Pulmonary embolism: risk-stratified management

Overview and definitions

Venous thromboembolism (VTE), clinically presenting as deep vein thrombosis (DVT) or PE, is globally the third most frequent acute cardiovascular syndrome behind myocardial infarction and stroke.^[1] In the majority of cases, PE originates from DVT in a lower limb, and only rarely from upper-limb DVT (mostly following venous catheterisation).^[1]

• Two guidelines frame this page: the 2019 ESC guideline for acute PE, developed in collaboration with the European Respiratory Society (ERS), and the 2026 AHA/ACC multisociety guideline, a de novo guideline for adult patients (18 years of age or more) with acute PE.^[1][3]
• ESC class and level on this page are quoted from the formal recommendation tables of the European Respiratory Journal publication of the ESC guideline, and AHA/ACC COR and LOE from the formal tables of the JACC publication of the 2026 guideline.

• The absence of haemodynamic instability does not exclude beginning (and possibly progressing) RV dysfunction, and thus an elevated PE-related early risk.^[1]

• In this large population, further assessment is necessary to determine the level of risk and adjust management decisions accordingly; ESC 2019 recommends validated criteria for diagnosing PE in suspected PE without haemodynamic instability (Class I, level B) and, once PE is confirmed, further stratification into intermediate- and low-risk categories (Class I, level B).^[1][2]

• A note on wording: ESC 2019 categorises the risk factors for the index VTE event in line with the International Society on Thrombosis and Haemostasis, and avoids terms such as provoked, unprovoked or idiopathic VTE.^[1]

• The 2026 AHA/ACC text says treatment may be divided into an initiation phase, an initial treatment phase (3 to 6 months) and an extended treatment phase.^[3]

Epidemiology and risk factors

^[1]

• Time trend analyses in European, Asian and North American populations suggest that case fatality rates of acute PE may be decreasing.^[1]
• The ESC also notes a tendency towards overdiagnosis of (subsegmental or even non-existent) PE, which might lead to a false drop in case fatality rates by inflating the denominator.^[1]

VTE is considered to be a consequence of the interaction between patient-related, usually permanent, risk factors and setting-related, usually temporary, risk factors.^[1]

^[1]

The risk of VTE varies with cancer type; pancreatic cancer, haematological malignancies, lung, gastric and brain cancer carry the highest risk.^[1] Combined oral contraceptives (containing both an oestrogen and a progestogen) are associated with an approximately two- to six-fold increase in VTE risk over baseline.^[1] In children, PE is usually associated with DVT and is rarely unprovoked; serious chronic medical conditions and central venous lines are considered likely triggers.^[1]

Pathophysiology

• Acute PE interferes with both circulation and gas exchange, and RV failure due to acute pressure overload is considered the primary cause of death in severe PE.^[1]
• Pulmonary artery pressure (PAP) increases if more than 30–50% of the total cross-sectional area of the pulmonary arterial bed is occluded by thromboemboli.^[1]
• PE-induced vasoconstriction, mediated by the release of thromboxane A2 and serotonin, contributes to the initial increase in pulmonary vascular resistance (PVR).^[1]

1. Anatomical obstruction and hypoxic vasoconstriction in the affected lung area lead to an increase in PVR and a proportional decrease in arterial compliance.^[1]
2. The abrupt increase in PVR results in RV dilation, which alters the contractile properties of the RV myocardium via the Frank–Starling mechanism.^[1]
3. The rise in RV pressure and volume increases wall tension and myocyte stretch, and the RV contraction time is prolonged.^[1]
4. With systemic vasoconstriction, these compensatory mechanisms increase PAP, improving flow through the obstructed bed and temporarily stabilising systemic blood pressure (BP).^[1]
5. The adaptation is limited: a non-preconditioned, thin-walled RV is unable to generate a mean PAP above 40 mmHg.^[1]
6. Prolongation of RV contraction into early diastole in the left ventricle (LV) leads to leftward bowing of the interventricular septum; LV filling is impeded in early diastole, which may reduce cardiac output (CO) and contribute to systemic hypotension and haemodynamic instability.^[1]
7. Although RV infarction is uncommon after PE, it is likely that an imbalance between oxygen supply and demand can damage cardiomyocytes; systemic hypotension is a critical element, impairing the coronary driving pressure to the overloaded RV.^[1]

^[1]

• Respiratory failure in PE is predominantly a consequence of haemodynamic disturbances.^[1]

• Zones of reduced flow in obstructed arteries, combined with zones of overflow in the capillary bed served by non-obstructed vessels, result in ventilation/perfusion mismatch, which contributes to hypoxaemia.^[1]

• In about one-third of patients, right-to-left shunting through a patent foramen ovale can be detected by echocardiography; it may lead to severe hypoxaemia and an increased risk of paradoxical embolisation and stroke.^[1]

• Acute RV failure, defined as a rapidly progressive syndrome with systemic congestion resulting from impaired RV filling and/or reduced RV flow output, is a critical determinant of clinical severity and outcome in acute PE.^[1]

• An inflammatory response might explain the secondary haemodynamic destabilisation that sometimes occurs 24–48 h after acute PE, although early recurrence may be an alternative explanation in some cases.^[1]

Clinical presentation

• The clinical signs and symptoms of acute PE are non-specific; in most cases PE is suspected in a patient with dyspnoea, chest pain, pre-syncope or syncope, or haemoptysis.^[1]

• Haemodynamic instability is a rare but important presentation, as it indicates central or extensive PE with severely reduced haemodynamic reserve.^[1]

• Dyspnoea may be acute and severe in central PE; in small peripheral PE it is often mild and may be transient. In pre-existing heart failure or pulmonary disease, worsening dyspnoea may be the only symptom indicative of PE.^[1]

• Chest pain is frequent and is usually caused by pleural irritation due to distal emboli causing pulmonary infarction; in central PE it may have a typical angina character, possibly reflecting RV ischaemia.^[1]

• Syncope may occur and is associated with a higher prevalence of haemodynamic instability and RV dysfunction; ESC 2019, citing a study that was recent at the time, says acute PE may be a frequent finding in patients presenting with syncope (17%), even in the presence of an alternative explanation.^[1]

• PE may be asymptomatic or discovered incidentally during diagnostic work-up for another disease.^[1]

• Hypoxaemia is frequent, but up to 40% of patients have normal arterial oxygen saturation and 20% have a normal alveolar–arterial oxygen gradient; hypocapnia is also often present.^[1]

• Electrocardiographic changes indicative of RV strain, such as T-wave inversion in V1–V4, a QR pattern in V1, an S1Q3T3 pattern, and incomplete or complete right bundle branch block, are usually found in more severe cases; in milder cases the only abnormality may be sinus tachycardia, present in 40% of patients.^[1]

• Atrial arrhythmias, most frequently atrial fibrillation, may be associated with acute PE.^[1]

• A chest X-ray is frequently abnormal and, although usually non-specific in PE, may help exclude other causes of dyspnoea or chest pain.^[1]

Differential diagnosis

• In suspected PE with haemodynamic instability, the clinical probability is usually high and the ESC differential diagnosis includes cardiac tamponade, acute coronary syndrome, aortic dissection, acute valvular dysfunction and hypovolaemia.^[1]
• In central PE, chest pain may have a typical angina character, possibly reflecting RV ischaemia, and requires differential diagnosis from an acute coronary syndrome or aortic dissection.^[1]

^[1]

• For unstable patients taken directly to the catheterisation laboratory with suspected acute coronary syndrome, ESC 2019 says pulmonary angiography may be considered as a diagnostic procedure once the acute coronary syndrome has been excluded, provided that PE is a probable alternative and particularly if catheter-directed treatment is a therapeutic option.^[1]

