272 Original article
Evaluation of serum endothelial cell specific molecule-1 (endocan) levels as a biomarker in patients with pulmonary thromboembolism Aygu¨l Gu¨zela, Latif Duranb, Nurhan Ko¨ksala, Aysun C ¸ ag˘lar Torunc, Hasan Alac¸amd, Birsen Cirit Ekiza and Naci Murate The aim of this study was to investigate the relationship between pulmonary thromboembolism (PTE) and serum endocan levels. The study included 46 patients with a diagnosis of PTE and control group (25 healthy individuals). Serum endocan levels in all participants’ blood samples were measured. The average age of the individuals was 61.76 W 16.39 years. There was a significant difference in the serum endocan levels between the patients and those of the control group [321.93 ng/l (111.35–2511.33) and 192.77 ng/l (118.30–309.02), respectively; P < 0.030]. The serum endocan levels in the submassive [469.41 ng/l (258.13–800.54)] and the massive PTE groups [719.18 ng/l (319.84–2511.33)] were statistically higher than those in the control group [192.77 ng/l (118.30–309.02)] (P < 0.001 and P < 0.001, respectively). In addition, there was a statistically significant difference between the serum endocan levels of the nonmassive PTE group [188.57 ng/l (111.35–685.56)] and the submassive PTE group (P < 0.01). The serum endocan levels correlated with the international normalization ratio (INR), right ventricular dilatation (RVD) and SBP (r U 0.418, P U 0.004; r U 0.659, P < 0.001;
Introduction Pulmonary thromboembolism (PTE) is a disease with high mortality rates that occurs as a result of the blockage of the pulmonary artery or its branches with a thrombus or embolus that develops in the systemic veins. Among the venous thromboembolic disease group, PTE has the highest mortality and morbidity [1,2]. It is difficult to clinically diagnose PTE because it does not present with specific signs and symptoms. Early diagnosis and treatment may reduce mortality from 30 to 3–10% [3–5]. Clinical signs and symptoms may vary according to the severity of the vascular obstruction; the number, size and location of the embolisms; the patient’s age; and whether the patient has cardiopulmonary disease. Ninety percent of patients suspected of having a PTE show clinical symptoms, either alone or in combination, of dyspnoea, chest pain and syncope [6–8]. In the diagnosis of PTE, arterial blood gas analysis, Ddimer, lung X-ray, lower extremity venous Doppler ultrasonography, ventilation-perfusion scintigraphy, computed tomography, pulmonary angiography, magnetic resonance angiography and pulmonary arteriography are used when there is insufficient history and the physical examination is inconclusive [9,10]. Pulmonary 0957-5235 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
r U S0.425, P U 0.003, respectively). In conclusion, serum endocan levels can be considered a practicable biomarker to determine the severity of PTEs and follow-up thrombolytic therapy. Blood Coagul Fibrinolysis 25:272–276 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Blood Coagulation and Fibrinolysis 2014, 25:272–276 Keywords: biomarker, chest, endocan, endothelial cell-specific molecule-1, pulmonary thromboembolism a
Department of Chest Disease, bDepartment of Emergency, Faculty of Medicine, Department of Pedodontics, Faculty of Dentistry, dDepartment of Medical Biochemistry, Faculty of Medicine and eDepartment of Industrial Engineering, Faculty of Engineering, Ondokuz Mayıs University, Samsun, Turkey c
Correspondence to Aygu¨l Gu¨zel, MD, Department of Chest Disease, Faculty of Medicine, Ondokuz Mayıs University, Samsun, 55139, Turkey Tel: +90 362 312 19 19 4086; e-mail: [email protected] Received 2 July 2013 Revised 30 November 2013 Accepted 7 December 2013
