2026 AHA/ACC Pulmonary Embolism Guidelines: Key Recommendations
The 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN guideline introduces a new severity classification system—the AHA/ACC Acute Pulmonary Embolism Clinical Categories—to enhance precision in risk stratification and guide evidence-based therapeutic decisions. 1, 2
New Risk Stratification Framework
The 2026 guideline replaces older terminology ("massive," "submassive," "non-massive") with a clinical category system that focuses on early PE-related mortality risk rather than anatomical clot burden. 1, 2, 3
High-risk PE is defined by shock, cardiac arrest, obstructive shock, or persistent hypotension (systolic BP < 90 mmHg for ≥15 minutes not caused by arrhythmia, hypovolemia, or sepsis), carrying >15% early mortality. 1, 2, 4
Intermediate-risk PE comprises hemodynamically stable patients with evidence of right ventricular (RV) dysfunction on imaging (RV/LV ratio >0.9 on CTPA or RV dilatation on echo) and/or elevated cardiac biomarkers (troponin, BNP/NT-proBNP), with 3-15% mortality. 1, 2, 4
Low-risk PE includes hemodynamically stable patients without RV dysfunction or biomarker elevation, with <1% mortality risk. 1, 2, 4
Diagnostic Approach
Clinical Probability Assessment
Use validated prediction rules (Wells or revised Geneva score) to stratify every patient into low, intermediate, or high clinical probability before ordering any tests. 4, 5
The revised Geneva score assigns points for: prior VTE (3 points), heart rate 75-94 bpm (3 points) or ≥95 bpm (5 points), recent surgery/fracture (2 points), hemoptysis (2 points), active cancer (2 points), unilateral leg pain (3 points), pain on deep venous palpation with unilateral edema (4 points), age >65 years (1 point). 5
Immediately assess for hemodynamic instability to identify high-risk PE requiring urgent reperfusion therapy. 4, 1, 2
D-dimer Testing
Measure D-dimer only in patients with low or intermediate clinical probability using highly sensitive assays; never measure D-dimer in high-probability patients because a normal result does not safely exclude PE. 4, 5
Age-adjusted D-dimer cutoffs (age × 10 µg/L for patients >50 years) maintain >97% sensitivity while significantly increasing specificity. 6
Imaging Strategy
Computed tomography pulmonary angiography (CTPA) is the first-choice imaging test for hemodynamically stable patients with elevated D-dimer or high clinical probability. 4, 5
Accept a PE diagnosis when CTPA shows segmental or more proximal filling defects in patients with intermediate or high clinical probability. 4, 5
Reject a PE diagnosis when CTPA is normal in patients with low or intermediate clinical probability. 4, 5
Ventilation-perfusion (V/Q) scintigraphy is a valid alternative when CTPA is contraindicated (contrast allergy, renal impairment); a normal perfusion scan excludes PE. 4, 5
Do not perform CT venography as an adjunct to CTPA—it adds radiation without diagnostic benefit. 4, 7
Identification of proximal deep-vein thrombosis by compression ultrasound in a patient with suspected PE confirms VTE and justifies anticoagulation. 4, 5
Treatment of High-Risk PE
Immediate Anticoagulation
Initiate intravenous unfractionated heparin (UFH) immediately with a weight-adjusted bolus (80 U/kg, typically 5,000-10,000 units) followed by continuous infusion (400-600 units/kg/day or 30,000-40,000 units/24 hours), even before imaging confirmation. 4, 7
Target aPTT 1.5-2.5 times control, measured 4-6 hours after treatment initiation. 4
Reperfusion Therapy
Administer systemic thrombolytic therapy immediately to all high-risk PE patients without high bleeding risk—this is a Class I, Level A recommendation that reduces mortality (OR 0.45; 95% CI 0.22-0.92). 7, 3
Alteplase dosing: 100 mg IV infused over 2 hours, or 0.6 mg/kg over 15 minutes (maximum 50 mg) in cardiac arrest situations. 7, 4
Major bleeding occurs in 21.9% of thrombolysis patients versus 11.9% with heparin alone, but the mortality benefit outweighs bleeding risk in high-risk PE. 7