Clinical probability

• Pre-test probability can be assessed either by implicit (empirical) clinical judgement or by prediction rules; as clinical judgement lacks standardisation, explicit rules were developed, the most frequently used being the revised Geneva rule and the Wells rule.^[1]
• In suspected PE without haemodynamic instability, ESC 2019 recommends that the diagnostic strategy be based on clinical probability, assessed either by clinical judgement or by a validated prediction rule (Class I, level A).^[2]

The revised Geneva rule as printed in ESC 2019 Table 5 (the ESC places the Wells rule in its supplementary data):^[1]

^[1]

The Wells score as tabulated in the 2026 AHA/ACC guideline (Table 3):^[3]

^{[3] [1]}

• The Pulmonary Embolism Rule-out Criteria (PERC) were developed for emergency department patients to select, on clinical grounds, those whose likelihood of PE is so low that work-up should not even be started. They comprise eight variables: age under 50 years; pulse under 100 beats per minute; arterial oxygen saturation above 94%; no unilateral leg swelling; no haemoptysis; no recent trauma or surgery; no history of VTE; and no oral hormone use.^[1]

• A validation study and a randomised non-inferiority study suggested safe exclusion of PE in patients with low clinical probability who also met all PERC criteria, but the low overall prevalence of PE in these studies does not support generalisability.^[1]

• The 2026 AHA/ACC guideline recommends a targeted history and comprehensive physical examination in patients presenting with symptoms suggestive of acute PE, to assist in determining the clinical pretest probability (COR 1, LOE A).^[3]

D-dimer

• The negative predictive value of D-dimer is high, and a normal level renders acute PE or DVT unlikely; the positive predictive value of an elevated level is low, so D-dimer is not useful for confirming PE.^[1]
• D-dimer is more frequently elevated in cancer, in hospitalised patients, in severe infection or inflammatory disease, and during pregnancy, and the number needed to test to exclude one PE rises from 3 in the general emergency department population to 10 or more in these situations.^[1]
• Quantitative enzyme-linked immunosorbent assay (ELISA) or ELISA-derived assays have a sensitivity of 95% or more and can be used to exclude PE in patients with low or intermediate pre-test probability.^[1]

^[2]

• The YEARS footnote to that table says these cut-offs may be used: PE is excluded in patients without clinical items (signs of DVT, haemoptysis, and whether an alternative diagnosis is less likely than PE) and D-dimer under 1000 µg/L, or in patients with one or more clinical items and D-dimer under 500 µg/L.^[2]

• ESC 2019 text: D-dimer should not be measured in patients with a high clinical probability of PE, owing to a low negative predictive value in this population (the formal row, in suspected PE without haemodynamic instability: D-dimer measurement is not recommended in patients with high clinical probability, as a normal result does not safely exclude PE, even when using a highly sensitive assay; Class III, level A), and it is less useful in hospitalised patients because the number that needs to be tested to obtain a clinically relevant negative result is high.^[1][2]

• Point-of-care assays have a lower sensitivity and negative predictive value than laboratory-based tests, so the ESC says they should only be used in patients with a low pre-test probability.^[1]

• The 2026 AHA/ACC guideline makes parallel statements. AHA/ACC 2026: in adults undergoing evaluation for PE who have a low or intermediate clinical probability of PE (under 50%) by risk assessment, an age-adjusted D-dimer value below the threshold (age × 10 μg/L for fibrinogen equivalent units assays) effectively excludes PE and the need for imaging (COR 2a, LOE B-R).^[3]

• AHA/ACC 2026: in adults with suspected PE, the YEARS algorithm can be useful to identify which patients do not need imaging (COR 2a, LOE B-R); its footnote uses a D-dimer threshold of 500 μg/L with 1 or more YEARS criteria (clinical signs of DVT, haemoptysis, and/or PE as the most likely diagnosis) and 1000 μg/L with none.^[3]

• The AHA/ACC text gives 2% as the accepted safety threshold (failure rate) for diagnostic tools in PE.^[3]

^{[7] [6]}

Imaging: CTPA, V/Q scanning and the rest

• Multidetector CT pulmonary angiography (CTPA) is the method of choice for imaging the pulmonary vasculature in suspected PE and allows visualisation down to the subsegmental level.^[1]
• In PIOPED II (mainly four-detector CTPA), sensitivity was 83% and specificity 96%.^[1]
• A negative CTPA had a negative predictive value of 96% and 89% with low and intermediate clinical probability, but only 60% with high probability; a positive CTPA had a positive predictive value of 92–96% with intermediate or high probability but 58% with low probability.^[1]
• ESC 2019 text: clinicians should therefore consider further testing in case of discordance between clinical judgement and the CTPA result.^[1]

Selected rows of the ESC 2019 diagnosis table for suspected PE without haemodynamic instability (CUS = lower-limb compression ultrasonography; V/Q = ventilation/perfusion lung scintigraphy):^[2]

^[2]

ESC 2019 Table 6, imaging tests for the diagnosis of PE:^[1]

^[1]

• ESC 2019 text: being a lower-radiation and contrast medium-sparing procedure, the V/Q scan may preferentially be applied in outpatients with low clinical probability and a normal chest X-ray, in young (particularly female) patients, in pregnant women, in patients with a history of contrast medium-induced anaphylaxis and in patients with severe renal failure.^[1]

• A three-tier report is preferable: normal scan (excluding PE), high-probability scan (considered diagnostic of PE in most patients), and non-diagnostic scan.^[1]

• The 2026 AHA/ACC guideline recommends imaging for patients with symptoms and signs suggestive of acute PE who are high probability (above 50%) by a validated score or have an elevated D-dimer, to confirm or exclude PE (COR 1, LOE A).^[3]

• AHA/ACC 2026: a positive CTPA or a high-probability V/Q scan is sufficient to diagnose PE (COR 1, LOE A), and CTPA is recommended in preference to a V/Q scan to confirm the diagnosis (COR 1, LOE B-R).^[3]

• AHA/ACC 2026: in suspected PE when CTPA cannot be performed, a V/Q scan in preference to contrast-enhanced MRA is reasonable to improve diagnostic yield (COR 2a, LOE B-R).^[3]

• AHA/ACC 2026: an echocardiogram is not recommended to confirm or refute the diagnosis (COR 3: No Benefit, LOE B-NR), and in suspected acute PE, CT venography of the inferior vena cava and leg veins is not recommended as a routine adjunct to CTPA to diagnose venous thrombosis (COR 3: No Benefit, LOE B-R).^[3]

• ESC 2019 text: echocardiography is not mandatory in the routine work-up of haemodynamically stable patients with suspected PE, although it may help in the differential diagnosis of acute dyspnoea; with a reported negative predictive value of 40–50%, a negative result cannot exclude PE.^[1]

• A pulmonary ejection acceleration time under 60 ms with a peak systolic tricuspid gradient under 60 mmHg (the 60/60 sign), or depressed RV free wall contractility compared with the apex (McConnell sign), is suggestive of PE.^[1]

• However, these findings are present in only about 12% and 20% of unselected PE patients, respectively.^[1]

• Mobile right-heart thrombi are detected in under 4% of unselected patients with PE and may reach 18% in the intensive care setting; they essentially confirm the diagnosis and are associated with high early mortality, especially with RV dysfunction.^[1]