angiography remains the gold standard method of diagnosis, with a morbidity rate of 1% and a mortality rate of 0.5% [11] Diagnostic methods are invasive and expensive. They also include high-dose radiation, and the results are difficult to assess. Thus, clinicians have to use noninvasive methods of PTE such as clinical markers, the use of which has increased in recent years [12–14]. The relationship between PTE and cardiac troponin I, troponin T, B-type natriuretic peptide (BNP) and N-terminal pro b type natriuretic peptide (NT-proBNP), procalcitonin, which was shown to increase in acute PTE and be correlated with complications and the risk of death, has been studied [15–17]. Endocan is a dermatan sulfate proteoglycan, which can be measured in serum and is expressed in lung endothelial cells. It plays an important role in endothelial-dependent pathological diseases, such as inflammatory disorders, tumour progression and adhesion, and migration and angiogenesis, and is acceptable as a potential endothelial cell marker [18]. Levels of endocan are increased in diseases with vascular endothelial involvement such as renal carcinoma, breast cancer, glioma and small cell lung cancer, and this increase was shown to be an important prognostic factor in the literature [19–21]. Very few DOI:10.1097/MBC.0000000000000071
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Serum endocan levels in pulmonary thromboembolism Gu¨zel et al. 273
studies have investigated endocan serum levels in lung diseases. One study [22] found that endocan plays an active role in the pathogenesis of trauma-related acute lung injury and that low endocan levels are an indicator of endothelial deterioration in the lung. Another study [20] reported that the tissue expression of endocan is high in lung cancer and that it stimulates proangiogenic growth factor in the tumoural endothelium. An increased serum endocan level was also found to determine the prognosis in lung cancer [23]. This study aimed to investigate the relationship between PTE and serum endocan levels and whether the endocan level could be used as a marker in determining the severity of PTE.
Materials and methods Approval for the study was obtained from the Medical Research Ethics Committee of Ondokuz Mayis University, and all stages of the study adhered to the tenets of the Declaration of Helsinki. The study included 46 patients who presented to the Ondokuz Mayis University Medical Faculty, Emergency and Chest Disease clinic with a diagnosis of PTE [24] and a healthy age and sex-matched control group of 25 individuals. Patients included in the PTE group were admitted to the emergency service in the first 24 h after the onset of symptoms, had not undergone treatment for an embolism prior to their presentation, were older than 18 years and had no additional disease (acute coronary syndrome, acute ischemic cerebrovascular disease, acute peripheral arterial occlusion, or chronic lung, heart or kidney disease). During the study, the patients’ age, sex and risk factors for PTE were recorded, as well as the results of the physical examination, chest radiograph, ECG, echocardiography (ECHO) and spiral chest computed tomography (CT) scan. The patients were grouped clinically as massive [right ventricular dilatation (RVD) þ < 90 mmHg SBP], submassive (RVD þ 90 mmHg SBP) and low risk (normal right ventricular findings and BP) according to right ventricular dysfunction findings [25] and SBP [26]. Blood collection
Blood was collected from the patients and the control group and placed in tubes with no anticoagulant. The tubes were left to congeal for 30 min, followed by centrifugation at 3000g for 10 min. The serum samples derived were placed in Eppendorf tubes and stored at 808C until they were analysed. One night before testing the samples with the ELISA, the serum samples were kept at þ48C to thaw. Measurement of endocan levels
Levels of endothelial cell specific molecule 1 were measured in the serum samples by ELISA. After thawing, the samples were vortexed and quantified by ELISA in
accordance with the manufacturer’s instructions (Catalogue number: CK-E90514; Hangzhou Eastbiopharm Corporation, China). The results are presented in ng/l.
Data analysis
All the data were evaluated using the packaged software SPSS version 21.0 (SPSS Inc., Chicago, Illinois, USA). The independent sample t-test was used to compare continuous variables exhibiting a normal distribution. The nonparametric Mann–Whitney U-test was used for data with a nonnormal distribution. Spearman’s rank correlation analysis was used for correlations. Raw data from the databases were pooled, and the medians (min. – max.), the mean standard deviations and the percentages were calculated. The statistical significance level was accepted to be P value less than 0.05.
