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Background: No data on the incidence of pleural effusion (PE) in Chinese patients with pulmonary embolism are available to date. The aim of the current study was to investigate the frequency of PE in a Chinese population of patients with pulmonary embolism. Methods: This was a retrospective observational single-center study. All data of computed tomography pulmonary angiography (CTPA) performed over 6-year period on adult patients with clinically suspected pulmonary embolism were analyzed. Results: From January 2008 until December 2013, PE was identified in 423 of 3141 patients (13.5%) with clinically suspected pulmonary embolism who underwent CTPA. The incidence of PE in patients with pulmonary embolism (19.9%) was significantly higher than in those without embolism (9.4%) (P < 0.001). Majority of PEs in pulmonary embolism patients were small to moderate and were unilateral. The locations of emboli and the numbers of arteries involved, CT pulmonary obstruction index, and parenchymal abnormalities at CT were not associated with the development of PE. Conclusions: PEs are present in about one fifth of a Chinese population of patients with pulmonary embolism, which are usually small, unilateral, and unsuitable for diagnostic thoracentesis.

Pulmonary arterial smooth muscle cell (PASMC) migration plays a key role in vascular remodeling, which occurs during development of chronic thromboembolic pulmonary hypertension (CTEPH). Activation of the renin-angiotensin system (RAS) contributes to vascular remodeling observed in many diseases, including idiopathic pulmonary arterial hypertension. However, the role of RAS imbalance in CTEPH has not been characterized. Here, we hypothesize that RAS imbalance regulates vascular remodeling by promoting PASMC migration in CTEPH. Serum renin and angiotensin II levels in patients with CTEPH were quantified by ELISA. The pulmonary endarterectomy tissues were stained and analyzed by immunohistochemistry. PASMCs were isolated and verified by immunofluorescence staining. PASMC migration was determined by Transwell assay. Phosphorylation and protein level were detected by Western blotting. Serum levels of renin and angiotensin II were increased in patients with CTEPH {renin [median (25th percentile, 75th percentile) in pg/ml], 1,199.94 [690.85, 1,656.90] vs. 595.43 [351.48, 936.43], P0.001; angiotensin II [in pg/ml], 63.97 [45.97, 345.24] vs. 56.85 [11.20, 90.37], P0.05}. The migration of PASMCs isolated from patients with CTEPH was enhanced compared with control. Angiotensin II promoted the migration of PASMCs via activation of angiotensin II receptor 1 and phosphorylation of ERK1/2, whereas angiotensin-(1-7) counteracted this effect through activation of the Mas receptor and ERK1/2. These results demonstrate that the renin-angiotensin system regulates migration of PASMCs from patients with CTEPH via the ERK1/2 pathway. Our findings suggest that angiotensin-(1-7) or reagents targeting the renin-angiotensin system will be beneficial in the development of novel therapies for CTEPH.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening condition characterized by single or recurrent pulmonary embolisms, which promotes pulmonary vascular remodeling. There is significant relationship between red cell distribution width (RDW) and pulmonary hypertension; however, the usefulness of RDW as biomarker for the diagnosis of CTEPH remains poorly defined.This study sought to assess the change and the diagnostic value of RDW in CTEPH.This retrospective study included 56 CTEPH patients and 56 sex- and age-matched healthy controls treated at Beijing Chao-Yang Hospital. Correlations between RDW and hematological and hemodynamic parameters were assessed. A logistic regression model was applied to test independent parameters in relation to the diagnosis of CTEPH, and receiver operating characteristic curve was plotted to determine the diagnostic value of RDW in CTEPH.RDW values were significantly higher in CTEPH patients (13.82% ± 1.14%) compared with healthy controls (12.75% ± 0.49%) and in World Health Organization (WHO), functional class III-IV cases (14.39% ± 1.24%) compared with class I-II cases (13.32% ± 0.78%) (both P = 0.000). RDW levels in CTEPH patients showed negative correlations with hemoglobin (r = -0.357, P = 0.007) and cardiac index (r = -0.288, P = 0.031), and positive correlations with pulmonary vascular resistance (r = 0.292, P = 0.029) and WHO functional class (r = 0.450, P = 0.001). Moreover, RDW was an independent parameter in the diagnosis of CTEPH (95% confidence interval: 2.866-13.698, P = 0.000); in particular, an RDW level ≥ 13.05% was the most useful cut-off value, with a sensitivity of 82.1% and a specificity of 71.4%.Increased RDW level may be an acceptable diagnostic parameter for CTEPH.

