m and 10^-5 m ) did not influence the changes in Ppa and lung weight induced by hypoxia or angiotensin II (0.3 μg). BQ123 did, however, suppress (P < 0.05) the increase in Ppa and lung weight induced by 5 nM ET-1. Thus, it appears unlikely that ET-1 is involved in changes in pulmonary vascular tone during acute HPV.     

Airway and blood vessel interaction during lung development

In the adult lung the pulmonary arteries run alongside the airways and the pulmonary veins show a similar branching pattern to the arteries, though separated from them. During early fetal development the airways act as a template for pulmonary blood vessel development in that the vessels form by vasculogenesis around the branching airways. In later lung development the capillary bed is essential for alveolar formation. This paper reviews evidence for the interaction of the airways and blood vessels in both normal and abnormal lung development.     

肺段的冠状断层解剖:断层标本与多层螺旋CT图像对照研究

目的：研究肺段在冠状断面上的划分及分布。方法：利用20例胸部连续冠状断层标本、2例多层螺旋CT图像、5侧游离肺剥离标本和7侧肺管道铸型，追踪观察了肺叶和肺段的支气管、肺动脉和肺静脉，并据此在冠状断面上划分了肺段。结果：肺段主要分布于从胸骨角至脊柱的10个断面里，气管权层面是在冠状断面上划分肺段的最佳开始层面。在冠状断面上有6个划分肺段的关键层面：①升主动脉层面，划分肺段的标志性结构尖段静脉、外侧段静脉、尖后段静脉、左前段静脉和上舌段静脉均出现；②肺动脉权层面，于肺动脉权下方可见到左、右上肺静脉，在Il例(55％)标本中m现尖后段静脉、前段静脉和舌静脉干同Here入左上二肺静脉的情形；③气管权层面，左、右肺上叶支气管及其分支显示清晰，于气管权下方可见到左、右下肺静脉汇入左心房；④中间支气管层面，可见到两肺下叶肺段支气管、肺动脉和肺静脉的起源；⑤胸主动脉层面，主要为两肺上段和外后底段的支气管和血管；⑥脊柱层面，两肺下叶主要表现为上段、外侧底段和后底段的支气管和血管。结论：通过仔细辨认肺段支气管、肺动脉和肺静脉，可在冠状断面上精确划分肺段。     

右肺门支气管和血管在横断面上的配布特点

目的：探讨有肺门支气管、肺动脉和肺静脉在横断面上的配布特点。方法：在44例成人胸部连续横断层标本和5例螺旋CT图像上，追踪观察了有侧第一、二、三肺门处支气管、肺动脉和肺静脉的分支(或属支)及其毗邻关系。结果：从气管权开始，至底段上、下静脉出现，以7个典型横断面便可清晰显示有肺门管道结构的配布规律：①在气管权层面，尖段动脉、尖段支气管和后段静脉于奇静脉弓右侧由内向外依次排列；②在右肺上叶支气管层面，后段静脉居后段支气管与前段支气管之间；③在中间支气管层面，右肺上叶动脉上行于中间支气管前方，两者的深面为尖段静脉、前段静脉和后段静脉；④在叶间动脉层面，右肺上叶静脉、叶间动脉和中间支气管由前向后依次排列，在33例(75％)标本中可见到下叶上段动脉的起源；⑤于中间支气管权层面，中、下叶动脉走行于中、下叶支气管外侧；⑥于基底干支气管层面，在11例(25％)标本中可见中叶静脉直接汇入左心房，内侧底段支气管常与上段静脉段问支同时出现；⑦于底段上、下静脉层面，以各底段支气管为中心，相应动脉呈周围性分布，底段上、下静脉呈向心性走行。结论：通过寻找标志性结构，在横断面上可准确识别有肺门处肺叶和肺段的支气管、肺动脉和肺静脉。     

慢性肺动脉高压肺血管力学特性的评价

本文以风心病二尖瓣病变合并被动性肺动脉高压为研究对象,借助右心导管技术和利用压力波形面积确定动脉顺应性的改进方法,通过测定肺血管阻力和顺应性,以评价慢性肺动脉高压肺血管力学特性的变化规律。发现慢性肺动脉高压患者肺动脉血管阻力明显升高（P＜0.01）;而反映血管壁固有结构的零压顺应性Co明显下降(P＜0.01),与术前肺动脉平均压呈显著负相关(r＝－0.745P＜0.05);扩血管药物试验提示不同程度肺动脉高压组的肺血管阻力均有显著下降(P＜0.01),轻度肺高压组零压顺应性和平均压顺应性均明显升高(P＜0.01);而重度肺高压组零压顺应性Co无明显变化(P＞0.05)。由此我们认为慢性肺高压肺血管都存在不同程度的重建,肺血管外周血管阻力和顺应性是影响其肺动脉压力水平的主要因素。     