Results Demographic and clinical findings
Seventy-one individuals (46, PTE group; 25, control group) were included in the study. The average age of the individuals was 61.76 16.39 years. The most common risk factors were age (65 years) (17 patients, 37.0%) and immobilization (11 patients, 23.9%). The other risk factors are presented in Table 1. On admittance to the Emergency Department, the most common complaint of the patients was dyspnoea (29 patients, 63%). This was followed by syncope (12 patients, 26.1%) and retrosternal chest pain (5 patients, 10.9%). Tachypnea (30 patients, 65.2%) and tachycardia (23 patients, 32.4%) were the most common physical findings detected at admission (Table 1). Comparison of demographic and blood count analyses of the patients with PE and controls was represented in Table 2. All the patients were classified into one of three groups (nonmassive, submassive or massive) according to their echocardiographic findings and SBP. There were 29 patients (63.0%) in the nonmassive group, six patients (13.0%) in the submassive group and 11 patients (24.0%) in the massive group (Table 1). PTE was detected generally in the segmental pulmonary artery (63.0%, 29 patients) with CT angiography. Other PTEs found on CT angiography were in the lobar artery (32.6%, 15 patients) and the main pulmonary artery (6.5%, three patients) (Table 1). Sinus tachycardia (46.5%) and S1Q3T3 (32.6%) were the most common ECG signs in the patients with a PTE. In the ECHO findings, 76.1% of the patients had pulmonary hypertension, and 36.9% had right ventricle dilatation and septal paradoxical movement. Other ECG and ECHO findings of the patients are presented in Table 1. Forty-two of the patients were treated with low-molecular weight heparin, and four patients were treated with tissue plasminogen activator. Most of the patients (89.1%) were followed up in the Chest Disease Department. All the observation results
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
274 Blood Coagulation and Fibrinolysis 2014, Vol 25 No 3
Table 1 Demographic, clinical and imaging features of all patients with pulmonary thromboembolism Risk factors (n, %) Immobilization Cancer History of PTE and DVT History of surgery Cardiac failure History of long-term trip Age of patients 65 years No. of factors Patient complaints on admission (n, %) Retrosternal chest pain Dyspnoea Syncope Physical signs (n, %) Ral Hypotension Hypertension Tachycardia Bradicardia Tachypnoea Fewer Electrocardiographic findings (n, %) Sinus tachycardia S1Q3T3 ST-T alterations Normal Echocardiography findings (n, %) Septal paradoxical movement Tricuspid valve regurgitation Left ventricle dilatation Right ventricle dilatation Pulmonary hypertension Pulmonary artery pressure (mean SD) PTE settlement in CT angiography Main pulmonary artery Lobar artery Segmental artery Results of treatment (n, %) Discharge in a healthy individual Exitus Total (n, %)
11 (23.9) 7 (15.2) 6 (13.0) 3 (6.5) 9 (19.6) 2 (4.6) 17 (37.0) 3 (6.5) 5 (10.9) 29 (63.0) 12 (26.1) 13 11 13 23
(28.3) (23.9) (28.3) (32.4) 1 (2.3) 30 (65.2) 2 (4.6) 20 (46.5) 15 (32.6) 3 (6.5) 8 (17.4) 17 (36.9) 9 (19.5) 12 (26.1) 17 (36.9) 35 (76.1) 47.84 17.33 3 (6.5) 15 (32.6) 29 (63.0) 39 (84.8) 7 (15.2) 46 (100.0)
CT, computed tomography; DVT, deep vein thrombosis; PTE, pulmonary thromboembolism; SD, standard deviation.
are represented in Table 1. Only seven patients died because of PTE in this period. Evaluation of endocan levels
There was a significant difference in the serum endocan levels between the patients and the control group
Table 2
[321.93 ng/l (111.35–2511.33) and 192.77 ng/l (118.30– 309.02), respectively; P < 0.030]. With respect to the PTE subgroups, no significant difference was found between the nonmassive PTE group [188.57 ng/l (111.35–685.56)] and the control (P ¼ 0.597). However, the serum endocan levels in the submassive [469.41 ng/l (258.13–800.54)] and massive PTE groups [719.18 ng/l (319.84–2511.33)] were statistically higher than those in the control group [192.77 ng/l (118.30–309.02)] (P < 0.001 and P < 0.001, respectively) (Fig. 1). In addition, there was a statistically significant difference in the serum endocan levels between the nonmassive PTE group and the submassive PTE group (P < 0.01) (Fig. 1). The endocan levels were correlated with the INR, RVD and SBP (r ¼ 0.418, P ¼ 0.004; r ¼ 0.659, P < 0.001; r ¼ 0.425, P ¼ 0.003, respectively). The endocan levels were not correlated with age and serum D-dimer levels (r ¼ 0.195, P ¼ 0.195 and r ¼ 0.316, P ¼ 0.078, respectively). Also, endocan levels were not correlated with other cardiac issues (cardiac failure, hypertension, septal paradoxical movement, tricuspid valve regurgitation, left ventricule dilatation, pulmonary hypertension).
