Heart India

: 2021  |  Volume : 9  |  Issue : 1  |  Page : 83--89

Clinical profile, risk stratification of patients with acute pulmonary embolism

Keyur Patel1, Sanjeev Bhatia1, Jit Brahmbhatt1, Vishal Sharma1, Zeeshan Mansuri1, Kamal Sharma1, Sharad Jain1, Krutika Patel2, Pinkesh Parmar3, Dignesh Vasava3,  
1 Department of Cardiology, U. N. Mehta Institute of Cardiology and Research Centre, B. J. Medical College, Ahmedabad, Gujarat, India
2 Research Department, U. N. Mehta Institute of Cardiology and Research Centre, B. J. Medical College, Ahmedabad, Gujarat, India
3 Department of Cardiology, U. N. Mehta Institute of Cardiology and Research Centre, Civil Hospital Campus, Ahmedabad, Gujarat, India

Correspondence Address:
Dr. Vishal Sharma
Department of Cardiology, U. N. Mehta Institute of Cardiology and Research Centre, B. J. Medical College, Ahmedabad, Gujarat


Context: To study the demographics and clinical profile of patients with acute pulmonary embolism (PE) and impact of management as per risk stratification on outcome of patients with acute PE. Materials and Methods: Prospective observational study of demographics, clinical profile, risk stratification, management, and outcome of patients presenting with acute PE from August 2016 to July 2017. Results: One hundred and fifty patients who were detected to have acute pulmonary thromboembolism with a mean age of 45.08 years, with 70% being males, were included in the study. There were 6 (4%) patients in high-risk group, 69 (46%) patients in intermediate-high subgroup, 39 (26%) patients in intermediate-low subgroup and 36 (24%) patients in low-risk group as per the ESC 2019 guidelines using sPESI score, shock/hypotension, right ventricle (RV) dysfunction and cardiac marker elevation. 72 patients (52%) had antecedent deep vein thrombosis (DVT) of which 60 patients has proximal, whereas 12 patients had distal DVT. One hundred and forty-seven patients (98%) had moderate-to-severe TR, 117 patients (78%) had evidence of right atrium/RV dysfunction and 27 patients (18%) had evidence of thrombus in the heart. Computed tomography pulmonary angiogram showed middle pulmonary artery thrombus/dilatation in 63 patients (42%), saddle thrombus in 18 patients (12%), partial thrombus in the left pulmonary artery (LPA) and right pulmonary artery (RPA) in 84 (56%) and 75 (50%) patients, respectively. Majority (86%) of patients with tenecteplase; 9 (10.3%) patients with streptokinase and 3 (3.4%) was thrmobolysed with alteplase. Conclusion: PE can present with unexplained dyspnea and atypical chest pain, among other signs and symptoms. Early diagnosis, risk stratification, and guideline-directed prompt management can lead to favorable outcome.

How to cite this article:
Patel K, Bhatia S, Brahmbhatt J, Sharma V, Mansuri Z, Sharma K, Jain S, Patel K, Parmar P, Vasava D. Clinical profile, risk stratification of patients with acute pulmonary embolism.Heart India 2021;9:83-89

How to cite this URL:
Patel K, Bhatia S, Brahmbhatt J, Sharma V, Mansuri Z, Sharma K, Jain S, Patel K, Parmar P, Vasava D. Clinical profile, risk stratification of patients with acute pulmonary embolism. Heart India [serial online] 2021 [cited 2021 Sep 28 ];9:83-89
Available from: https://www.heartindia.net/text.asp?2021/9/1/83/312481

Full Text


Venous thromboembolism (VTE), clinically presenting as deep vein thrombosis (DVT) or pulmonary embolism (PE), is globally the third-most frequent acute cardiovascular syndrome behind myocardial infarction and stroke in some Western countries.[1] In epidemiological studies, annual incidence rates for PE range from 39 to 115/100 000 population; for DVT, incidence rates range from 53 to 162 per 100000 population.[2],[3]

