Pulmonary Vessels In Patients Research Articles

Pulmonary vascular stenosis scoring in fibrosing mediastinitis.

This study aims to develop a scoring system for evaluating the degree of pulmonary vascular stenosis in fibrosing mediastinitis (FM). A retrospective single-centre study was conducted on 56 patients with FM in China between April 2014 and August 2021. The involvement of pulmonary vessels in patients with FM was assessed using dual-phase computed tomography pulmonary angiography, and we found that 85.7% of the patients had both pulmonary artery (PA) and vein (PV) involvement. PA involvement was mainly located proximal to both the upper PA and the bilateral basal trunk levels in the lower lungs. The involvement of the superior PV was more common than that of the inferior PV, and the right inferior PV was the least involved. Most of these lesions exhibited moderate or severe stenosis. Additionally, a scoring system for evaluating the degree of pulmonary vascular stenosis was developed. A correlation analysis revealed a negative correlation between the final pulmonary vascular score and the pulmonary arterial pressure, pulmonary vascular resistance, and maximum tricuspid regurgitation velocity. The calculated score of 17.1 was the best cut-off value for the diagnosis of mild and severe pulmonary hypertension (PH). We successfully developed a scoring system for pulmonary vascular stenosis that can be used to evaluate the severity of pulmonary vessel involvement and PH. This scoring system may be relevant in the future development of target-based strategies for percutaneous interventions.

The HRCT Imaging Findings of the Peripheral Pulmonary Vessels in Patients with Pulmonary Hypertension (PH)

The prominence of the pulmonary vasculature and/or tortuosity (n = 16) and dilatation of the central PA (n = 39) with RV hypertrophy were frequently observed. The interlobular septal thickening (n = 18, 45%), and centrilobular (perivascular) ground glass opacities (n = 6, 15%) were clearly depicted on gapless HRCT. PA aneurysmal dilatation and irregular dilatation with arterio-venous fistula were observed in 2 (5%) and 3 cases (7.5%), respectively. Bronchial artery dilatation was observed in 5 cases.

Impairment of the NKT-STAT1-CXCL9 Axis Contributes to Vessel Fibrosis in Pulmonary Hypertension Caused by Lung Fibrosis.

Rationale: Pulmonary hypertension (PH) is a common, severe comorbidity in interstitial lung diseases such as pulmonary fibrosis (PF), and it has limited treatment options. Excessive vascular fibrosis and inflammation are often present in PH, but the underlying mechanisms are still not well understood. Objectives: To identify a novel functional link between natural killer T (NKT) cell activation and vascular fibrosis in PF-PH. Methods: Multicolor flow cytometry, secretome, and immunohistological analyses were complemented by pharmacological NKT cell activation invivo, invitro, and ex vivo. Measurements and Main Results: In pulmonary vessels of patients with PF-PH, increased collagen deposition was linked to a local NKT cell deficiency and decreased IL-15 concentrations. In a mouse model of PH caused by lung fibrosis, pharmacological NKT cell activation using a synthetic α-galactosylceramide analog (KRN7000) restored local NKT cell numbers and ameliorated vascular remodeling and right ventricular systolic pressure. Supplementation with activated NKT cells reduced collagen deposition in isolated human pulmonary arterial smooth muscle cells (hPASMCs) and in ex vivo precision-cut lung slices of patients with end-stage PF-PH. Coculture with activated NKT cells induced STAT1 signaling in hPASMCs. Secretome analysis of peripheral blood mononuclear cells identified CXCL9 and CXCL10 as indicators of NKT cell activation. Pharmacologically, CXCL9, but not CXCL10, potently inhibited collagen deposition in hPASMCs via the chemokine receptor CXCR3. Conclusions: Our results indicate that the absence of NKT cells impairs the STAT1-CXCL9-CXCR3 axis in PF-PH and that restoration of this axis by NKT cell activation may unravel a novel therapeutic strategy to target vascular fibrosis in interstitial lung disease.