• ESC 2019 text: lower-limb compression ultrasonography (CUS) shows a DVT in 30–50% of patients with PE, and a proximal DVT in a patient suspected of PE is considered sufficient to warrant anticoagulation without further testing; those patients should still undergo risk assessment for PE severity and early death. The formal rows (suspected PE without haemodynamic instability): accepting the diagnosis of VTE (and PE) if CUS shows a proximal DVT in a patient with clinical suspicion of PE is recommended (Class I, level A), and if a positive proximal CUS is used to confirm PE, assessment of PE severity should be considered to permit risk-adjusted management (Class IIa, level C).^[1][2]

• In suspected PE, CUS can be limited to a four-point examination (bilateral groin and popliteal fossa); incomplete compressibility of the vein is the only validated criterion.^[1]

Putting the diagnostic pathway together

Suspected PE with haemodynamic instability

1. In suspected high-risk PE, as indicated by haemodynamic instability, bedside echocardiography or emergency CTPA (depending on availability and clinical circumstances) is recommended for diagnosis (ESC 2019, Class I, level C).^[2]
2. IV anticoagulation with unfractionated heparin (UFH), including a weight-adjusted bolus injection, is recommended without delay in patients with suspected high-risk PE (ESC 2019, Class I, level C).^[2]
3. Bedside transthoracic echocardiography (TTE) is the most useful initial test; in a highly unstable patient, echocardiographic RV dysfunction is sufficient to prompt immediate reperfusion without further testing.^[1]
4. In a haemodynamically compromised patient with suspected PE, unequivocal signs of RV pressure overload, especially the 60/60 sign, McConnell sign or right-heart thrombi, justify emergency reperfusion if immediate CT angiography is not feasible in a patient with high clinical probability and no other obvious cause for RV pressure overload.^[1]
5. As soon as the patient is stabilised with supportive treatment, final confirmation of the diagnosis by CT angiography should be sought.^[1]

Suspected PE without haemodynamic instability

1. A diagnostic strategy based on clinical probability, assessed by clinical judgement or a validated prediction rule, is recommended (ESC 2019, Class I, level A), as is the use of validated criteria for diagnosing PE (Class I, level B).^[2]
2. Initiation of anticoagulation is recommended without delay in patients with high or intermediate clinical probability while the diagnostic work-up is in progress (ESC 2019, Class I, level C).^[2]
3. Low or intermediate probability, or PE-unlikely: plasma D-dimer, preferably using a highly sensitive assay, is recommended for outpatients or emergency department patients to reduce the need for unnecessary imaging and irradiation (ESC 2019, Class I, level A); in the emergency department, a negative ELISA D-dimer combined with clinical probability can exclude PE in about 30% of patients with suspected PE.^[1][2]
4. In most centres, multidetector CTPA is the second-line test after an elevated D-dimer and the first-line test with high clinical probability; it is diagnostic when it shows a clot at least at the segmental level.^[1]
5. Where V/Q scintigraphy is readily available, it is a valid option for patients with an elevated D-dimer and a contraindication to CTPA, and may be preferred to avoid unnecessary radiation, particularly in younger patients and in female patients in whom thoracic CT might raise the lifetime risk of breast cancer.^[1]

• False-negative CTPA results have been reported in patients with high clinical probability, but they are infrequent and the 3-month thromboembolic risk was low in such patients, so the need for, and nature of, further tests remains controversial.^[1]

Risk stratification

• Risk stratification is mandatory for determining the appropriate management.^[1]
• Initial risk stratification of suspected or confirmed PE based on haemodynamic instability is recommended to identify patients at high risk of early mortality (ESC 2019, Class I, level B).^[2]
• In patients without instability, the ESC assesses two sets of criteria: indicators of PE severity, mostly related to RV dysfunction, and comorbidity or other aggravating conditions that may adversely affect early prognosis.^[1]

Clinical scores: PESI and sPESI

• Tachycardia, low systolic BP, respiratory insufficiency (tachypnoea and/or low arterial oxygen saturation) and syncope, alone or in combination, have been associated with an unfavourable short-term prognosis.^[1]
• The principal strength of the Pulmonary Embolism Severity Index (PESI) lies in the reliable identification of patients at low risk for 30-day mortality (PESI classes I and II); because the original PESI includes 11 differently weighted variables, a simplified version (sPESI) was developed and validated.^[1]

^{[3] [1]}

• In patients without haemodynamic instability, ESC 2019 says clinical prediction rules integrating PE severity and comorbidity, preferably the PESI or sPESI, should be considered for risk assessment in the acute phase (Class IIa, level B).^[2]
• Overall, a PESI of class I–II or an sPESI of 0 is a reliable predictor of low-risk PE.^[1]

Right ventricular imaging and biomarkers

• Echocardiography: an RV/LV diameter ratio of 1.0 or more and a tricuspid annular plane systolic excursion (TAPSE) under 16 mm are the findings most frequently reported in association with unfavourable prognosis (ESC 2019).^[1]

• Meta-analyses have suggested that echocardiographic RV dysfunction is associated with elevated short-term mortality in patients who appear haemodynamically stable, but its positive predictive value for PE-related death was low (under 10%) in one meta-analysis.^[1]

• CT: in a meta-analysis of 49 studies (more than 13 000 patients), an RV/LV ratio of 1.0 or more was associated with a 2.5-fold risk of all-cause mortality (OR 2.5, 95% CI 1.8–3.5) and a five-fold risk of PE-related mortality (OR 5.0, 95% CI 2.7–9.2); RV/LV ratios of 1.0 or more (instead of 0.9) may be more appropriate to indicate poor prognosis.^[1]

• Troponin: between 30% (conventional assays) and 60% (high-sensitivity assays) of patients have elevated troponin I or T, but on its own it has relatively low specificity and positive predictive value for early mortality in normotensive patients.^[1]

• In a cohort of 526 normotensive patients, high-sensitivity troponin T under 14 pg/mL had a negative predictive value of 98% for an adverse in-hospital outcome.^[1]

• Natriuretic peptides: a meta-analysis found that 51% of 1132 unselected patients with acute PE had elevated B-type natriuretic peptide (BNP) or N-terminal (NT)-proBNP on admission, and those patients with elevated levels had a 10% risk of early death and a 23% risk of an adverse clinical outcome; low levels can exclude an unfavourable early outcome with high sensitivity and negative predictive value.^[1]

• Lactate: arterial levels of 2 mmol/L or more predict PE-related complications in unselected and in initially normotensive patients.^[1]

• ESC 2019: assessment of the RV by imaging (TTE or CTPA) or by laboratory biomarkers (cardiac troponins or natriuretic peptides) should be considered, even in the presence of a low PESI or a negative sPESI (Class IIa, level B).^[2]

• ESC 2019: in patients without haemodynamic instability, validated scores combining clinical, imaging and laboratory prognostic factors may be considered to further stratify severity (Class IIb, level C).^[2]

ESC 2019 risk classes

• The ESC 2019 classification of PE severity and the risk of early (in-hospital or 30-day) death (Table 8). Its footnote e qualifies the clinical-parameters criterion of both intermediate classes (quoted in the intermediate-low row); footnote b refers to the guideline’s Figure 3 and Supplementary Table 3 for prognostically relevant TTE or CTPA findings and cut-offs; footnote c (further biomarkers) is given below the table:^[1][2]

^{[1] [2]}

• Testing for biomarkers such as troponin or natriuretic peptides is not necessary for immediate therapeutic decisions in high-risk PE.^[1]
• ESC 2019 Table 8 footnote c: further biomarkers, such as N-terminal pro B-type natriuretic peptide (NT-proBNP) of 600 ng/L or more, heart-type fatty acid-binding protein (H-FABP) of 6 ng/mL or more, or copeptin of 24 pmol/L or more, may provide additional prognostic information; they have been validated in cohort studies but, at the time of the guideline, had not been used to guide treatment decisions in randomised controlled trials.^[1]