VTE is a common and potentially life-threatening condition. It continues to be under diagnosed and undertreated. Awareness among Indians regarding this potentially life-threatening disease is low. Contrary to earlier belief, the incidence of VTE in Asia and India is comparable to that in Western countries.[4],[5] The risk of VTE is especially high in hospitalized patients, in a majority of whom it is clinically silent. It is one of the most common causes of unplanned readmission and preventable death.[3]

The clinical manifestations of acute PE are highly variable, ranging from pulseless electrical activity to mild dyspnea, which can cloud the diagnosis.[6] PE should be a part of the differential diagnosis in patients who present with new or worsening dyspnea, chest pain, or hypotension. Based on the physician's level of suspicion, the diagnostic workup may include a clinical decision rule, biomarkers (e.g., D-dimer), and/or imaging modalities, such as computed tomography (CT) angiography or a ventilation-perfusion scan. Additional evaluations may be performed with troponins, B-type natriuretic peptide (BNP), Pro-BNP, and/or echocardiography. PE is commonly classified as massive (high-risk), submassive (intermediate-risk), and low-risk to help determine the required treatment.[1] Risk stratification scores are used to determine management and the risk of complications and associated mortality. Myocardial infarction and heart failure increase the risk of PE.[7],[8]

Conversely, patients with VTE have an increased risk of subsequent myocardial infarction and stroke, or peripheral arterial embolization.[9]

There are very few studies from Asian countries, especially in India. The current study was conducted in Western Indian, considering to need to improve the knowledge about characterize the clinical profile, management, and outcomes of patients with PE.

 Materials and Methods

This prospective-observational single-center study carried out in the Department of cardiology at U. N. Mehta Institute of Cardiology and Research Centre. The study design was approved by the Ethical Committee of the institute. The manuscript is in accordance with the Helsinki Declaration and with ethical guidelines from our studies committee. One hundred and fifty patients of PE from August 2015 to December 2018 with computed tomographic pulmonary angiography (CTPA) showing thrombus in pulmonary arteries fulfilling inclusion and exclusion criteria formed study population. Informed consent of all the patients was taken prior enrolment into the study.

Patients with aged 18 years and above admitted with clinical features suggestive of acute PE and demonstration of thrombus in pulmonary arteries by echo or CTPA were included in the study. Patients with suspected case of PE and D-dimer-positive patients without demonstration of thrombus in the pulmonary artery were excluded from the study.

Patients underwent detailed evaluation including history, clinical examinations, and laboratory investigation. Detailed history regarding risk factors of PE is taken in all patients. All patients underwent basic and relevant biochemical investigations. Clinical probability of all patients was assessed by using Wells simplified score and Revised Geneva score.

Patients with high probability of PE were evaluated with D-dimer and cardiac biomarkers and two-directional echocardiography (2D Echo) was done in all patients to look for right atrium/right ventricle (RA/RV) dilatation, RV dysfunction, right ventricular systolic pressure (RVSP), thrombus in the middle pulmonary artery (MPA) and its branches, left ventricular function and ejection fraction. Chest X-ray was done in all patients to look for other causes of dyspnea. CTPA done in all patients to look for thrombus, location, number and RV function. Ultrasonography of the lower limbs was done in all patients. Patients were risk-stratified on the basis of ESC guidelines 2019 in to low risk, intermediate, and high risk. Intermediate-high risk was again stratified into intermediate-low and intermediate-high risk.[6]

All the patients with high and intermediate-risk group and four patients with intermediate low-risk group received thrombolysis in addition to standard unfractionated heparin and oral anticoagulant therapy. All low-risk patients were treated with standard heparin, followed by oral anticoagulation.

Tenecteplase was given as an intravenous weight-adjusted bolus (given over 5s) at a dose ranging from 30 to 50 mg (0.5 mg/kg), with a 5 mg step-up for every 10 kg increase from 60 to 90 kg. Heparin infusion was continued for 2 days keeping activated partial thromboplastin time (APTT) 50–70s.