Robot-assisted bronchial sleeve left upper lobectomy for locally advanced bronchopulmonary squamous cell carcinoma after neoadjuvant chemotherapy: a case report

: For patients with central bronchopulmonary malignancies, sleeve lobectomy serves as an alternative to pneumonectomy. In recent years, robotic-assisted technique has been innovatively developed and applied in sleeve lobectomy. Here, we introduce a patient treated with chemotherapy who received robotic bronchial sleeve lobectomy without pulmonary vessel anastomosis in our department. The patient was a 53-year-old male smoker, who had suffered irritable cough for 6 months. During surgery we found that the tumor was tightly adhered to the pulmonary artery. Robotic scissors were used to separate the tumor from the surface of the pulmonary artery. Finally, the tumor was removed along with the relevant bronchus, and the pulmonary artery remained intact. The tumor margins were verified as negative by fast frozen pathology during the procedure. This experience in our department demonstrates the advantages of robot-assisted bronchial lobectomy in preserving pulmonary vessels in patients with pulmonary arterial adventitia involvement.

Native Endogenous Fluorescence Imaging Detects Vascular Occlusions in Patients with COVID-19

Background: A number of histopathological reports showed the presence of widespread thrombosis and associated morphology in pulmonary vessels of patients with COVID-19. Later, we identified vascular occlusions with neutrophils and neutrophil extracellular traps (NETs), as major components, in autopsy tissue from patients with COVID-19.Methods: We, here investigated 109 lung specimens from 17 patients with COVID-19 and compared them with 11 lung specimens from two patients who succumbed to pulmonary embolism and acute cardiac. Healthy lung specimens from four patients served as controls. We studied these autopsy lung specimens using immunohistochemistry and native endogenous fluorescence.Findings: We present a label-free imaging technique using native endogenous fluorescence that enables the visualization of occluded vessels. We demonstrate that native endogenous fluorescence identified occluded vessels in tissue specimens from patients with COVID-19.Interpretation: Label-free detection of occluded vessels enabled the detection of affected occluded vessels in lung specimens of patients with COVID-19 where the occluding components showed varying contents of neutrophil-derived materials.Funding Statement: Deutsche Forschungsgemeinschaft (DFG), EU, Volkswagen-StiftungDeclaration of Interests: All authors have no conflicts of interests to declare.Ethics Approval Statement: An institutional approval from each local Ethical Committee was obtained (permit #193_13B; permit # 174_20B; EK 092/20; EK 119/20; EK 460/20).

STUDY OF THE PULMONARY HYPERTENSION AND PULMONARY VESSELS MEASUREMENTS USING COMPUTED TOMOGRAPHY

The purpose of the study was to study the pulmonary vessels in patients with pulmonary hypertension using Computed Tomography scan (CT) This is a prospective ,analytical study. this study was conducted at Khartoum Hospital (Sudan); in the period between November 2020 - January 2021 a sample of (100) patients with clinically diagnosed as pulmonary hypertension was enrolled, their mean ages were (47.92 ± 19.03) years, the sample included both genders, (42) patients were females while (58) were males and their ages were ranged from (3 - 80) years old. (CTPA) scans were acquired, all patients were examined by using multislice (CT) scanner, the data collected by special designed sheet from findings and analyzed statistically by using an (SPSS) Statistics software package.
 The sample was directed to study the relationship of pulmonary hypertension with the presence of pulmonary vessels measurements; the patient's age and gender correlation with the pulmonary hypertension were investigated. The results find that the right and left main pulmonary arteries diameters changes were found to be significantly related to the presence of pulmonary hypertension, while there was no significant difference in the main pulmonary artery diameters measurements. The study concluded that CT for pulmonary artery plays an important role in the diagnostic evaluation of patients with pulmonary hypertension this due to it is easily accessible and excellent non-invasive method for the visualization and measurement of pulmonary artery and to know the possible cause of pulmonary hypertension.