^{[1] [2] [3]}

The 2026 AHA/ACC clinical categories

• The 2026 AHA/ACC guideline presents five categories (A–E) with subcategories, ranging from low to high risk for adverse outcomes, to enhance the precision of severity classification, prognosis assessment and therapeutic decision-making.^[3]

^[3]

• A respiratory modifier, R, is added to the category when the respiratory modifier criteria are met (e.g. C3R, D2R); in Category C it is applied when hypoxaemia or tachypnoea is present or supplemental oxygen is needed, and in Category E (E-R) respiratory failure is defined by the need for noninvasive or invasive positive pressure ventilation.^[3]

• Two footnotes to the AHA/ACC category figure read: systolic blood pressure under 90 or a decrease of more than 40 mm Hg lasting under 15 min or responding to IV fluids; and any of lactate above 2 mmol/L, acute kidney injury, urine output under 0.5 mL/kg/h, mental status change, cardiac index under 2.2 L/min/m², mean arterial pressure under 60 mm Hg, or an increased shock score or stage (SCAI stage, CPES score).^[3]

• Categories A and B: use of the Hestia, PESI and/or sPESI scores is recommended to identify a low risk for short-term adverse outcomes (COR 1, LOE B-R).^[3]

• Haemodynamically stable patients in categories C and D: a validated PE-specific risk score is reasonable to identify a higher risk for short-term adverse outcomes (COR 2a, LOE B-NR).^[3]

• Category C (elevated clinical severity score without features of hypotension or shock): measurement of at least 1 cardiac biomarker (troponin or BNP) is recommended to assist with risk stratification for short-term complications and/or mortality (COR 1, LOE B-NR).^[3]

• Categories C to E undergoing evaluation at an acute care facility: measurement of lactate (venous or arterial) is recommended to assist with risk stratification for short-term complications and/or mortality (COR 1, LOE B-NR).^[3]

• Categories C–D (elevated clinical severity score but no shock): RV imaging is recommended for short-term risk stratification (COR 1, LOE A), and echocardiography over CT is preferred for short-term risk stratification when there is no evidence of persistent hypotension or shock (COR 2a, LOE B-NR).^[3]

• Patients with acute PE who undergo CTPA: reporting the numerical RV/LV ratio (measured by internal diameter assessed on axial or reformatted 4D-chamber view) is recommended over subjective quantification for risk stratification (COR 1, LOE B-R).^[3]

• A 2026 correction replaced Table 4 of the 2026 AHA/ACC guideline (optimal methods of RV dysfunction assessment on echocardiogram); the corrected table gives RV/LV end-diastolic ratio above 0.9 as the RV/LV criterion and states that a TAPSE of 1.7 cm or less is abnormal.^[3][4]

• ESC 2019 instead names an RV/LV diameter ratio of 1.0 or more and a TAPSE under 16 mm as the findings most frequently reported with unfavourable prognosis, so quote each threshold with its body.^[1]

Management: high-risk PE and resuscitation

• ESC 2019: treatment follows the risk class: primary reperfusion for high-risk PE; anticoagulation with monitoring for intermediate-high risk, with rescue reperfusion reserved for patients who develop signs of haemodynamic instability; and, for carefully selected low-risk patients, early discharge with home treatment should be considered if proper outpatient care and anticoagulant treatment can be provided (Class IIa, level A).^[1][2]

^{[1] [2]}

ESC 2019 recommendations for acute-phase treatment of high-risk PE (Table 4 definition); after haemodynamic stabilisation, anticoagulation continues as in intermediate- or low-risk PE:^[2]

^[2]

• Primary reperfusion, in most cases systemic thrombolysis, is the ESC treatment of choice for high-risk PE; surgical embolectomy or catheter-directed treatment are alternative reperfusion options in patients with contraindications to thrombolysis, if expertise with either of these methods and the appropriate resources are available on-site.^[1]
• ESC 2019 text: patients recovering from high-risk PE can be switched to oral anticoagulation after reperfusion and stabilisation; as they were excluded from the phase III NOAC trials, the timing should be based on clinical judgement, and the specifications concerning the higher initial dose of apixaban or rivaroxaban (for 1 and 3 weeks after PE diagnosis, respectively), or the minimum overall period (5 days) of heparin anticoagulation before switching to dabigatran or edoxaban, must be followed.^[1]

^[1]

• ESC 2019 text: accelerated IV rtPA (100 mg over 2 h) is preferable to prolonged infusions of first-generation agents (streptokinase and urokinase); UFH may be given during alteplase infusion but should be stopped during streptokinase or urokinase infusion.^[1]
• ESC 2019 text: reteplase, desmoteplase and tenecteplase had also been investigated, but at the time of the guideline none of these agents was approved for use in acute PE, and, at that time, preliminary reports on reduced-dose rtPA needed confirmation by solid evidence before any recommendation could be made (the 2026 AHA/ACC text on lower-dose thrombolysis is given below).^[1][3]
• The greatest benefit is seen when lysis starts within 48 h of symptom onset, but it can still be useful after 6–14 days of symptoms.^[1]
• A meta-analysis of thrombolysis trials that included (but were not confined to) patients with high-risk PE, defined mainly as cardiogenic shock, showed a significant reduction in the combined outcome of mortality and recurrent PE, achieved with a 9.9% rate of severe bleeding and a 1.7% rate of intracranial haemorrhage.^[1]

^[1]

• ESC 2019 text: if central venous pressure is low, a modest (500 mL or less) fluid challenge can be used, as it may increase the cardiac index, but further volume loading should be withheld if there are signs of elevated central venous pressure.^[1]

• Norepinephrine can improve systemic haemodynamics, and the ESC says its use should be limited to patients in cardiogenic shock.^[1]

• ESC 2019 text: supplemental oxygen is indicated with arterial oxygen saturation under 90%; intubation should be performed only if the patient cannot tolerate or cope with non-invasive ventilation, and, in high-risk PE, positive end-expiratory pressure should be applied with caution because positive intrathoracic pressure induced by mechanical ventilation may reduce venous return and worsen low CO due to RV failure.^[1]

• ESC 2019 text (narrative, no class row): in cardiac arrest presumably caused by PE, advanced life support guidelines should be followed; thrombolytic therapy should be considered, and once it is given, cardiopulmonary resuscitation should continue for at least 60–90 min before resuscitation attempts are stopped.^[1]

• AHA/ACC 2026 recommends vasopressors and/or inotropes for cardiogenic shock due to PE (categories D2–E2) to improve cardiac output and systemic perfusion (COR 1, LOE C-LD), and says deep sedation and mechanical ventilation should not be performed in categories C–E unless clinically indicated, to avoid haemodynamic collapse (COR 3: Harm, LOE C-LD).^[3]

• AHA/ACC 2026: for acute, refractory cardiogenic shock from known or suspected acute PE (category E2), it is reasonable to institute veno-arterial ECMO, provided appropriate resources are available, to stabilise haemodynamics and improve oxygenation (COR 2a, LOE B-NR), and unstable patients (category E) should not be transferred to another centre before they are stabilised (COR 3: Harm, LOE C-EO).^[3]

Management: intermediate- and low-risk PE

ESC 2019 recommendations for acute-phase treatment of intermediate- or low-risk PE:^[2]

^[2]

• The Class III NOAC row (severe renal impairment, pregnancy and lactation, antiphospholipid antibody syndrome) carries a renal footnote: dabigatran is not recommended with creatinine clearance (CrCl) under 30 mL/min; edoxaban should be given at 30 mg once daily with CrCl 15–50 mL/min and is not recommended under 15 mL/min; rivaroxaban and apixaban are to be used with caution at CrCl 15–29 mL/min and are not recommended under 15 mL/min.^[2]
• The same table notes that the risk-to-benefit ratios of surgical embolectomy or catheter-directed procedures have not yet been established in intermediate- or low-risk PE.^[2]