To evaluate the dynamic changes of inflammation-related indices in blood during the development of venous thromboembolism (VTE) and the association between these indices and VTE.A total of 95 VTE hospitalized patients(41 males,54 females) were recruited from Department of Respiratory and Critical Care Medicine, Beijing Chaoyang Hospital from January 2010 to December 2010. Comparisons of inflammation-related indices including white blood cell (WBC), neutrophil (NE), fibrinogen (FBG), C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were conducted between VTE patients and normal ranges. And the dynamic changes of these indices during the development of VTE were evaluated. Then they were divided into subgroups according to disease stage, gender, age, VTE type, body mass index, smoking status and clinical manifestations. And statistical analyses were performed to elucidate the associations between these indices and VTE.The levels of NE and CRP in VTE patients (0.72, 15.0 mg/L) and ESR in male VTE patients (20.0 mm/1 h) were elevated compared with normal ranges; while WBC (male 7.27×10(9)/L, female 8.67×10(9)/L), FBG (male 3621 mg/L, female 3201 mg/L) and female ESR (19.5 mm/1 h) in VTE patients were within the normal ranges. The level of CRP was higher in acute (mean rank order value: 49.72) and sub-acute (mean rank order value: 44.80) VTE patients than chronic VTE patients (mean rank order value: 30.25). The level of FBG, CRP and ESR in patients ≥ 50 years old increased versus those50 years old (mean rank order values 48.83 vs 34.53, 44.32 vs 28.90 and 45.95 vs 27.84 respectively), the patients whose body mass index (BMI)25 kg/m(2) had higher WBC level than those whose BMI ≥ 25 kg/m(2) (mean rank order values 52.96 vs 36.46); smoking VTE patients had elevated FBG and CRP levels than non-smoking VTE patients (mean rank order values 57.75 vs 42.69 and 53.92 vs 37.75 respectively); compared with those without clinical manifestations of periphery pulmonary artery involved, the patients with clinical manifestations had higher levels of FBG, CRP and ESR (mean rank order values 59.24 vs 37.39, 52.68 vs 33.19 and 50.08 vs 36.55 respectively). The above differences had statistical significance (all P0.05).Some inflammation-related indices frequently used in clinical settings become elevated in VTE patients. Part of these indices show higher levels in VTE acute and sub-acute stages, and in older, non-obese, smoking and periphery pulmonary artery involved VTE patients.

Pulmonary capillary hemangiomatosis (PCH) is a rare disease and no Chinese case has been reported yet. The disease is often misdiagnosed and its clinical characteristics are incompletely described. The aim of this study was to describe two Chinese cases and to clarify the clinical and radiographic parameters of patients with PCH.Two PCH cases were presented and other cases were searched from the English literature. All available clinical and radiographic data were collected from 62 literature reported PCH cases. A pooled analysis of total 64 cases was made.Dyspnea and hemoptysis were the most common clinical symptoms of PCH. Pulmonary hypertension (PH) was found in 78% of the reported cases. PCH typically showed characteristic diffuse or patchy ground-glass opacities (GGOs) and/or multiple ill-defined centrilobular nodules in the computed tomography.The diagnosis of PCH requires a high clinical suspicion. However, both clinical presentations and radiographic studies often provide clues to the diagnosis, which may prompt early lung biopsy for a definite diagnosis.