Discussion PTE is a preventable disease with high morbidity and mortality. It accounts for 5–15% of hospital mortality [27]. With early diagnosis and treatment, the mortality rate decreases from 30 to 3–10% [3]. Nonspecific clinical signs and symptoms of PTE reduce the likelihood of an antemortem clinical diagnosis. Therefore, the identification of underlying risk factors is important in the diagnosis of PTE. Advanced age, a previous history of PTE, chemotherapy, active cancer, long-term chronic disease, congenital or acquired thrombophilia, pregnancy, oral contraceptive use, hip or leg fracture, a history of previous surgery and trauma are considered risk factors [6]. The mortality rate of 15.2% in our study is consistent with that in the literature. The most common risk factors in the current study were advanced age (65 years) and immobilization.
Comparison of demographic and laboratory features of the patients with PE and controls
Age (years) Sex, male ratio (n, %) BMI (kg/m2) WBC (109/l) Hb (g/dl) PLT (109/l) MPV (fl) PDW (%) PCT (%) D-dimer (ng/ml) INR Troponin
PTE group n ¼ 46
Control group n ¼ 25
P
59.04 19.05 19/46 (41.3) 27.50 (20.30–40.10) 10.26 4.40 12.42 2.24 251.50 (59.00–609.00) 7.52 1.13 55.15 (14.80–88.00) 0.19 (0.06–0.52) 5051.28 3512.12 1.17 0.21 0.01 (0–1.05)
66.76 7.90 11/25 (44.0) 27.70 (20.30–40.10) 7.53 1.64 12.82 1.56 210.00 (144.00–295.00) 7.93 0.84 43.30 (13.90–55.70) 0.22 (0.12–0.36) – – –
0.059 0.827 0.842
Evaluation of serum endothelial cell specific molecule-1 (endocan) levels as a biomarker in patients with pulmonary thromboembolism Aygu¨l Gu¨zela, Latif Duranb, Nurhan Ko¨ksala, Aysun C ¸ ag˘lar Torunc, Hasan Alac¸amd, Birsen Cirit Ekiza and Naci Murate The aim of this study was to investigate the relationship between pulmonary thromboembolism (PTE) and serum endocan levels. The study included 46 patients with a diagnosis of PTE and control group (25 healthy individuals). Serum endocan levels in all participants’ blood samples were measured. The average age of the individuals was 61.76 W 16.39 years. There was a significant difference in the serum endocan levels between the patients and those of the control group [321.93 ng/l (111.35–2511.33) and 192.77 ng/l (118.30–309.02), respectively; P < 0.030]. The serum endocan levels in the submassive [469.41 ng/l (258.13–800.54)] and the massive PTE groups [719.18 ng/l (319.84–2511.33)] were statistically higher than those in the control group [192.77 ng/l (118.30–309.02)] (P < 0.001 and P < 0.001, respectively). In addition, there was a statistically significant difference between the serum endocan levels of the nonmassive PTE group [188.57 ng/l (111.35–685.56)] and the submassive PTE group (P < 0.01). The serum endocan levels correlated with the international normalization ratio (INR), right ventricular dilatation (RVD) and SBP (r U 0.418, P U 0.004; r U 0.659, P < 0.001;
Introduction Pulmonary thromboembolism (PTE) is a disease with high mortality rates that occurs as a result of the blockage of the pulmonary artery or its branches with a thrombus or embolus that develops in the systemic veins. Among the venous thromboembolic disease group, PTE has the highest mortality and morbidity [1,2]. It is difficult to clinically diagnose PTE because it does not present with specific signs and symptoms. Early diagnosis and treatment may reduce mortality from 30 to 3–10% [3–5]. Clinical signs and symptoms may vary according to the severity of the vascular obstruction; the number, size and location of the embolisms; the patient’s age; and whether the patient has cardiopulmonary disease. Ninety percent of patients suspected of having a PTE show clinical symptoms, either alone or in combination, of dyspnoea, chest pain and syncope [6–8]. In the diagnosis of PTE, arterial blood gas analysis, Ddimer, lung X-ray, lower extremity venous Doppler ultrasonography, ventilation-perfusion scintigraphy, computed tomography, pulmonary angiography, magnetic resonance angiography and pulmonary arteriography are used when there is insufficient history and the physical examination is inconclusive [9,10]. Pulmonary 0957-5235 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