Statistical Methods

All statistical studies were carried out using IBM Statistical Package for the Social Sciences (SPSS) vs 20. (Chicago, IL, USA). Quantitative variables were expressed as the mean ± standard deviation, and qualitative variables were expressed as percentage (%). Parametric values between two groups were performed using the independent sample test or ANOVA. Categorical variables were compared using the Chi-square test. A nominal significance was taken as a two-tailed P < 0.05.


A total of 150 patients were admitted during the study period with clinical diagnosis to have PE if there is evidence of thrombus in CT pulmonary angiogram or 2D-Echo. The mean age of the cohort was 45.08 ± 14.10 year, with 70% being males and 30% of females. Baseline characteristics and risk factors are shown in [Table 1] and [Table 2].{Table 1}{Table 2}

Risk stratification of patients was done according to ESC 2019 guidelines with the help of 4 variables, which include shock, RV dysfunction, simplified PESI score, and cardiac enzymes.[6] Out of 150 patients, 8 (4%) had high risk, 69 (46%) had intermediate-high risk; 39 (26%) patients had intermediate low risk and rest 36 (24%) patients belonged to low risk group showed in [Figure 1]. The purpose of this for better management and outcome of further treatment.{Figure 1}

All PE risk factors with risk stratification mentioned in [Table 3]. The most common finding in electrocardiograph (ECG) is sinus tachycardia shows 6 (100%) patients with high risk, 66 (95.7%) with intermediate-high risk, 24 (61.5%) in intermediate-low risk and 30 (83.3%) statistically significant P < 0.0001 followed by ST-T changes shows maximum (66.7%) in low-risk group with statistically nonsignificant (P 0.06) similarly right axis deviation shows maximum (41.7%), most of the patients (46.2%) with incomplete RBBB in the intermediate low group (P 0.001) and almost 50% patients with S1Q3T3 pattern in high-risk group (P 0.001).{Table 3}

Chest X-ray was done in all patients. Among 150 patients, 129 (86%) patients had a normal chest radiograph and remaining 21 patients, 15 (10%) had pleural effusion, 3 (2%) had cardiomegaly and all 3 (2%) patient had fibrosis suggestive of old pulmonary Koch's in intermediate high-risk group. 2D ECHO was used as a screening tool in all patients in this study. Out of 150 patients, 117 (78%) of patients had RV dysfunction which was assessed by tricuspid annular plane systolic excursion. RA and RV dilatation were present in 129 (86%) of patients in our study. All patients in high-risk group show abnormal echocardiography (P < 0.0001). Mean RVSP was 72 ± 4.38 mmHG in the high risk group and comparatively low 54.58 ± 10.23 in low-risk group (P < 0.0001). Majority of patients in the study had Tricuspid regurgitation at presentation. 129 (86%) had moderate TR and 18 (12%) had severe TR. Definitive evidence of thrombus in MPA and its branches were observed in 6 (8.7%) intermediate high-risk patients and 3 (7.7%) in intermediate low-risk patients on 2D Echo screening. 50% of patients with high risk shows endogenic material in RPA.

Among 150 patients who underwent CTPA, 63 (42%) had dilated main pulmonary artery; 18 (12%) had saddle thrombus; 75 (50%) had right main pulmonary artery partial thrombus; 84 (56%) had LPA partial thrombus. 63 (42%) patients had thrombus seen in segmental and sub-segmental vessels [Figure 2]. Lower limb venous ultrasonography was done in all patients. Out of 150 patients, 72 (48%) patients had evidence of deep venous thrombosis; 80 patients had proximal and 12 patients had distal vein thrombosis.{Figure 2}