Intermediate-risk PE

• For most cases of acute PE without haemodynamic compromise, parenteral or oral anticoagulation (without reperfusion) is adequate treatment, and ESC 2019 says normotensive patients with at least one indicator of elevated PE-related risk, or with aggravating conditions or comorbidity, should be hospitalised.^[1]

• ESC 2019 text: patients with RV dysfunction on echocardiography or CTPA accompanied by a positive troponin test should be monitored over the first hours or days because of the risk of early haemodynamic decompensation and circulatory collapse.^[1]

• Routine primary reperfusion, especially full-dose systemic thrombolysis, is not recommended (ESC 2019) because the risk of potentially life-threatening bleeding appears too high for the expected benefit; rescue thrombolysis, or alternatively surgical embolectomy or catheter-directed treatment, should be reserved for patients who develop haemodynamic instability.^[1]

• In PEITHO, the mean time between randomisation and death or haemodynamic decompensation was 1.79 ± 1.60 days in the placebo (heparin-only) arm.^[1]

• Therefore, ESC 2019 says it appears reasonable to leave patients with intermediate-high-risk PE on LMWH over the first 2–3 days and ensure they remain stable before switching to oral anticoagulation.^[1]

^[5]

• The ESC adds that PEITHO findings do not support thrombolysis to prevent long-term sequelae after intermediate-risk PE, although clinical follow-up was available for only 62% of the population.^[1]
• The 2026 AHA/ACC text places PEITHO patients in its categories C3–D2 and notes that rescue thrombolysis was beneficial in patients who collapsed after initial anticoagulation alone.^[3]

AHA/ACC 2026: advanced therapy by category

Selected AHA/ACC 2026 rows on reperfusion (purpose clauses and category conditions as printed):^[3]

^[3]

• The AHA/ACC text names standard-dose rt-PA (100 mg in 2 hours) as the most commonly used agent, although there are no head-to-head trials to suggest superiority of any agent; it adds that evidence is emerging that lower-dose thrombolysis (25–50 mg rt-PA) may be as efficacious and associated with less major bleeding.^[3]
• Its overall view: the data suggest that patients with the highest PE mortality risk and lowest bleeding risk would obtain the greatest net benefit from thrombolysis, and those with the lowest mortality and highest bleeding risk would obtain the least benefit and are likely to be harmed.^[3]

Catheter-directed treatment and surgery (ESC narrative)

• Catheter-directed treatment uses a catheter passed into the pulmonary arteries via the femoral route for mechanical fragmentation, thrombus aspiration or, more commonly, a pharmacomechanical approach with in situ reduced-dose thrombolysis.^[1]
• Most knowledge comes from registries and pooled case series, in which overall procedural success (haemodynamic stabilisation, correction of hypoxia and survival to discharge) has reached 87%, although these results may be subject to publication bias.^[1]
• In one randomised trial of 59 patients with intermediate-risk PE, ultrasound-assisted thrombolysis was associated with a larger decrease in RV/LV diameter ratio at 24 h than heparin alone, without an increased risk of bleeding.^[1]
• The ESC says these results should be interpreted with caution, given the small numbers treated, the lack of studies directly comparing catheter-directed with systemic thrombolysis, and the lack of randomised data on clinical efficacy outcomes.^[1]
• Surgical embolectomy is usually carried out on cardiopulmonary bypass, without aortic cross-clamping or cardioplegic arrest, with incision of the two main pulmonary arteries; in a Society of Thoracic Surgeons database analysis of 214 patients having surgical embolectomy for high-risk (38) or intermediate-risk (176) PE, in-hospital mortality was 12%, and 32% in those with pre-operative cardiac arrest.^[1]

Low-risk PE: early discharge and home treatment

• ESC 2019: carefully selected patients with low-risk PE should be considered for early discharge and continuation of treatment at home, if proper outpatient care and anticoagulant treatment can be provided (Class IIa, level A).^[2]

• As a general rule, the ESC says early discharge should be considered when three sets of criteria are fulfilled: low risk of early PE-related death or serious complications; no serious comorbidity or aggravating condition mandating hospitalisation; and proper outpatient care and anticoagulant treatment can be provided, considering anticipated compliance and the healthcare and social infrastructure.^[1]

• Hestia: a bedside checklist integrating PE severity, comorbidity and feasibility of home treatment; if the answer to one or more questions is yes, the patient cannot be discharged early. In a single-arm management trial, the 3-month rate of recurrent VTE was 2.0% (0.8–4.3%) in patients discharged within 24 h.^[1]

• ESC 2019 text, PESI: more standardised than Hestia but with a less comprehensive list of aggravating conditions; moreover, the sPESI excludes all patients with cancer from the low-risk category; if a PESI or sPESI approach is chosen, it must be combined with an assessment of the feasibility of early discharge and home treatment.^[1]

• ESC 2019 text: both the Hestia rule and the PESI or sPESI appear capable of reliably identifying patients at low PE-related risk and free of serious comorbidity, so either may be used for triage according to local experience and preference.^[1]

• ESC 2019 text: it is wise to exclude RV dysfunction and right heart thrombi if immediate or early (within the first 24–48 h) discharge is planned.^[1]

^[3]

• AHA/ACC 2026: for patients diagnosed with acute PE in a clinic or emergency department, it is reasonable to use a decision tool (options include the Hestia rule, the PESI and the sPESI) to identify suitability for outpatient treatment (COR 2a, LOE B-R).^[3]
• AHA/ACC 2026: for select patients in categories A and B diagnosed in a clinic or emergency department, outpatient treatment is a reasonable option compared with hospitalisation when the rate of 90-day adverse outcomes is low and it aligns with patient goals (COR 2a, LOE B-R); patients discharged must have immediate access to anticoagulant medication and rapid, reliable, expert follow-up.^[3]

Anticoagulation: drug choice and doses

• ESC 2019: in high or intermediate clinical probability, anticoagulation should be started while awaiting diagnostic results, usually with subcutaneous weight-adjusted LMWH or fondaparinux, or IV UFH.^[1]
• ESC 2019 text: based on pharmacokinetic data, an equally rapid anticoagulant effect can also be achieved with a NOAC, and phase III trials showed non-inferior efficacy of single-oral-drug strategies using higher doses of apixaban for 7 days or rivaroxaban for 3 weeks.^[1]
• ESC 2019: if anticoagulation is initiated parenterally, LMWH or fondaparinux is recommended over UFH for most patients (Class I, level A, acute-phase table for intermediate- or low-risk PE); its text explains that they carry a lower risk of inducing major bleeding and heparin-induced thrombocytopenia. ESC 2019 text: UFH is largely restricted to patients with overt haemodynamic instability or imminent haemodynamic decompensation in whom primary reperfusion treatment will be necessary (the formal rows: IV UFH including a weight-adjusted bolus is recommended without delay in suspected high-risk PE, and UFH including a weight-adjusted bolus without delay in high-risk PE; both Class I, level C); ESC 2019 text (no class row): UFH is also recommended for serious renal impairment (CrCl 30 mL/min or less) or severe obesity.^[1][2]

^{[1] [2] [3]}

• In a meta-analysis cited by the ESC, the primary efficacy outcome occurred in 2.0% with NOACs vs 2.2% with VKAs (RR 0.88, 95% CI 0.74–1.05), and major bleeding in 1.1% vs 1.7% (RR 0.60, 95% CI 0.41–0.88).^[1]