Microparticles in COVID-19 as a link between lung injury extension and thrombosis.

Procoagulant microparticles are associated with the extent of lung injuries in #COVID19 and pulmonary thrombosis https://bit.ly/3eX2LPc

Thrombotic Lesion of the Pulmonary Vessels in Patients with Pulmonary Embolism

After suffering pulmonary embolism (PE), doctors are confronted with various consequences of the disease, from asymptomatic residual pulmonary thrombosis to the formation of chronic thromboembolic pulmonary hypertension (CTEPH). There is also a subgroup of patients who have undergone pulmonary embolism, who experience shortness of breath during physical exertion, absent before pulmonary embolism, or shortened dyspnea preceding PE, combined with residual thrombosis of pulmonary artery (PA) and normal average pressure in PA at rest during catheterization of the right heart (CRH). This condition is defined as chronic thromboembolic pulmonary disease or post thromboembolic syndrome. Pathogenetic aspects of this condition are not fully investigated. It is important to predict the development of postembolic syndrome and to develop algorithms for the diagnosis, treatment and rehabilitation of patients with symptoms and residual pulmonary thrombosis. In case of the development of pulmonary vasculopathy in some patients who have undergone pulmonary embolism, a severe life-threatening condition forms - CTEPH, characterized by an increase in pressure in the pulmonary artery, right heart failure due to the presence of organized blood clots that have entered the pulmonary vascular bed during PE. The volume of thrombotic masses does not always correlate with clinical symptoms, which indicates the importance of microvascular remodeling. If CTEPH is suspected, a diagnostic algorithm is required, including ventilation-perfusion scintigraphy, CT angiopulmonography and catheterization of the right heart. Treating a patient with CTEPH is a difficult task fora doctor. The timely referral of the patient to the center where they are involved in treatment, including surgery and CTEPH is extremely important. Timely performed thrombendarterectomy in some cases allows to completely cure the patient. In the case of inoperable CTEPH or residual pulmonary hypertension after thrombendarterectomy, balloon angioplasty of the PA is used as well as drug treatment with specific drugs that reduce the pressure in the PA (riociguat), endothelin receptor antagonists (bosentan, macitentan), prostanoids (inhalant illoprost) phosphodiesterase-5 inhibitor and combined therapy. In this article we considered some consequences directly related to PE: asymptomatic residual pulmonary thrombosis, chronic thromboembolic pulmonary disease, chronic thromboembolic pulmonary hypertension.

Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19

BackgroundProgressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19.MethodsWe examined 7 lungs obtained during autopsy from patients who died from Covid-19 and compared them with 7 lungs obtained during autopsy from patients who died from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection and 10 age-matched, uninfected control lungs. The lungs were studied with the use of seven-color immunohistochemical analysis, micro–computed tomographic imaging, scanning electron microscopy, corrosion casting, and direct multiplexed measurement of gene expression.ResultsIn patients who died from Covid-19–associated or influenza-associated respiratory failure, the histologic pattern in the peripheral lung was diffuse alveolar damage with perivascular T-cell infiltration. The lungs from patients with Covid-19 also showed distinctive vascular features, consisting of severe endothelial injury associated with the presence of intracellular virus and disrupted cell membranes. Histologic analysis of pulmonary vessels in patients with Covid-19 showed widespread thrombosis with microangiopathy. Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza (P<0.001). In lungs from patients with Covid-19, the amount of new vessel growth — predominantly through a mechanism of intussusceptive angiogenesis — was 2.7 times as high as that in the lungs from patients with influenza (P<0.001).ConclusionsIn our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection. The universality and clinical implications of our observations require further research to define. (Funded by the National Institutes of Health and others.)