sPESI score was 1 in 90% of patients with troponin-I positivity and 10% of patients with troponin negativity with P < 0.0001. This is suggestive of troponin is increased in correlation with sPESI. RV dysfunction was present in 96.7% of patients with troponin positive and 50% of patients with negative troponin had RV dysfunction with P = 0.0004 suggest that troponin I is a marker of RV dysfunction and help in the probability of diagnosis. All patients with high risk and intermediate high risk had troponin I positive as per guidelines. In this study, all high risk and intermediate high risk had positive troponin-I. Out of 36 patients with intermediate low risk 13% had troponin positive and 45% had negative with P = 0.03. All patients with low risk had negative troponin-I. Mean hemoglobin was 13.1 ± 1.40 g/dl; mean serum creatinine was 1.11 ± 0.54 mg/dl; mean serum glutamic pyruvic transaminase 119.36 ± 295.66 IU/L, mean troponin-I was 0.32 ± 0.68 ng/ml; mean D-dimer value was 5772.43 ± 2339.19, mean prothrombin time was 16.68 ± 8.49 and mean APTT was 38.59 ± 16.34. All blood investigations are relatively high in intermediate high-risk group. The outcome in all subgroups with an overall mortality of 3 (2%) seen in high-risk group and 147 (98%) patients were discharged [Table 4].{Table 4}

As per that risk stratification, all massive PE patients required thrombosis and in submassive PE patient's use of thrombolysis is to be balanced against risk of death and bleeding and minor PE is to be treated with anticoagulation.

By taking into consideration like cardiac enzymes and simplified PESI score, patients with submassive PE are further divided into intermediate-high and low risk group and was managed accordingly. In this study, 96 (64%) were managed with thrombolysis plus anticoagulation and 21 (42%) patients were treated with anticoagulation. Majority (86%) of patients with tenectaplase; 9 (10.3%) patients with streptokinase and 3 (3.4%) was thrmobolysed with alteplase.

High risk all patients were thrombolysed with tenectaplase; and improved in terms of resolution of dyspnea, chest pain, and hemoptysis. Heart rate and oxygen saturation (SaO2) return to normal and inotropic support tapered slowly. Twenty-three patients were intermediate high risk and all of them were thrombolysed; twenty patients with tenectaplase and rest three with streptokinase injection.

All patients in intermediate high-risk groups were hemodynamically stable, but all patients had sPESI score 1 or >1, RV dysfunction present on imaging test and positive cardiac biomarkers. In the presence of all these factors, these groups are prone for hemodynamical collapse and early mortality. All patients were thrombolysed to avoid these complications. Post thrombolysis, all patients showed improvement in dyspnea, chest pain, and cough.

Thirty-nine patients were intermediate low risk and 12 of them were thrombolysed; 12 with tenectaplase and 3 with alteplase. All 12 patients presented with dyspnoea and on evaluation found to have hypoxemia. The echocardiographic finding showed RV dysfunction and/or cardiac biomarker elevation. All of them had sPESI score >1 suggested risk of hemodynamic collapse.

All these factors were taken into consideration, and patients were thrombolysed in view of high-risk benefit ratio. Post thrombolysis, all 12 patients had improvement in dyspnea and resolution of hypoxemia, and heart rate normalized. On echocardiography, RV function improved in 9 patients and 3 had mild RV dysfunction, and all twelve showed regression of TR.


PE and DVT are separate but related aspects of the same dynamic disease process, now termed VTE.[10],[11] Male: female ratio in our study was 2.3:1. This is consistent with the study done by Calwin et al. from Chennai.[12] In that study, the mean age of the patient population was 52.1 years and 62.8% were male and 37.2% were female. In our study, smoking was major risk factor present in 52% of the patients. Studies done by Mitchell et al. also showed smoking as the major risk factor for acute PE and was found in 22 (41.5%) of the patients.[13] Landmark study PIOPED II, also depicted smoking was one of the major risk factors found in approximately 43% of the patients, which is similar to our study findings.[14] Apart from smoking chronic lung disease found to be another important risk factor. In our study, chronic lung disease was present in 20% of patients, which is comparable to the PIOPED II study, in which it was observed in 26% of patients.[10]