Pulmonary endarterectomy is safe and effective surgical treatment for chronic thromboembolic pulmonary hypertension. This study aimed to evaluate the efficacy of pulmonary endarterectomy in treatment of thromboembolic pulmonary hypertension.A retrospective study of 15 patients who underwent pulmonary endarterectomy in Beijing Chaoyang Hospital was performed. Obvious pulmonary hypertension and hypoxemia were observed in all patients. Bilateral pulmonary endarterectomy was performed under cardiopulmonary bypass with profound hypothermic circulatory arrest.Two patients (2/15) died of residual postoperative pulmonary hypertension and bleeding complication. The other 13 cases had significant decrease in systolic pulmonary artery pressure ((92.8 +/- 27.4) mmHg vs. (49.3 +/- 18.6) mmHg) and pulmonary vascular resistance ((938.7 +/- 464.1) dynesxsxcm(-5) vs. (316.8 +/- 153.3) dynesxsxcm(-5)), great improvement in cardiac index ((2.31 +/- 0.69) Lxmin(-1)xm(-2) vs. (3.85 +/- 1.21) Lxmin(-1)xm(-2)), arterial oxygen saturation (0.67 +/- 0.11 vs. 0.96 +/- 0.22) and mixed venous O(2) saturation (0.52 +/- 0.12 vs. 0.74 +/- 0.16) postoperatively compared to preoperative data. Mid-term follow-up showed that the cardiac function of all cases returned to NYHA class I or II, with great improvement in 6-minute walking distance ((138 +/- 36) m) and quality of life.Bilateral pulmonary endarterectomy using cardiopulmonary bypass with the aid of deep hypothermia and circulatory arrest can effectively reduce pulmonary hypertension and provide good mid-term hemodynamic and symptomatic results with low surgical mortality rate and few complications.

To evaluate the acute effects of inhaled iloprost on hemodynamics and oxygenation in chronic thromboembolic pulmonary hypertension (CTEPH).A prospective study was made. Eighteen patients with CTEPH were enrolled. At right heart catheterisation, iloprost was inhaled at 20 microg for 10 - 15 min. Compare the value of heart rate (HR), mean blood pressure (mBP), mean pulmonary arterial hypertension (mPAP), right atrium pressure (RAP), pulmonary arterial wedge pressure (PAWP), cardiac output (CO), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), arterial partial pressure of oxygen (PaO2), arterial oxygen saturation (SaO2), mixed venous saturation (SvO2), pulmonary shunt fraction (Qs/Qt), alveolar-arterial partial pressure of oxygen [P ( A-a) O2] before to after inhaled iloprost in these patients.Significant changes (before to after inhalation): mPAP, (53 +/- 11) to (47 +/- 14) mm Hg (P0.01); PVR, (821 +/- 194) to (681 +/- 199) dyn x s x cm(-5) (P0.01); RAP, (10 +/- 6) to (7 +/- 6) mm Hg (P0.01). However, HR, PAWP, mBP, CO and SVR had no significant changes. At the same time, inhaled iloprost significantly decreased PaO2 from (58 +/- 11) to (52 +/- 6) mm Hg (P0.01) and increased Qs/Qt from (27 +/- 11)% to (33 +/- 9)% (P0.01)and P(A-a) O2 from (86 +/-39) to (93 +/- 38) mm Hg (P0.01).Inhaled iloprost might instantly improve hemodynamics in CTEPH, but at the same time it increased arteriovenous shunts which resulted in lower PaO2.

To analyze the treatment effect of deep venous thrombosis (DVT) in acute pulmonary thromboembolism (PTE) with thrombolytic and anticoagulant therapy.Post hoc analysis of data from a prospective multicenter randomized control thrombolytic and anticoagulant trial of 516 patients with acute symptomatic PTE from June 2002 to December 2004. Thrombolytic therapy was performed in patients with massive and sub-massive PTE and anticoagulant therapy was given in patients with non-massive PTE. A total of 362 patients that accepted compression ultrasonography (CUS) before and 14 days after treatment constituted this study.The ratio of detected DVT by CUS 14 days after treatment was reduction than that before treatment (chi2=22.667, P0.001), but 11.6% patients had new or recurrent DVT. The rates of recanalization in thrombolysis group and anticoagulant group were 56.5% and 47.8% respectively (chi2=1.435, P=0.231). The results after three months follow up showed not recovery in 30.4% DVT patients and new or recurrent DVT in 10.4% patients.The normalization rate of DVT is low during 14 days treatment, and recurrence rate is high. Thrombolysis has no better rate of recanalization than anticoagulant. The prognosis of DVT hasn't improved significantly during short term treatment.