• ESC key message: prefer a NOAC over the traditional LMWH–VKA regimen unless the patient has contraindication(s) to this type of drug.^[1]

• AHA/ACC 2026: in acute PE without an absolute contraindication, anticoagulation is recommended to reduce recurrent VTE and death (COR 1, LOE B-R).^[3]

• AHA/ACC 2026, categories C1–E1 needing initial parenteral therapy: LMWH is recommended over UFH to reduce recurrent VTE and major bleeding (COR 1, LOE B-R).^[3]

• AHA/ACC 2026, patients eligible for oral anticoagulation: direct oral anticoagulants (DOACs) are recommended over VKAs, unless contraindicated, to prevent recurrent VTE and reduce major bleeding (COR 1, LOE B-R).^[3]

• AHA/ACC 2026, suspected PE in category C2 or higher with low bleeding risk: therapeutic anticoagulation may be beneficial when imaging is delayed or not immediately accessible (COR 2a, LOE C-EO).^[3]

• AHA/ACC 2026, established thrombotic antiphospholipid antibody syndrome: a VKA is recommended in preference to a direct oral anticoagulant (DOAC) for prevention of venous and arterial thrombosis (COR 1, LOE A).^[3]

• AHA/ACC 2026, mild-to-moderate (stage 2–3) chronic kidney disease needing oral anticoagulation: a DOAC is recommended over a VKA to reduce major bleeding (COR 1, LOE A).^[3]

• AHA/ACC 2026, most patients on weight-based LMWH: anti-Xa monitoring and dose adjustment is not indicated to reduce recurrent VTE or bleeding (COR 3: No Benefit, LOE A).^[3]

• In a randomised, open-label study in high-risk antiphospholipid syndrome (triple positive for lupus anticoagulant, anticardiolipin and anti-β2-glycoprotein I), rivaroxaban was associated with an increased rate of thromboembolic and major bleeding events compared with warfarin (HR for the composite primary outcome 6.7, 95% CI 1.5–30.5); ESC 2019 stated that, at the time of the guideline, NOACs were not an alternative to VKAs for patients with antiphospholipid syndrome.^[1]

How long to anticoagulate

• ESC 2019 draws these conclusions from landmark trials of different durations of VKA treatment for VTE: all patients with PE should receive 3 months or more of anticoagulation; after withdrawal, recurrence risk is expected to be similar whether anticoagulants are stopped after 3–6 months or after longer periods; and extended oral anticoagulant treatment reduces the risk of recurrent VTE by up to 90%, a benefit partially offset by the risk of bleeding.^[1]

• In patients who have had a PE, VTE more frequently recurs as PE, and the case fatality rate of recurrent VTE after a PE is twice that after DVT.^[1]

• In one study after a first PE, recurrence after stopping treatment was about 2.5% per year with transient risk factors vs 4.5% per year when PE occurred without known cancer, known thrombophilia or any transient risk factor.^[1]

• ESC 2019 regimen and duration rows for patients without cancer; for the rows where extension should be considered, the patient’s bleeding risk should be assessed to identify and treat modifiable bleeding risk factors, and it may influence decision-making on the duration and regimen/dose of anticoagulant treatment; for therapeutic decisions in specific clinical situations, the rows where extension should be considered refer to ESC supplementary table 9:^[2]

^[2]

Risk factors for VTE as categorised in the 2026 AHA/ACC guideline (Table 9):^[3]

^[3]

• AHA/ACC 2026: after a first PE with no major reversible risk factor, continuing anticoagulation beyond the initial 3–6 months into the extended phase (without an anticipated stop date) is beneficial to prevent recurrent VTE (COR 1, LOE A).^[3]

• AHA/ACC 2026, first PE due to a major reversible risk factor: stopping at the end of the initial 3–6 months is recommended over continuing, to optimise the net clinical benefit (COR 1, LOE B-NR).^[3]

• AHA/ACC 2026, first PE due to a minor reversible risk factor: shared decision-making about stopping anticoagulation at the end of the initial treatment phase (3–6 months) versus continuing into the extended treatment phase is reasonable, to optimise the net clinical benefit of recurrent VTE versus bleeding (COR 2a, LOE B-NR).^[3]

• AHA/ACC 2026, extended phase: a DOAC, unless contraindicated, is recommended over a VKA to reduce bleeding (COR 1, LOE A), and half-dose apixaban or rivaroxaban is recommended to reduce bleeding (COR 1, LOE A).^[3]

• People who develop VTE without an identifiable risk factor have a high risk of recurrence after stopping anticoagulation (about 30%–40% at 10 years, per the AHA/ACC text).^[3]

• ESC 2019 text: the risk of major bleeding is higher in the first month of anticoagulant treatment, and then declines and remains stable over time; based on the evidence available at the time of the guideline, ESC risk factors include advanced age (particularly over 75 years), previous bleeding (if not associated with a reversible or treatable cause) or anaemia, active cancer, previous stroke (haemorrhagic or ischaemic), chronic renal or hepatic disease, concomitant antiplatelet therapy or non-steroidal anti-inflammatory drugs (to be avoided, if possible), other serious acute or chronic illness, and poor anticoagulation control.^[1]

• ESC 2019 text: thrombophilia testing (including antiphospholipid antibodies and lupus anticoagulant) may be considered when VTE occurs at a young age (e.g. under 50 years) without an otherwise identifiable risk factor, especially with a strong family history of VTE.^[1]

Cancer-associated PE

• Overall, LMWHs decreased recurrent VTE by 40% with major bleeding similar to VKAs, but only 3–9% of patients in the phase III NOAC treatment trials had cancer.^[1]
• In an open-label trial of edoxaban vs dalteparin in 1050 patients with cancer-associated thrombosis, edoxaban (60 mg once daily, reduced to 30 mg for moderate renal impairment, low body weight or a strong P-glycoprotein inhibitor) was started after 5 days of LMWH.^[1]
• Edoxaban was non-inferior for recurrent VTE or major bleeding over 12 months, but major bleeding was 6.9% vs 4.0%, a difference that appears to have been mainly accounted for by gastrointestinal cancer.^[1]
• A randomised, open-label pilot trial of rivaroxaban vs dalteparin in 406 patients with VTE and cancer observed a significant decrease in the risk of recurrent VTE with rivaroxaban (HR 0.43, 95% CI 0.19–0.99); the 6-month cumulative major bleeding rate was 6% vs 4% (HR 1.83, 95% CI 0.68–4.96) and clinically relevant non-major bleeding 13% vs 4%.^[1]

ESC 2019 rows for PE in patients with active cancer:^[2]

^[2]

• ESC 2019 says patients with acute PE and cancer, particularly gastrointestinal cancer, should be encouraged to continue LMWH for 3–6 months or more, as should patients in whom oral treatment is unfeasible because of intake or absorption problems and those with severe renal impairment; in all other cases, especially in patients with an anticipated low risk of bleeding and without gastrointestinal tumours, the choice between LMWH and edoxaban or rivaroxaban is left to the discretion of the physician and the patient’s preference.^[1]

• AHA/ACC 2026: for patients with PE and cancer offered anticoagulation into the extended phase, either a DOAC or LMWH is recommended over a VKA to reduce recurrent VTE (COR 1, LOE A).^[3]

• AHA/ACC 2026: in cancer with recurrent PE despite therapeutic LMWH, dose escalation of LMWH by 20% to 25% is reasonable to prevent future recurrent PE (COR 2a, LOE B-NR).^[3]

• Occult cancer, ESC 2019 text: the search after VTE may be restricted to careful history taking, physical examination, basic laboratory tests and a chest X-ray (if no CTPA was performed).^[1]