r U S0.425, P U 0.003, respectively). In conclusion, serum endocan levels can be considered a practicable biomarker to determine the severity of PTEs and follow-up thrombolytic therapy. Blood Coagul Fibrinolysis 25:272–276 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Blood Coagulation and Fibrinolysis 2014, 25:272–276 Keywords: biomarker, chest, endocan, endothelial cell-specific molecule-1, pulmonary thromboembolism a
Department of Chest Disease, bDepartment of Emergency, Faculty of Medicine, Department of Pedodontics, Faculty of Dentistry, dDepartment of Medical Biochemistry, Faculty of Medicine and eDepartment of Industrial Engineering, Faculty of Engineering, Ondokuz Mayıs University, Samsun, Turkey c
Correspondence to Aygu¨l Gu¨zel, MD, Department of Chest Disease, Faculty of Medicine, Ondokuz Mayıs University, Samsun, 55139, Turkey Tel: +90 362 312 19 19 4086; e-mail: [email protected] Received 2 July 2013 Revised 30 November 2013 Accepted 7 December 2013
angiography remains the gold standard method of diagnosis, with a morbidity rate of 1% and a mortality rate of 0.5% [11] Diagnostic methods are invasive and expensive. They also include high-dose radiation, and the results are difficult to assess. Thus, clinicians have to use noninvasive methods of PTE such as clinical markers, the use of which has increased in recent years [12–14]. The relationship between PTE and cardiac troponin I, troponin T, B-type natriuretic peptide (BNP) and N-terminal pro b type natriuretic peptide (NT-proBNP), procalcitonin, which was shown to increase in acute PTE and be correlated with complications and the risk of death, has been studied [15–17]. Endocan is a dermatan sulfate proteoglycan, which can be measured in serum and is expressed in lung endothelial cells. It plays an important role in endothelial-dependent pathological diseases, such as inflammatory disorders, tumour progression and adhesion, and migration and angiogenesis, and is acceptable as a potential endothelial cell marker [18]. Levels of endocan are increased in diseases with vascular endothelial involvement such as renal carcinoma, breast cancer, glioma and small cell lung cancer, and this increase was shown to be an important prognostic factor in the literature [19–21]. Very few DOI:10.1097/MBC.0000000000000071
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Serum endocan levels in pulmonary thromboembolism Gu¨zel et al. 273
studies have investigated endocan serum levels in lung diseases. One study [22] found that endocan plays an active role in the pathogenesis of trauma-related acute lung injury and that low endocan levels are an indicator of endothelial deterioration in the lung. Another study [20] reported that the tissue expression of endocan is high in lung cancer and that it stimulates proangiogenic growth factor in the tumoural endothelium. An increased serum endocan level was also found to determine the prognosis in lung cancer [23]. This study aimed to investigate the relationship between PTE and serum endocan levels and whether the endocan level could be used as a marker in determining the severity of PTE.