Acute pulmonary thromboembolism (PTE) patients with right ventricular dysfunction (RVD) may benefit from thrombolytic therapy but may end up with worse prognosis. RVD was assessed in prognosis to which a model on it was constructed to decide the indexes correlated to the best prognosis.This prospective study included 520 consecutive acute PTE patients from 41 hospitals in China between June 2002 and February 2005. All the patients were evaluated by transthoracic echocardiography (TTE), CT pulmonary angiography (CTPA), laboratory tests, and blood gas analysis. Physicians were asked to record all the clinical manifestations. Data from Univariate analysis demonstrated the parameters correlated with an 14-day clinically adverse outcomes. Multiple logistic regression analysis was used to decide the independent predictors and to construct a prognostic model.Mean age of the patients was 57.4 +/- 14.1 years and 323 of them (62.1%) were male. The 14-day mortality in normotensive patients with RVD was higher' (2.0% vs. 0.4%, P0.01) than those without. ROC curve showed the best cut-off values of RVED/LVED and SPAP for 14-day prognosis were 0.67 and 60 mm Hg, respectively. SPAP independently predicted 3-month clinical outcomes (P0.01). Results from Univariate analysis demonstrated that 24 parameters were correlated with an adverse 14-day clinical outcomes, which include palpation, syncope, panic, cyanosis, respiratory rateor = 30/min, pulseor = 110/min, jugular vein, accentuation of P2, murmurs in tricuspid area, time interval from onset, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), alveolar-arterial PO2 difference (PA-aO2), white blood cell (WBC)4.0 x 10(9)/L or10.0 x 10(9)/L, platelet, thrombus on TTE, RV/LV1.1, TRPG30 mm Hg, IVCmin8 mm, RVD, RVED/LVED0.6, SPAP60 mm Hg, RVWM, PTE range larger than two lobes or seven segments on CTPA. Furthermore, a multiple logistic regression model implied 8 predictors including RVD, RVED/LVED0.6, SPAP60 mm Hg, pulseor = 110/min, accentuation of P2, Syncope, CPK, WBC4.0 x 109/L or10.0 x 10(9)/L be independent predictors of an 14-day clinically adverse outcome (P0.01). This model seemed to fit well (P0.001). We chose a cut-off value as Por = 0.2 and compared the model to the original derivation samples. Data showed that the sensitivity (true positive rate) was 81.82%, specificity was 92.11%, false positive rate was 18.18%, coincidence was 91.14%, and the concordance rate was 80.96%.RVD seemed a nice discriminator for poor prognosis in normotensive patients. Early detection of RVD (especially RVED/LVED0.67 and/or SPAP60 mm Hg) was beneficial for identifying patients at high-risk and the multiple logistic regression model (P0.001) could be well fitted.

A cross-sectional study was carried out to observe the prevalence, incidence and risk factors of deep venous thrombosis (DVT) in patients from intensive care unit (ICU).Patients who were admitted to respiratory intensive care unit (RICU) and emergency intensive care unit (EICU) of Beijing Chaoyang Hospital and Beijing Anzhen Hospital were screened in our study. All patients enrolled underwent compression ultrasonography (CUS) within 48 h upon their admission to the ICUs. CUS was re-performed at 10 - 14 day, or when leaving ICU or at the time patients developed signs and symptoms (pain, heat, redness, edema) of DVT. Risk factors which were presumed associated with DVT were recorded. The main identified outcome was the presence of DVT. The secondary outcome was pulmonary thromboembolism (PTE).DVT was found in 30 patients of 252 patients within 48 h (11.90%). One hundred seventy-two patients were performed CUS two times or more. 26 patients (15.12%) had DVT. D-dimer, history of operation, kidney failure appeared to be independent risk factors for DVT in ICU patients. 13 patients were suspected PTE and 3 patients diagnosed as PTE.ICU doctors should pay more attention to DVT, which is relatively common in ICU patients.

To identify the risk factors of deep venous thrombosis(DVT) in patients with acute pulmonary thromboembolism (PTE).Post hoc analysis on data from a prospective multicenter through a randomized control trial on thrombolysis and anticoagulant among 454 patients with acute symptomatic PTE from June 2002 to December 2004. All patients were confirmed PTE by CT pulmonary angiography (CTPA) and/or ventilation perfusion scan or by magnetic resonance pulmonary angiography. Data of PTE patients with DVT was compared with those without DVT to identify the DVT risk factors. The effect of other variable on DVT was assessed by logistic regression analysis.When comparing the age, sex body weight index and underlying diseases including hypertension, coronary heart disease, chronic obstructive pulmonary disease, cerebral accident and malignant tumor between groups of DVT and no DVT,data showed that there was no statistically significant difference except for diabetes (chi2 = 4.481, P = 0.034) among them.However,results from multi-analysis showed that edema of lower-limb [odd ratio (OR), 2.255; 95% CI, 1.493 to 3.408], phlebitis (OR, 2.380; 95% CI, 1.426 to 3.973) and the entire swollen (calf swellingor =1 cm) larger than asymptomatic side (OR, 3.834; 95% CI, 2.561 to 5.738) were independent risk factors for DVT.Edema of lower-limb, phlebitis and calf swellingor =1 cm seemed to be risk factors for DVT.