• Occult cancer, AHA/ACC 2026: in acute PE without associated identifiable risk factors, a thorough history, physical examination and age-appropriate cancer screening should be obtained to diagnose undetected cancer (COR 1, LOE A); in acute PE generally, routine imaging with CT or positron emission tomography-CT (PET-CT) is not recommended to diagnose undetected cancer (COR 3: No Benefit, LOE A).^[3]

Vena cava filters and PE response teams

• ESC 2019: inferior vena cava (IVC) filters should be considered in acute PE with absolute contraindications to anticoagulation (Class IIa, level C) and in PE recurrence despite therapeutic anticoagulation (Class IIa, level C); routine use of IVC filters is not recommended (Class III, level A).^[2]
• AHA/ACC 2026: in PE when anticoagulation cannot be tolerated, IVC filters can be useful to reduce the short-term incidence of recurrent PE (COR 2a, LOE B-R), when anticoagulation cannot be tolerated but a filter is deemed necessary, retrievable IVC filters are recommended over permanent filters to reduce the short-term incidence of recurrent PE while minimising long-term adverse outcomes (COR 1, LOE B-R), and routine filter placement in therapeutically anticoagulated patients should not be performed (COR 3: Harm, LOE A).^[3]
• PREPIC-2 randomised 399 patients with PE and venous thrombosis to anticoagulation with or without a retrievable vena cava filter; the rate of recurrent VTE was low in both groups and did not differ between them.^[1]
• ESC 2019: set-up of a multidisciplinary team and programme for high- and (in selected cases) intermediate-risk PE should be considered, depending on the resources and expertise available in each hospital (Class IIa, level C).^[2]
• AHA/ACC 2026: a multidisciplinary pulmonary embolism response team (PERT) assessment is recommended for patients at increased risk of adverse outcomes (i.e. categories C–E) to improve in-hospital clinical care delivery (COR 1, LOE B-NR); its footnote adds that categories A or B with multiple comorbidities may also benefit from a PERT (e.g. category B with intracranial haemorrhage).^[3]

Special populations

Pregnancy (pointers)

• D-dimer levels continuously increase during pregnancy and are above the rule-out threshold in almost one-quarter of pregnant women in the third trimester.^[1]
• In a prospective management study of 498 women with suspected PE during pregnancy, a pregnancy-adapted YEARS algorithm combined with D-dimer ruled out PE without CTPA in women deemed to be at low PE risk; at 3 months, one woman in whom PE had been excluded on the basis of the algorithm developed a popliteal DVT (0.21%, 95% CI 0.04–1.2) and no women developed PE.^[1]

Selected ESC 2019 pregnancy rows:^[2]

^[2]

• LMWH is the ESC treatment of choice for PE in pregnancy; in contrast to VKAs and NOACs, it does not cross the placenta and so does not confer a risk of fetal haemorrhage or teratogenicity. Anticoagulation should continue for 6 weeks or more after delivery with a minimum overall duration of 3 months, and LMWH and warfarin can be given to breastfeeding mothers.^[1]
• ESC 2019 text: thrombolytic treatment should not be used peri-partum except in life-threatening PE; typically, UFH is used in the acute treatment of high-risk PE in pregnancy.^[1]
• AHA/ACC 2026: in pregnant patients with acute PE who can receive anticoagulation, either LMWH or UFH is recommended to prevent recurrent VTE (COR 1, LOE C-LD), and in pregnant patients with acute PE, DOACs and warfarin are potentially harmful and may result in miscarriages or fetal anomalies (COR 3: Harm, LOE C-LD).^[3]
• AHA/ACC 2026: in pregnant adults, it may be reasonable to use pregnancy-adapted YEARS criteria to identify those who do not need imaging (COR 2b, LOE B-NR).^[3]

Older adults, obesity and kidney disease

• D-dimer specificity in suspected PE falls steadily with age, to about 10% in patients over 80 years, and age-adjusted cut-offs may improve the performance of D-dimer testing in the elderly.^[1]
• ESC 2019 text (no class row): UFH is also recommended for patients with serious renal impairment (CrCl 30 mL/min or less) or severe obesity.^[1]
• See the NOAC renal footnote above for CrCl thresholds by drug (ESC 2019), and the AHA/ACC 2026 row: in mild-to-moderate (stage 2–3) chronic kidney disease with acute PE requiring oral anticoagulant therapy, a DOAC is recommended over a VKA to reduce major bleeding (COR 1, LOE A).^[2][3]

Complications and follow-up, including CTEPH

• Chronic thromboembolic pulmonary hypertension (CTEPH) is caused by persistent obstruction of pulmonary arteries by organised thrombi, with flow redistribution and secondary remodelling of the pulmonary microvascular bed.^[1]

• Its cumulative incidence has been reported between 0.1% and 9.1% in the first 2 years after symptomatic PE; in a Swiss screening study of 508 patients over 2 years, the 2-year cumulative incidence was 0.79%.^[1]

• The ESC diagnosis requires findings after at least 3 months of effective anticoagulation: mean PAP of 25 mmHg or more with pulmonary arterial wedge pressure of 15 mmHg or less at right heart catheterisation, in a patient with mismatched perfusion defects on V/Q scan.^[1]

• Persisting or deteriorating dyspnoea and poor physical performance are frequently present 6 months to 3 years after PE.^[1]

• ESC 2019 text: the patency of the pulmonary arterial bed is restored in the majority of survivors within the first few months, so no routine follow-up CTPA is needed in such patients.^[1]

• ESC 2019: routine clinical evaluation 3–6 months after acute PE is recommended (Class I, level B), for symptoms suggesting recurrence, bleeding, malignancy, or persistent or new-onset exercise limitation, and to decide on extension of anticoagulant treatment.^[2]

• ESC 2019: an integrated model of care (hospital specialists, appropriately qualified nurses and primary care physicians) is recommended to ensure optimal transition from hospital to community care (Class I, level C).^[2]

• ESC 2019: in symptomatic patients with mismatched perfusion defects persisting on V/Q scan (alternatively, dual-energy CT may be used, if appropriate expertise and resources are available on-site) beyond 3 months, referral to a pulmonary hypertension/CTEPH expert centre is recommended after taking into account echocardiography, natriuretic peptide levels and/or cardiopulmonary exercise testing (Class I, level C).^[2]

• ESC 2019: further diagnostic evaluation should be considered with persistent or new-onset dyspnoea or exercise limitation (Class IIa, level C), and may be considered in asymptomatic patients with risk factors for CTEPH (Class IIb, level C).^[2]

• ESC follow-up pathway: in persisting dyspnoea and poor physical performance, TTE should be considered to assess the probability of (chronic) pulmonary hypertension and thus possible CTEPH; a high echocardiographic probability of pulmonary hypertension, or intermediate probability with raised NT-proBNP or CTEPH risk factors, should prompt consideration of a V/Q scan, and mismatched perfusion defects on the V/Q scan indicate referral to a pulmonary hypertension or CTEPH expert centre for further diagnostic work-up.^[1]

• AHA/ACC 2026 uses the term chronic thromboembolic pulmonary disease (CTEPD). Clinical follow-up within the first week of discharge is beneficial to provide patient education, address barriers to anticoagulation, ensure adherence and detect bleeding complications (COR 1, LOE C-LD), and patients should have a visit at or before 3 months to discuss the duration of anticoagulation, review the need for further testing and assess persistent PE-related symptoms (COR 1, LOE C-EO).^[3]

• AHA/ACC 2026: patients should be asked about PE-related symptoms and functional limitation at every visit for at least 1 year to screen for CTEPD or other causes (COR 1, LOE C-LD); with ongoing dyspnoea and/or functional impairment after 3 months or more of therapeutic anticoagulation, a diagnostic evaluation for CTEPD is recommended (COR 1, LOE B-NR).^[3]