右肺肺段和亚肺段支气管和血管的矢状断层解剖学研究

目的：研究右肺肺段和亚肺段支气管和血管在矢状断面上的配布规律.方法：利用15例胸部连续矢状断层标本和2例多层螺旋CT图像,追踪观察了右肺肺段和亚肺段支气管和血管,并据此寻找在矢状断面上划分右肺肺段的方法.结果：在右主支气管杈层面上,右肺上叶动脉发出尖段动脉和前段动脉,右肺下叶支气管向后发出上段支气管、向下发出内侧底段支气管.在叶间动脉层面上,右肺上叶支气管发出尖、后、前段支气管,基底干支气管发出前、外侧和后底段支气管.在叶间动脉分叉层面上,后段静脉居前、后段支气管之间,尖段静脉与前段静脉合成尖前静脉,中叶支气管分为外、内侧段支气管,下叶动脉发出的段级动脉居相应支气管的上方.在右心房右侧第二层面上,右肺上、中叶的支气管和血管已为亚段级,在右肺下叶内,肺段支气管居中,其上、下方分别为相应的肺动脉和肺静脉.结论：在矢状断面上,右侧肺段内支气管和血管相对集中,且容易显示其发出处和长轴,故矢状断面是显示右肺肺段和亚肺段支气管和血管的优势断面.     

sPAP/PAAT Ratio as a New Index of Pulmonary Vascular Load: A Study in Normal Subjects and Ssc Patients with and without PH

In pulmonary hypertension (PH), the development of right ventricular (RV) dilatation and RV failure are signs of accelerated progression of the disease, resulting in an increased risk of cardiac death. Even the noninvasive assessment of systolic blood pressure in the pulmonary artery undertaken by echocardiography does not provide a measure of ventricle–pulmonary interaction. Some studies have shown the potential for echocardiography to indirectly evaluate pulmonary vascular resistance (PVR) and the acceleration time of pulmonary outflow (PAAT). We used systolic pulmonary artery pressure (sPAP) and pulmonary vascular resistance to develop an sPAP/PAAT ratio (strength/surface unit)/(time) for this study. From January 2017 to December 2018, 60 healthy subjects and 63 patients with systemic scleroderma (Ssc) (60 females, 3 males), 27 with PH and 36 without PH at two-dimensional echocardiographic/Doppler, were screened. In normal subjects, the mean sPAP/PAAT ratio was 0.26 ± 0.063, which indicated optimal pulmonary arterial ventricle coupling and biventricular function. The data derived from the analysis of the Ssc patients showed that those presenting pre-capillary PH at cardiac catheterization had an sPAP/PAAT ratio of 0.40 ± 0.05. There was a significant correlation between sPAP/PAAT with Walk Distance (WD) and PVR, but not with TAPSE. Interobserver variability was less than 5%. The sPAP/PAAT ratio is a new parameter that may indicate pulmonary vascular afterload and interaction, both in normal subjects and in patients with Ssc and PH.     

RhoA/Rho激酶信号通路与肺动脉高压

目前研究已发现RhoA/Rho激酶信号通路参与了人体多种疾病的形成,如高血压、冠心病、脑率中等.肺动脉高压的病理学改变包括内皮细胞的损伤、增殖,肺血管平滑肌细胞的高反应性,炎症细胞迁移和黏附以及肺小血管形成和栓塞;Rho激酶调节细胞的多种生物学行为和功能,如收缩、黏附、迁移、增殖、凋亡、基因表达等.研究表明RhoA/R...     

Can echocardiographically estimated pulmonary arterial elastance be a non-invasive predictor of pulmonary vascular resistance?

Introduction

Measurement of pulmonary vascular resistance (PVR) is essential in evaluating a patient with pulmonary hypertension.

Material and methods

Data from right heart catheterization (RHC) and echocardiograms performed within 90 days of each other on 45 non-consecutive adult patients were reviewed in this retrospective study. Patients were recruited using an assortment of strategies to ensure the presence of patients with a wide range of PVR.

Results

The linear regression equation between RHC-derived PVR and echocardiographic pulmonary arterial elastance (PAE) was: PVR = (562.6 × PAE) – 38.9 (R = 0.56, p < 0.0001). An adjustment for echocardiographic PAE was made by multiplying it by hemoglobin (in g/dl) and (right atrial area)^1.5 (in cm³). As RHC-derived PVR varies with blood hemoglobin, an adjustment for PVR was made for hemoglobin of 12 g/dl. Visualization of the XY scatter plot of adjusted PVR and adjusted PAE isolated a subset of patients with PVR higher than 8.8 Wood units, where a strong linear relationship existed (adjusted PVR = (0.89 × adjusted PAE) + 137.4, R = 0.89, p = 0.008).

Conclusions

The correlation coefficient of the regression equation connecting echocardiographic PAE and RHC-derived PVR was moderate. In a subset of patients with very high PVR and after appropriate adjustment, a strong linear relationship existed with an excellent correlation coefficient.     

肺动脉修复与重建的应用解剖学

目的 :为肺动脉修复与重建提供解剖学基础。方法 :对 3 0例成人尸体肺动脉心包外段的长度、外径、分支及奇静脉各段的长度、外径进行观测。结果 :左、右肺动脉出心包返折处的外径分别为 (13 .8±2 .6)mm ,(15 .3± 2 .8)mm ;发出下叶上支处的外径分别为 (8.4± 2 .1)mm ,(9.1± 2 .3 )mm。左、右肺动脉出心包处至下叶上支动脉起点处长度分别为 (4 .9± 0 .6)cm ,(3 .8± 0 .8)cm。奇静脉第 2段、第 3段 (奇静脉弓 )的长度分别为 (4 .2± 0 .9)cm ,(3 .1± 0 .6)cm。结论 :(1)如肿瘤侵犯肺动脉主干及其分支根部 ,动脉切除后可采用袖式吻合及侧壁扩大成形术 ;(2 )如右肺动脉侧壁切除缺损较大时 ,首选自体奇静脉片进行重建。