To study the changes of blood coagulative and fibrinolytic system and the function of pulmonary vascular endothelium in the course of acute pulmonary thromboembolism (PTE) and after anticoagulant or thrombolytic treatment.Twenty patients with acute non-massive PTE, 10 males and 10 females, aged (57 +/- 11) underwent anticoagulant treatment and 17 sex-, and age-matched acute massive PTE patients underwent thrombolytic treatment. The plasma level of D-dimer (D-D), thrombomodulin (TM), protein C (PC), protein S (PS), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), and antithrombin-III (AT-III) activity were measured by ELISA before and after normal subjects severed as control group were included in the study. The plasma level of D-D, PS, PC, TM, t-PA and PAI-1 were measured by a method of ELISA before the treatment and six days after the anticoagulant treatment or 24 hours after the thrombolytic treatment. AT-III activity was measured by chromo-substrate method at the same time points. Forty sex- and age-matched healthy persons were used as controls.The plasma levels of D-D, t-PA, PS, and TM level of the anticoagulant group were all significantly higher and the AT-III activity of the 2 treatment groups was significantly lower than those of the controls before treatment (all P0.05); the plasma levels of D-D, t-PA, PAI-1, PS, and TM of the thrombolytic group were ala significantly higher and the AT-III activity was significantly lower than those of the control group before the treatment (all P0.05). After anticoagulant therapy, the plasma levels of D-D, t-PA, PS, and PC were significantly lower than those before treatment (all P0.05), however, the plasma levels of PAI-1, TM, and AT-III activity after treatment did not differ significantly from those before treatment. The plasma levels of D-D, t-PA, PS, PC, and TM after treatment of the thrombolytic group were all significantly lower than those before treatment (all P0.05), however, the plasma levels of PAI-1, TM, and AT-III activity after treatment did not differ significantly from those before treatment.Apparent imbalance in the blood coagulative and fibrinolytic system and pulmonary vascular endothelium damage occur in the patients with acute PTE. Combination tests of plasma D-D, AT-III, PS, PC, TM, t-PA and PAI-1 can give a more comprehensive explanation of the imbalance in the blood coagulative and fibrolytic system. Anticoagulant treatment and thrombolytic treatment play important roles in the regulation of the imbalance of coagulative and fibrinolytic system and protection of the function of pulmonary vascular endothelium of PTE patients.

Acute pulmonary thromboembolism (APE) causes right ventricular dysfunction (RVD) and cardiac troponin I (cTnI) elevation. Patients with RVD and cTnI elevation have a worse prognosis. Thus, early detection of RVD and cTnI elevation is beneficial for risk stratification. In this study, we assessed 14-day adverse clinical events and combined RVD on transthoracic echocardiography (TTE) with cTnI in risk stratification among a broad spectrum of APE patients.The prospective multi-centre trial included 90 patients with confirmed APE from 12 collaborating hospitals. Acute RVD on TTE was diagnosed in the presence of at least 2 of the following: right ventricular dilatation (without hypertrophy), loss of inspiratory collapse of inferior vena cava (IVC), right ventricular (RV) hypokinesis, tricuspid regurgitant jet velocity2.8 m/s. The study patients were divided into two groups according to clinical and echocardiographic findings at presentation: Group I: 50 patients with RVD; Group II: 40 patients without RVD.More than half of the patients (50/90, 55.6%) had RVD. Nearly one third (26/90, 28.9%) of patients had elevated cTnI at presentation and only 4.2% on the fourth day after initial therapy. A multiple Logistic regression model implied RVD, right and left ventricular end-diastolic diameter ratio (RVED/LVED), and cTnI independently predict an adverse 14-day clinical outcome (P0.01). Receiver operating characteristics (ROC) curves revealed that the cut-off values of RVED/LVED and cTnI yielding the highest discriminating power were 0.65 and 0.11 ng/ml, respectively. Furthermore, the incidence of an adverse 14-day clinical event in patients with RVD and elevated cTnI was greater (40.7%) than in patients with elevated cTnI or positive RVD alone (0% and 8.3%, respectively) (P0.001).RVD, RVED/LVED, and cTnI are independent predictors of 14-day clinical outcomes. The patients with RVED/LVED greater than 0.65 and cTnI higher than 0.11 ng/ml at presentation possibly have adverse 14-day events. RVD combined with cTnI can identify a subgroup of APE patients with a much more guarded prognosis.