Materials and methods Approval for the study was obtained from the Medical Research Ethics Committee of Ondokuz Mayis University, and all stages of the study adhered to the tenets of the Declaration of Helsinki. The study included 46 patients who presented to the Ondokuz Mayis University Medical Faculty, Emergency and Chest Disease clinic with a diagnosis of PTE [24] and a healthy age and sex-matched control group of 25 individuals. Patients included in the PTE group were admitted to the emergency service in the first 24 h after the onset of symptoms, had not undergone treatment for an embolism prior to their presentation, were older than 18 years and had no additional disease (acute coronary syndrome, acute ischemic cerebrovascular disease, acute peripheral arterial occlusion, or chronic lung, heart or kidney disease). During the study, the patients’ age, sex and risk factors for PTE were recorded, as well as the results of the physical examination, chest radiograph, ECG, echocardiography (ECHO) and spiral chest computed tomography (CT) scan. The patients were grouped clinically as massive [right ventricular dilatation (RVD) þ < 90 mmHg SBP], submassive (RVD þ 90 mmHg SBP) and low risk (normal right ventricular findings and BP) according to right ventricular dysfunction findings [25] and SBP [26]. Blood collection
Blood was collected from the patients and the control group and placed in tubes with no anticoagulant. The tubes were left to congeal for 30 min, followed by centrifugation at 3000g for 10 min. The serum samples derived were placed in Eppendorf tubes and stored at 808C until they were analysed. One night before testing the samples with the ELISA, the serum samples were kept at þ48C to thaw. Measurement of endocan levels
Levels of endothelial cell specific molecule 1 were measured in the serum samples by ELISA. After thawing, the samples were vortexed and quantified by ELISA in
accordance with the manufacturer’s instructions (Catalogue number: CK-E90514; Hangzhou Eastbiopharm Corporation, China). The results are presented in ng/l.
Data analysis
All the data were evaluated using the packaged software SPSS version 21.0 (SPSS Inc., Chicago, Illinois, USA). The independent sample t-test was used to compare continuous variables exhibiting a normal distribution. The nonparametric Mann–Whitney U-test was used for data with a nonnormal distribution. Spearman’s rank correlation analysis was used for correlations. Raw data from the databases were pooled, and the medians (min. – max.), the mean standard deviations and the percentages were calculated. The statistical significance level was accepted to be P value less than 0.05.
Results Demographic and clinical findings
Seventy-one individuals (46, PTE group; 25, control group) were included in the study. The average age of the individuals was 61.76 16.39 years. The most common risk factors were age (65 years) (17 patients, 37.0%) and immobilization (11 patients, 23.9%). The other risk factors are presented in Table 1. On admittance to the Emergency Department, the most common complaint of the patients was dyspnoea (29 patients, 63%). This was followed by syncope (12 patients, 26.1%) and retrosternal chest pain (5 patients, 10.9%). Tachypnea (30 patients, 65.2%) and tachycardia (23 patients, 32.4%) were the most common physical findings detected at admission (Table 1). Comparison of demographic and blood count analyses of the patients with PE and controls was represented in Table 2. All the patients were classified into one of three groups (nonmassive, submassive or massive) according to their echocardiographic findings and SBP. There were 29 patients (63.0%) in the nonmassive group, six patients (13.0%) in the submassive group and 11 patients (24.0%) in the massive group (Table 1). PTE was detected generally in the segmental pulmonary artery (63.0%, 29 patients) with CT angiography. Other PTEs found on CT angiography were in the lobar artery (32.6%, 15 patients) and the main pulmonary artery (6.5%, three patients) (Table 1). Sinus tachycardia (46.5%) and S1Q3T3 (32.6%) were the most common ECG signs in the patients with a PTE. In the ECHO findings, 76.1% of the patients had pulmonary hypertension, and 36.9% had right ventricle dilatation and septal paradoxical movement. Other ECG and ECHO findings of the patients are presented in Table 1. Forty-two of the patients were treated with low-molecular weight heparin, and four patients were treated with tissue plasminogen activator. Most of the patients (89.1%) were followed up in the Chest Disease Department. All the observation results
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
274 Blood Coagulation and Fibrinolysis 2014, Vol 25 No 3
Table 1 Demographic, clinical and imaging features of all patients with pulmonary thromboembolism Risk factors (n, %) Immobilization Cancer History of PTE and DVT History of surgery Cardiac failure History of long-term trip Age of patients 65 years No. of factors Patient complaints on admission (n, %) Retrosternal chest pain Dyspnoea Syncope Physical signs (n, %) Ral Hypotension Hypertension Tachycardia Bradicardia Tachypnoea Fewer Electrocardiographic findings (n, %) Sinus tachycardia S1Q3T3 ST-T alterations Normal Echocardiography findings (n, %) Septal paradoxical movement Tricuspid valve regurgitation Left ventricle dilatation Right ventricle dilatation Pulmonary hypertension Pulmonary artery pressure (mean SD) PTE settlement in CT angiography Main pulmonary artery Lobar artery Segmental artery Results of treatment (n, %) Discharge in a healthy individual Exitus Total (n, %)
11 (23.9) 7 (15.2) 6 (13.0) 3 (6.5) 9 (19.6) 2 (4.6) 17 (37.0) 3 (6.5) 5 (10.9) 29 (63.0) 12 (26.1) 13 11 13 23
(28.3) (23.9) (28.3) (32.4) 1 (2.3) 30 (65.2) 2 (4.6) 20 (46.5) 15 (32.6) 3 (6.5) 8 (17.4) 17 (36.9) 9 (19.5) 12 (26.1) 17 (36.9) 35 (76.1) 47.84 17.33 3 (6.5) 15 (32.6) 29 (63.0) 39 (84.8) 7 (15.2) 46 (100.0)
CT, computed tomography; DVT, deep vein thrombosis; PTE, pulmonary thromboembolism; SD, standard deviation.