The most common clinical presentation of patients included in our study is dyspnea (94.4%) followed by chest pain (82%). The other symptoms being cough (17%) and hemoptysis (14%) and syncope (4%). This is consistent with our studies done in India. Study done by Shukla et al. showed the most common clinical presentation is dyspnea (100%) followed by chest pain (52%), syncope (30%), and cough (40%). The other symptoms being hemoptysis (10%).[15] Another study done by Mitchell et al. also showed dyspnea was the predominant symptom (71.7%) followed by syncope (17.0%), cough (15.1%), chest pain (7.6%), and hemoptysis (3.8%).[13] Stein et al. author of the landmark study PIOPED II demonstrated similar findings.[10] This confirms an important fact that the finding of solitary dyspnea in a patient provides a strong suspicion for PE.

The ECG, in addition to clinical symptoms, can be essential in directing the physician towards the diagnosis. ECG findings in Calwin et al. study were sinus tachycardia (91.4%) followed by RV strain pattern (65.7%), S1Q3T3 pattern (34.2%) and RBBB (20%).[12] Shukla et al. also showed ST-T depression in 80% of patients in his study. Other findings were S1Q3T3 IN 30%, RBBB in 13%, and low voltage in 66% of patients with PE.[15] About 78% had evidence of RV dysfunction and RA and RV dilatation was present 86% of patients. Majority of patients in the study had Tricuspid regurgitation at presentation. Forty-three (86%) had moderate TR and 6 (12%) had severe TR.

Definitive evidence of thrombus in MPA and its branches were observed in 9 (18%) patients on 2D Echo screening. A study done by Mitchell et al. from south India showed PAH was the main finding present in 85% of patients.[13] Other findings were RV dysfunction in 58% and definite evidence of thrombus in 5.7% of patients. Another study done by Shukla et al. depicted moderate-to-severe TR in 73% of patients and RV dilatation and dysfunction in 86% of patients, which is consistent with our study.[15] This implies its use as an important screening tool in a suspect of acute PE, especially if there is no prior cardiopulmonary disease. The abnormality was mainly in the form of a raised pulmonary artery pressure.

In the present study, CTPA findings; 63 (42%) had dilated main pulmonary artery; 18 (12%) had saddle thrombus; 75 (50%) had right main pulmonary artery partial thrombus; 84 (56%) had LPA partial thrombus. 63 (42%) patients had thrombus seen in segmental and subsegmental vessels. A study done by Calwin et al. showed 83% of patients had thrombus located in the main and lobar arteries. The remaining four patients (16.7%) had thrombus seen in subsegmental vessels.[12] Another study done by Shukla et al. showed MPA thrombus in 40% of patients, thrombus in MPA branches in 40% of patients and 20% of patients had segmental and subsegmental occlusion.[15] All high-risk and intermediate high-risk group patients had undergone thrmobolysis in the present study. Majority (86%) had been given tenectaplase, 10.3% had been given streptokinase and 3.4% had been given alteplase as thrombolytic agents. In the PEITHO study, majority study population was thrombolysed with tenectaplase and only 2.6% were treated with other agents.[16]

MAPPET-3 study stated in-hospital death or clinical deterioration requiring escalation of treatment is lower with heparin + alteplase than with heparin + placebo (11% vs. 25%, respectively; P = 0.006) and Rate of recurrent PE was low and bleeding incidence similar in both groups.[17] Results of PEITHO 2 will give a direction for further treatment of intermediate-risk patients.[18] PEITHO 2 trial protocol also does not stratify patients into intermediate high- and low-risk group. Konstantinides et al. show that >95% of patients with acute PE are hemodynamically stable at presentation and are thus not considered to be at high risk.[18]


Echocardiography, cardiac biomarkers and sPESI score are helpful for prognosis purpose. PE can present with unexplained dyspnea and atypical chest pain among other signs and symptoms. Early diagnosis, risk stratification, and guideline-directed prompt management can lead to favorable outcome.