To determine the prevalence of polymorphisms in the plasminogen activator inhibitor-1 (PAI-1) promoter 4G/5G polymorphisms in Chinese Han population and to investigate whether they are associated with pulmonary thromboembolism (PTE).Samples of peripheral venous blood were collected from 101 patients with PTE diagnosed by high probability of lung ventilation/perfusion scan and/or multi-slice CT pulmonary angiography (CTPA) as well as medical history and clinical manifestations, 67 males and 34 females, aged 48 +/- 15, and 101 age and sex-matched healthy controls from the same geographic area as controls. The genome DNA was extracted from the whole blood using potassium iodide-phenol-chloroform method. Polymerase chain reaction (PCR), denaturing high performance liquid chromatography (DHPLC), and sequence analysis were used to screen the single nucleotide polymorphisms and the genotype distribution of -675 4G/5G located in the promoter region of the PAI-1 gene.The frequencies of the allele 4G of PAI-1 gene in the controls were 0.495, significantly lower than in the PTE patients (0.733, chi(2) = 24.060, P0.01). The frequencies of the allele 5G of PAI-1 gene in the controls were 0.505, significantly higher than that in the PET patients. The genotype frequency of 4G4G of the PET patients was 57.4%, significantly higher than that of the controls (30.7%, P = 0.000). The genotype frequencies of 4G5G and 5G5G of the PET patients were 31.7% and 10.9% respectively, not significantly different from those of the controls (37.6 and 31.7% respectively). The presence of 4G allele of PAI-1 gene was found to be a greater risk factor for PTE. In comparison with the controls, the OR of 4G4G + 4G5G, 4G4G, and 4G5G in the PET patients were 3.794 (1.786 - 8.060), 5.443 (2.416 - 12.260), and 2.450 (1.067 - 5.623) respectively with the P values of 0.001, 0.000, and 0.035 respectively.The 4G/5G and 4G/4G genotypes are associated with the pathogenesis of PET.T.

To explore the changes of blood coagulative and fibrinolytic systems and functions of pulmonary vascular endothelium in patients with pulmonary thromboembolism (PTE).Twenty patients with acute massive PTE, 40 patients with acute non-massive PTE and 40 control subjects without PTE were included in the study. D-Dimer (D-D), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor1 (PAI-1), plasma protein S (Ps), plasma protein C (Pc), thrombomodulin (TM), anticardiolipin antibody (ACA) and homocysteine (Hcy) were measured by the method of ELISA. Antithrombin-III (AT-III) activity was measured by chromo-substrate method.The levels of D-D, t-PA, PAI-1, and TM were (1.46 +/- 0.62) mg/L, (11.4 +/- 6.9) microg/L, (88.2 +/- 27.5) microg/L, (6.8 +/- 1.1) microg/L respectively in patients with acute massive PTE and (0.92 +/- 0.27) mg/L, (6.6 +/- 1.5) microg/L, (60.1 +/- 26.1) microg/L, and (6.30 +/- 1.50) mg/L in patients with acute non-massive PTE. The levels of both PET groups were significantly higher than those of the control subjects [(0.38 +/- 0.10) mg/L, (4.7 +/- 1.4) microg/L, (35.7 +/- 9.2) microg/L, (3.0 +/- 0.5) microg/L and P0.05]. The levels of AT-III were (86.0 +/- 11.8)% in patients with acute massive PTE and (90.1 +/- 9.0)% in patients with acute non-massive PTE. The levels of AT-III in both groups were significantly lower than those of the control subjects, which were (102.6 +/- 9.2)% (P0.01 and P0.05 respectively). The levels of ACA-IgG, IgM and IgA in patients with acute massive PTE and non-massive PTE were also significantly higher than those in the control group (P0.05).Imbalance of blood coagulation and fibrolytic systems and pulmonary vascular endothelium damage occur in patients with PTE.