• AHA/ACC 2026: for patients undergoing diagnostic evaluation for CTEPD, it is reasonable to obtain both TTE and a lung perfusion scan (planar V/Q, V/Q SPECT or SPECT/CT) over an echocardiogram alone, to exclude CTEPD or determine whether additional diagnostic testing is needed (COR 2a, LOE B-NR; footnote: in a patient with a normal echocardiogram at the time of acute PE, a repeated echocardiogram at 3 to 6 months is low yield and may be omitted); after acute PE with resolution of symptoms and low suspicion for CTEPD, a follow-up CTPA or lung perfusion scan is not beneficial to assess the degree of thrombus resolution (COR 3: No benefit, LOE B-NR); for CTEPD with pulmonary hypertension, referral to a centre with expertise in managing CTEPD is recommended to optimise evaluation and management (COR 1, LOE C-LD).^[3]

Prognosis and disposition

• ESC 2019 recommends initial risk stratification by haemodynamic instability to identify patients at high risk of early mortality (Class I, level B); in ESC Table 7, an sPESI of 0 carries a 30-day mortality risk of 1.0% and an sPESI of 1 point or more 10.9%.^[1][2]
• In prospective cohorts of patients treated at home, with or without a short admission, 3-month rates of recurrence, major bleeding and death were 1.75%, 1.43% and 2.83%.^[1]
• ESC key message: if you suspect acute PE, start anticoagulation as soon as possible while the work-up is ongoing, unless the patient is bleeding or has absolute contraindications.^[1]

Evidence, guidelines and regional differences

^{[1] [2] [3]}

In Australia and New Zealand

• A working group of experts completed an evidence-based guideline for the diagnosis and management of DVT and PE on behalf of the Thrombosis and Haemostasis Society of Australia and New Zealand (THANZ).^[8]

• The THANZ guideline summary’s main recommendations state that the diagnosis of VTE should be established with imaging and may be excluded using clinical prediction rules combined with D-dimer testing.^[8]

• Proximal DVT or PE caused by a major surgery or trauma that is no longer present: anticoagulation for 3 months.^[8]

• Proximal DVT or PE that is unprovoked or associated with a transient (non-surgical) risk factor: anticoagulation for 3–6 months.^[8]

• Proximal DVT or PE that is recurrent (two or more) and provoked by active cancer or antiphospholipid syndrome: extended anticoagulation.^[8]

• For extended therapy, therapeutic or low-dose direct oral anticoagulants (DOACs) can be prescribed and are preferred over warfarin in the absence of contraindications; routine thrombophilia testing is not indicated.^[8]

• Thrombolysis or a suitable alternative is indicated for massive (haemodynamically unstable) PE, and most patients with acute VTE should be treated with a factor Xa inhibitor and assessed for extended anticoagulation.^[8]

• The THANZ guideline summary uses the term unprovoked, which ESC 2019 avoids, so name the source when quoting either.^[1][8]

• For pregnancy, the Society of Obstetric Medicine of Australia and New Zealand (SOMANZ) publishes a position statement on PE in pregnancy and post-partum.^[9]

• A single-centre Australian group, developing a consensus-based, evidence-informed algorithm for PE risk stratification and management at its institution, noted that catheter-based therapy is becoming commonplace internationally but that there is no published guidance on a standard approach to when to use these therapies in the Australian setting.^[10]

Exam pearls

• High-risk PE = haemodynamic instability: cardiac arrest, obstructive shock, or persistent hypotension (systolic under 90 mmHg, or a drop of 40 mmHg or more, for over 15 min, not caused by new-onset arrhythmia, hypovolaemia or sepsis) (ESC 2019).^[1]
• Within the ESC 2019 intermediate-risk group: intermediate-high = both RV dysfunction and a raised cardiac biomarker (particularly a positive troponin); intermediate-low = the RV appears normal and/or biomarkers are normal.^[1]
• ESC 2019, suspected PE without haemodynamic instability: D-dimer measurement is not recommended with high clinical probability (Class III, level A); with low or intermediate probability, or PE-unlikely, as an alternative to the fixed D-dimer cut-off, a negative age-adjusted D-dimer (age × 10 μg/L, over 50 years) should be considered for excluding PE (Class IIa, level B).^[2]
• YEARS (ESC footnote, which says these cut-offs may be used): PE is excluded with no clinical items and D-dimer under 1000 µg/L, or with one or more items and D-dimer under 500 µg/L.^[2]
• PEITHO (randomised, double-blind; tenecteplase plus heparin vs placebo plus heparin in normotensive intermediate-risk PE with RV dysfunction on echocardiography or CT and a positive troponin I or T): death or haemodynamic decompensation within 7 days 2.6% vs 5.6%; extracranial bleeding 6.3% vs 1.2%; stroke 2.4% vs 0.2%.^[5]
• ESC 2019: rescue thrombolysis is recommended for haemodynamic deterioration on anticoagulation (Class I, level B); routine primary thrombolysis is not recommended in intermediate- or low-risk PE (Class III, level B; footnote: the risk-to-benefit ratios of surgical embolectomy or catheter-directed procedures have not yet been established in intermediate- or low-risk PE).^[2]
• NOACs are not recommended in severe renal impairment, pregnancy and lactation, or antiphospholipid antibody syndrome (ESC 2019, Class III, level C); the row footnote defines the renal limits by drug: dabigatran is not recommended with CrCl under 30 mL/min; edoxaban 30 mg once daily at CrCl 15–50 mL/min and not recommended under 15 mL/min; rivaroxaban and apixaban with caution at 15–29 mL/min and not recommended under 15 mL/min.^[2]
• Active cancer (ESC 2019): weight-adjusted subcutaneous LMWH should be considered for the first 6 months over VKAs (Class IIa, level A); edoxaban (Class IIa, level B) or rivaroxaban (Class IIa, level C) should be considered as alternatives to weight-adjusted subcutaneous LMWH in patients without gastrointestinal cancer.^[2]

References10ShowHide

1. [1]Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J, 2020.PMID 31504429
2. [2]Konstantinides SV, Meyer G, Becattini C, 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 Respir J, 2019.PMID 31473594
3. [3]Creager MA, Barnes GD, Giri J, et al. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2026.PMID 41712898
4. [4]Creager MA, Barnes GD, Giri J, et al. Correction to: 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/ SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 2026.PMID 42441758
5. [5]Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med, 2014.PMID 24716681
6. [6]van der Hulle T, Cheung WY, Kooij S, et al. Simplified diagnostic management of suspected pulmonary embolism (the YEARS study): a prospective, multicentre, cohort study. Lancet, 2017.PMID 28549662
7. [7]Righini M, Van Es J, Den Exter PL, et al. Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA, 2014.PMID 24643601
8. [8]Tran HA, Gibbs H, Merriman E, et al. New guidelines from the Thrombosis and Haemostasis Society of Australia and New Zealand for the diagnosis and management of venous thromboembolism. Med J Aust, 2019.PMID 30739331
9. [9]Lowe SA, Barrett HL, Cutts BA, et al. Update on pulmonary embolism in pregnancy and post-partum: The Society of Obstetric Medicine of Australia and New Zealand Position Statement on Pulmonary Embolism in Pregnancy and Post-partum. Aust N Z J Obstet Gynaecol, 2021.PMID 34435660
10. [10]Dunn A, Lee E, Harrison B, et al. Multidisciplinary management of intermediate and high-risk pulmonary embolism in the era of mechanical thrombectomy: a local practice guideline. Intern Med J, 2026.PMID 41454751