are represented in Table 1. Only seven patients died because of PTE in this period. Evaluation of endocan levels
There was a significant difference in the serum endocan levels between the patients and the control group
Table 2
[321.93 ng/l (111.35–2511.33) and 192.77 ng/l (118.30– 309.02), respectively; P < 0.030]. With respect to the PTE subgroups, no significant difference was found between the nonmassive PTE group [188.57 ng/l (111.35–685.56)] and the control (P ¼ 0.597). However, the serum endocan levels in the submassive [469.41 ng/l (258.13–800.54)] and massive PTE groups [719.18 ng/l (319.84–2511.33)] were statistically higher than those in the control group [192.77 ng/l (118.30–309.02)] (P < 0.001 and P < 0.001, respectively) (Fig. 1). In addition, there was a statistically significant difference in the serum endocan levels between the nonmassive PTE group and the submassive PTE group (P < 0.01) (Fig. 1). The endocan levels were correlated with the INR, RVD and SBP (r ¼ 0.418, P ¼ 0.004; r ¼ 0.659, P < 0.001; r ¼ 0.425, P ¼ 0.003, respectively). The endocan levels were not correlated with age and serum D-dimer levels (r ¼ 0.195, P ¼ 0.195 and r ¼ 0.316, P ¼ 0.078, respectively). Also, endocan levels were not correlated with other cardiac issues (cardiac failure, hypertension, septal paradoxical movement, tricuspid valve regurgitation, left ventricule dilatation, pulmonary hypertension).
Discussion PTE is a preventable disease with high morbidity and mortality. It accounts for 5–15% of hospital mortality [27]. With early diagnosis and treatment, the mortality rate decreases from 30 to 3–10% [3]. Nonspecific clinical signs and symptoms of PTE reduce the likelihood of an antemortem clinical diagnosis. Therefore, the identification of underlying risk factors is important in the diagnosis of PTE. Advanced age, a previous history of PTE, chemotherapy, active cancer, long-term chronic disease, congenital or acquired thrombophilia, pregnancy, oral contraceptive use, hip or leg fracture, a history of previous surgery and trauma are considered risk factors [6]. The mortality rate of 15.2% in our study is consistent with that in the literature. The most common risk factors in the current study were advanced age (65 years) and immobilization.
Comparison of demographic and laboratory features of the patients with PE and controls
Age (years) Sex, male ratio (n, %) BMI (kg/m2) WBC (109/l) Hb (g/dl) PLT (109/l) MPV (fl) PDW (%) PCT (%) D-dimer (ng/ml) INR Troponin
PTE group n ¼ 46
Control group n ¼ 25
P
59.04 19.05 19/46 (41.3) 27.50 (20.30–40.10) 10.26 4.40 12.42 2.24 251.50 (59.00–609.00) 7.52 1.13 55.15 (14.80–88.00) 0.19 (0.06–0.52) 5051.28 3512.12 1.17 0.21 0.01 (0–1.05)
66.76 7.90 11/25 (44.0) 27.70 (20.30–40.10) 7.53 1.64 12.82 1.56 210.00 (144.00–295.00) 7.93 0.84 43.30 (13.90–55.70) 0.22 (0.12–0.36) – – –
0.059 0.827 0.842