Quantitative CT Evaluation of Small Pulmonary Vessels in Patients with Acute Pulmonary Embolism

The objective of this study was to investigate the correlation between the computed tomography (CT) cross-sectional area (CSA) of small pulmonary vessels and the CT obstruction index in patients with acute pulmonary embolism (PE) and the correlation between the changes in these measurements after anticoagulant therapy. Fifty-two patients with acute PE were selected for this study. We measured the CSA less than 5 mm2 on coronal reconstructed images to obtain the percentage of the CSA (%CSA < 5). CT angiographic index was obtained based on the Qanadli method for the evaluation of the degree of pulmonary arterial obstruction. Spearman rank correlation analysis was used to evaluate the relationship between the initial and the follow-up values and changes in the %CSA < 5 and the CT obstruction index. There was no significant correlation between the %CSA < 5 and CT obstruction index on both initial (ρ = -0.03, P = 0.84) and follow-up (ρ = -0.03, P = 0.82) assessments. In contrast, there was a significant negative correlation between the changes in %CSA < 5 and the CT obstruction index (ρ = -0.59, P < 0.0001). Although the absolute %CSA < 5 and CT obstruction index were not significantly correlated, the changes in the values of the two parameters had a significant correlation. Changes in %CSA < 5, which can be obtained easily, can be used as biomarker of therapeutic response in patients with acute PE.

Prolyl-4 Hydroxylase 2 (PHD2) Deficiency in Endothelial Cells and Hematopoietic Cells Induces Obliterative Vascular Remodeling and Severe Pulmonary Arterial Hypertension in Mice and Humans Through Hypoxia-Inducible Factor-2α.

Vascular occlusion and complex plexiform lesions are hallmarks of the pathology of severe pulmonary arterial hypertension (PAH) in patients. However, the mechanisms of obliterative vascular remodeling remain elusive; hence, current therapies have not targeted the fundamental disease-modifying mechanisms and result in only modest improvement in morbidity and mortality. Mice with Tie2Cre-mediated disruption of Egln1 (encoding prolyl-4 hydroxylase 2 [PHD2]; Egln1(Tie2)) in endothelial cells and hematopoietic cells exhibited spontaneous severe PAH with extensive pulmonary vascular remodeling, including vascular occlusion and plexiform-like lesions, resembling the hallmarks of the pathology of clinical PAH. As seen in patients with idiopathic PAH, Egln1(Tie2) mice exhibited unprecedented right ventricular hypertrophy and failure and progressive mortality. Consistently, PHD2 expression was diminished in lung endothelial cells of obliterated pulmonary vessels in patients with idiopathic PAH. Genetic deletions of both Egln1 and Hif1a or Egln1 and Hif2a identified hypoxia-inducible factor-2α as the critical mediator of the severe PAH seen in Egln1(Tie2) mice. We also observed altered expression of many pulmonary hypertension-causing genes in Egln1(Tie2) lungs, which was normalized in Egln1(Tie2)/Hif2a(Tie2) lungs. PHD2-deficient endothelial cells promoted smooth muscle cell proliferation in part through hypoxia-inducible factor-2α-activated CXCL12 expression. Genetic deletion of Cxcl12 attenuated PAH in Egln1(Tie2) mice. These studies defined an unexpected role of PHD2 deficiency in the mechanisms of severe PAH and identified the first genetically modified mouse model with obliterative vascular remodeling and pathophysiology recapitulating clinical PAH. Thus, targeting PHD2/hypoxia-inducible factor-2α signaling is a promising strategy to reverse vascular remodeling for treatment of severe PAH.

Possible role of Krüppel-like factor 5 in the remodeling of small airways and pulmonary vessels in chronic obstructive pulmonary disease.