Although the results of our study strongly suggest risk stratification using ECG and echocardiogram, it is limited by being a single center experience with a small group of patients. More studies in future are required comprising a multicenter analysis with a large patient cohort to add to the current knowledge and formulate an effective risk stratification model for sub-massive PE patients. Such a model shall be helpful both regarding improving patient outcomes and early decision-making the need for aggressive management pathways.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing GJ, Harjola VP, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS) The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Heart J 2020;41(4):543-603.
2Oger E. Incidence of venous thromboembolism: A community-based study in Western France. EPI-GETBP Study Group. Groupe d'Etude de la Thrombose de Bretagne Occidentale. Thromb Haemost 2000;83:657-60.
3Martin C, Sobolewski K, Bridgeman P, Boutsikaris D. Systemic thrombolysis for pulmonary embolism: A Review. P T 2016;41:770-5.
4Agarwal S, Lee AD, Raju RS, Stephen E. Venous thromboembolism: A problem in the Indian/Asian population? Indian J Urol 2009;25:11-6.
5Pawar P, Ayyappan MK, Jagan J, Rajendra N, Mathur K, Raju R. Analysis of patients with venous thromboembolism in a multi-specialty tertiary hospital in South India. Indian J Vascular Endov Surg 2020;7:29.
6Authors/Task Force Members, Konstantinides SV, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galiè N, et al. 2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC) Endorsed by the European Respiratory Society (ERS). Europ Heart J 2014;35:3033-80.
7Anderson DR, Kovacs MJ, Dennie C, Kovacs G, Stiell I, Dreyer J, et al. Use of spiral computed tomography contrast angiography and ultrasonography to exclude the diagnosis of pulmonary embolism in the emergency department. J Emerg Med 2005;29:399-404.
8Kearon C, Ginsberg JS, Douketis J, Turpie AG, Bates SM, et al. An evaluation of D-dimer in the diagnosis of pulmonary embol- ism: A randomized trial. Ann Intern Med 2006;144:812-21.
9Rodger MA, Maser E, StiellI, Howley HE, Wells PS. The inter observer reliability of pretest probability assessment in patients with suspected pulmonary embolism. Thromb Res 2005;116:101-7.
10Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, et al. Clinical characteristics of patients with acute pulmonary embolism: Data from PIOPED II. Am J Med 2007;120:871-9.
11Pinjala R, ENDORSE-India investigators. Venous thromboembolism risk & prophylaxis in the acute hospital care setting (ENDORSE), a multinational cross-sectional study: Results from the Indian subset data. Indian J Med Res 2012;136:60-7.
12Davidsingh SC, Srinivasan N, Balaji P, Kalaichelvan U, Mullasari AS. Study of clinical profile and management of patients with pulmonary embolism–Single center study. indian heart journal 2014;66(2):197-202.
13Mitchell AM, Jones AE, Tumlin JA, Kline JA. Prospective study of the incidence of contrast-induced nephropathy among patients evaluated for pulmonary embolism by contrast-enhanced computed tomography. Acad Emerg Med 2012;19:618-25.
14Goldhaber SZ. Echocardiography in the management of pulmonary embolism. Arch Intern Med 2002;136:691e700.
15Shukla AN, Thakkar B, Jayaram AA, Madan TH, Gandhi GD. Efficacy and safety of tenecteplase in pulmonary embolism. J Thromb Thrombolysis 2014;38:24-9.
16Konstantinides SV, Vicaut E, Danays T, Becattini C, Bertoletti L, Beyer-Westendorf J, et al. Impact of thrombolytic therapy on the long-term outcome of intermediate-risk pulmonary embolism. J Am Coll Cardiol 2017;69:1536-44.
17Konstantinides S, Geibel A, Heusel G, Heinrich F, Kasper W; Management Strategies and Prognosis of Pulmonary Embolism-3 Trial Investigators. Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. N Engl J Med 2002;347:1143-50.
18Konstantinides SV, Barco S, Lankeit M, Meyer G. Management of pulmonary embolism: An update. J Am Coll Cardiol 2016;67:976-90.