BackgroundSmall airway remodeling is an important cause of the airflow limitation in chronic obstructive pulmonary disease (COPD). A large population of patients with COPD also have pulmonary hypertension. Krüppel-like factor 5 (KLF5) is a zinc-finger transcription factor that contributes to tissue remodeling in cardiovascular diseases. Here, we evaluate the possible involvement of KLF5 in the remodeling of small airways and pulmonary vessels in COPD.MethodsLung tissues were obtained from 23 control never-smokers, 17 control ex-smokers and 24 ex-smokers with COPD. The expression of KLF5 in the lung tissues was investigated by immunohistochemistry. We investigated whether oxidative/nitrosative stress, which is a major cause of the pathogenesis in COPD, could augment the production of KLF5. We examined the role of KLF5 in the stress-mediated tissue remodeling responses. We also investigated the susceptibility of KLF5 expression to nitrosative stress using bronchial fibroblasts isolated from the lung tissues.ResultsThe expression of KLF5 was up-regulated in the small airways and pulmonary vessels of the COPD patients and it was mainly expressed in bronchial fibroblasts and cells of the pulmonary vessels. The extent of the KLF5 expression in the small airway of the COPD group had a significant correlation with the severity of the airflow limitation. Oxidative/nitrosative stress augmented the production of KLF5 in lung fibroblasts as well as the translocation of KLF5 into the nuclei. Silencing of KLF5 suppressed the stress-augmented differentiation into myofibroblasts, the release of collagens and metalloproteinases. Bronchial fibroblasts from the patients with COPD highly expressed KLF5 compared to those from the control subjects under basal condition and were more susceptible to the induction of KLF5 expression by nitrosative stress compared to those from the control subjects.ConclusionWe provide the first evidence that the expression of KLF5 is up-regulated in small airways and pulmonary vessels of patients with COPD and may be involved in the tissue remodeling of COPD.

Pulmonary Vessel Cross-sectional Area before and after Liver Transplantation: Quantification with Computed Tomography

Pulmonary vascular complications of liver disease have a substantial impact on morbidity and mortality in patients who undergo liver transplant. The effect of liver transplantation on the pulmonary vasculature in patients without pulmonary vascular disease, however, has not been described. This study was undertaken to characterize the regional effect of liver transplant on the cross-sectional area (CSA) of pulmonary vessels. We performed a single-center, retrospective, cohort study of patients who had a liver transplant between 2002 and 2012 and who had chest computed tomography scans within 1 year before and after transplant. Using ImageJ software, we measured the CSA of small pulmonary vessels (0-5 mm(2)) and the total lung CSA to calculate the percent CSA of pulmonary vessels <5 mm (%CSA<5) at the level of the aortic arch, carina, and right inferior pulmonary vein (RIPV). Pretransplant and posttransplant, %CSA<5 were compared, and associations of pretransplant %CSA<5 with clinical parameters were measured. There was a significant decrease in %CSA<5 at the level of the RIPV (0.19% [interquartile range {IQR}, 0.15-0.26] before vs. 0.15% [IQR, 0.12-0.21] after; P = .0003), with a median change of -16.2% (IQR, -39.3 to 3.9) posttransplant. Changes at the level of the aortic arch and carina were not significant. Pretransplant RIPV %CSA<5 was not significantly correlated with severity of liver disease or oxygenation but was inversely correlated with percent change in %CSA<5 (r = -0.39; P = .0039). This is the first study to describe a significant regional change in the pulmonary vessels of patients without known pulmonary vascular disease who undergo liver transplant.

Nuclear Factor κ-B Is Activated in the Pulmonary Vessels of Patients with End-Stage Idiopathic Pulmonary Arterial Hypertension

ObjectivesTo assess activation of the inflammatory transcription factor NF-kappa B (NF-κB) in human idiopathic pulmonary arterial hypertension (PAH).BackgroundIdiopathic PAH is a severe progressive disease characterized by pulmonary vascular remodeling and excessive proliferation of vascular cells. Increasing evidence indicates that inflammation is important in disease pathophysiology.MethodsNF-κB-p65 and CD68, CD20 and CD45 were measured by immunohistochemistry and confocal microscopy on lung specimens from patients with idiopathic PAH (n = 12) and controls undergoing lung surgery (n = 14). Clinical data were recorded for all patients including invasive pulmonary hemodynamics for the PAH patients. Immunohistochemical images were analyzed by blinded observers to include standard pulmonary vascular morphometry; absolute macrophage counts/mm2 and p65-positivity (p65+) using composite images and image-analysis software; and cytoplasmic:nuclear p65+ of individual pulmonary arterial endothelial and smooth muscle cells (PASMC) in 10–20 pulmonary arteries or arterioles per subject. The expression of ET-1 and CCL5 (RANTES) in whole lung was determined by RT-qPCR.ResultsMacrophage numbers were increased in idiopathic PAH versus controls (49.0±4.5 vs. 7.95±1.9 macrophages/100 mm2, p<0.0001): these macrophages demonstrated more nuclear p65+ than in macrophages from controls (16.9±2.49 vs. 3.5±1.25%, p<0.001). An increase in p65+ was also seen in perivascular lymphocytes in patients with PAH. Furthermore, NF-κB activation was increased in pulmonary arterial endothelial cells (62.3±2.9 vs. 14.4±3.8, p<0.0001) and PASMC (22.6±2.3 vs. 11.2±2.0, p<0.001) in patients with PAH versus controls, with similar findings in arterioles. Gene expression of both ET-1 mRNA ((0.213±0.069 vs. 1.06±0.23, p<0.01) and CCL5 (RANTES) (0.16±0.045 vs. 0.26±0.039, p<0.05) was increased in whole lung homogenates from patients with PAH.ConclusionsNF-κB is activated in pulmonary macrophages, lymphocytes, endothelial and PASMC in patients with end-stage idiopathic PAH. Future research should determine whether NF-κB activation is a driver or bystander of pulmonary vascular inflammation and if the former, its potential role as a therapeutic target.

Quantitative assessment of cross-sectional area of small pulmonary vessels in patients with COPD using inspiratory and expiratory MDCT

ObjectivesStructural and functional changes in pulmonary vessels are prevalent at the initial stages of chronic obstructive pulmonary disease (COPD). These vascular alterations can be assessed using cross-sectional area (CSA) of small pulmonary vessels. However, neither in non-COPD smokers nor in COPD patients it has been defined whether the structural changes of pulmonary vessels detected by paired inspiratory and expiratory CT scans are associated with emphysematous changes. We quantified the CSA and low attenuation area (LAA) and evaluated the changes in these parameters in the inspiratory and expiratory phases. Materials and methodsFifty consecutive non-COPD smokers and COPD patients were subjected to multi detector-row CT and the percentage of vessels with a CSA less than 5mm2 as well as the percentage LAA for total lung area (%CSA<5, %LAA, respectively) were calculated. ResultsThe %CSA<5 correlated negatively with %LAA. The %CSA<5 was lower in COPD patients with emphysema as compared with non-COPD smokers and COPD patients with or without mild emphysema. In addition, the %CSA<5 was lower in the no/mild emphysema subgroup as compared with non-COPD smokers. The respiratory phase change of %CSA<5 in COPD patients was greater than that in non-COPD smokers. ConclusionThe percentage of small pulmonary vessels decreased as emphysematous changes increase, and this decrease was observed even in patients with no/mild emphysema. Furthermore, respiratory phase changes in CSA were higher in COPD patients than in non-COPD smokers.

Effect of neoadjuvant chemotherapy on the crispness of pulmonary vessels in patients with lung cancer

Neoadjuvant chemotherapy is one of the hot points of lung cancer therapy,which has been proven to be able to improve resection rate and 5-year survival of patients.But its effect on operation safety is not clear yet.The aim of this study is to confirm the effect of neoadjuvant chemotherapy on pulmonary arterial wall so as to assess its safety for operation in patients with lung cancer. Thirty-two patients underwent lobectomy or pneumonectomy with mediastinal lymphadenectomy after a neoadjuvant chemotherapy,compared with 36 patients surgically treated only.During the operation,the changes of thoracic structure were observed.After the operation,the pulmonary artery specimens were detected pathologically. The incidence of pleural fibrosis and thickening of pulmonary arterial tunica adventitia in neoadjuvant chemotherapy group was significantly higher than those of control group(59.38% vs 22.22%,P < 0.01;68.75% vs 19.44%,P < 0.01).The incidence of tunica intima,internal elastic membrane and tunica media damage in neoadjuvant chemotherapy group was also markedly higher than those of control group(65.62% vs 33.33%,P < 0.01;59.38% vs 19.44%,P < 0.01;71.88% vs 22.22%,P < 0.01). Neoadjuvant chemotherapy may lead to pleural fibrosis and thickening of pulmonary arterial tunica adventitia and increase crispness of pulmonary arterial wall,which may increase difficulty and risk of operation.

Elevated plasma procoagulant and fibrinolytic markers in patients with chronic obstructive pulmonary disease.

There is clinical and pathological evidence of thrombosis in pulmonary vessels of patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate the presence of hypercoagulability and determine the extent of this abnormality in COPD patients. We measured plasma levels of thrombin antithrombin III complex (TAT), fibrinopeptide A (FPA), tissue plasminogen activator-plasminogen activator inhibitor (tPA-PAI): markers of coagulation-fibrinolysis-system, and also beta-thromboglobulin (beta-TG): a marker of platelet activation, in 40 COPD patients and in 20 control subjects. Measurements were also repeated 12 months after entry in all patients. TAT, FPA, tPA-PAI, and beta-TG concentrations were significantly higher in COPD than in control subjects. At 12 months follow-up, deltaA-aDO2 and delta%FEV1 were significantly higher in patients with high TAT or tPA-PAI levels than in patients with low levels and TAT, FPA and tPA-PAI levels remained elevated, although beta-TG levels decreased after domiciliary O2 therapy. Our results showed an enhanced prothrombotic process in COPD patients, which could potentially account for the increased thrombosis in pulmonary vessels in these patients.

Evidence for local platelet activation in pulmonary vessels in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease

To investigate the relationships between local platelet activation in pulmonary vessels and pulmonary artery pressure circulating platelet aggregates and plasma beta-thromboglobulin (beta-TG) levels were evaluated in peripheral venous blood and blood from different sites of pulmonary circulation (right ventricle, pulmonary artery and arteriolo-capillary bed) in 29 patients with COPD. Fifteen had pulmonary hypertension and 14 normal pulmonary artery pressure. In normotensive COPD no significant differences could be found in platelet aggregation and beta-TG levels among different sampling sites. On the contrary in patients with pulmonary hypertension a significant increase of platelet aggregates and beta-TG levels was found in blood withdrawn from the arteriolo-capillary bed. A significant correlation was demonstrated between platelet aggregation and both mean pulmonary artery pressure and pulmonary vascular resistance. These results indicate that in patients with pulmonary hypertension secondary to COPD a local platelet activation in pulmonary vessels does occur and may contribute to the maintainance of elevated pulmonary vascular resistance.

Pulmonary veno-occlusive disease after chemotherapy

A case of pulmonary veno-occlusive disease (PVOD) in a 41-year-old woman who had received chemotherapy (bleomycin, mitomycin-C, and cis-platinum) for metastatic cervical carcinoma is reported. Before her death, pulmonary hypertension and right ventricular heart failure had been attributed to lung toxicity induced by chemotherapy, but the postmortem findings were characteristic of PVOD. The authors support the view that PVOD is a syndrome, not a distinct entity, and present the case as a further example of the many situations in which PVOD can arise. Whether the lesions of the pulmonary veins developed as a result of the chemotherapy or whether the two conditions were associated by chance must remain, for now, a subject of speculation. Pathologists are urged to devote special attention to the examination of the pulmonary vessels in patients who have received chemotherapy.