Surgical pulmonary embolectomy is indicated when thrombolysis is absolutely contraindicated or fails to improve hemodynamics within one hour—mortality has decreased with modern techniques. 7, 3
Catheter-based embolectomy or thrombus fragmentation may be considered when neither thrombolysis nor surgery is feasible, though evidence is limited. 7, 3
Veno-arterial ECMO can bridge patients with profound circulatory collapse to definitive reperfusion. 7
Hemodynamic Support
Use norepinephrine (or vasopressin) for hypotension; dobutamine (or dopamine) for low cardiac output with normal blood pressure. 7, 4
Avoid aggressive fluid boluses >500 mL—they worsen RV afterload and can precipitate RV failure. 7, 4
Avoid diuretics and vasodilators as they may worsen cardiovascular collapse. 4
Treatment of Intermediate- and Low-Risk PE
Anticoagulation Strategy
Start anticoagulation immediately in patients with high or intermediate clinical probability while diagnostic work-up proceeds. 4, 7
For hemodynamically stable patients, prefer low-molecular-weight heparin (LMWH) or fondaparinux over UFH. 4, 7
UFH is reserved for severe renal impairment (CrCl <30 mL/min), severe obesity, or when reperfusion therapy is planned. 7
Systemic thrombolysis is not routinely recommended for intermediate- or low-risk PE (Class III, Level A). 7, 4
Rescue thrombolysis may be used only for patients who deteriorate hemodynamically despite adequate anticoagulation. 7, 4
Oral Anticoagulant Selection
For all eligible patients, a direct oral anticoagulant (NOAC)—apixaban, rivaroxaban, edoxaban, or dabigatran—is preferred over warfarin (Class I, Level A). 7, 4
NOAC contraindications include: CrCl <25-30 mL/min, antiphospholipid antibody syndrome, pregnancy/lactation, and for edoxaban, CrCl >95 mL/min. 7, 4
When warfarin is chosen, overlap with parenteral anticoagulation for ≥5 days and until INR 2.0-3.0 (target 2.5) on two consecutive readings ≥24 hours apart. 7, 4
Duration of Anticoagulation
All patients require a minimum of 3 months of therapeutic anticoagulation (Class I, Level A). 7, 4
Provoked PE (major transient risk factor such as surgery, trauma, immobilization, pregnancy): stop anticoagulation after 3 months (Class I, Level A). 7, 4
Unprovoked PE: continue indefinitely if bleeding risk is low-to-moderate; annual recurrence risk exceeds 5% and outweighs bleeding risk (Class I, Level A). 7, 4
Recurrent VTE (≥1 prior episode not related to transient risk factor): continue anticoagulation indefinitely (Class I, Level A). 7, 4
Antiphospholipid antibody syndrome: continue vitamin K antagonist indefinitely; NOACs are contraindicated (Class I, Level A). 7, 4
Active cancer: continue anticoagulation indefinitely with LMWH or a NOAC (edoxaban or rivaroxaban preferred). 7
After the first 6 months, reduced-dose apixaban (2.5 mg twice daily) or rivaroxaban (10 mg daily) may be used for extended anticoagulation. 4
Outpatient Management
Patients classified as PESI class I-II, sPESI = 0, or meeting Hestia criteria are suitable for outpatient treatment. 7, 6
Exclusion criteria for outpatient care: hemodynamic instability (HR >110 bpm, SBP <100 mmHg), SpO₂ <90% on room air, active bleeding or high bleeding risk, severe pain requiring opioids, advanced chronic kidney disease (eGFR <30 mL/min), severe liver disease, or lack of adequate home support. 7
Inferior Vena Cava (IVC) Filters
Routine placement of IVC filters is not recommended (Class III, Level A). 7, 4
Retrievable filters may be used only when: (a) anticoagulation is absolutely contraindicated, (b) anticoagulation cannot be initiated within 1 month of symptomatic VTE, or (c) recurrent PE occurs despite therapeutic anticoagulation. 7
Special Populations
Pregnancy
Therapeutic fixed-dose LMWH (weight-adjusted based on early-pregnancy weight) is the anticoagulant of choice; NOACs are absolutely contraindicated (Class I, Level A). 7, 4
Thrombolysis in pregnancy is reserved for life-threatening hemodynamic instability due to high maternal hemorrhage risk. 7
Renal Impairment
When CrCl <30 mL/min, NOACs are contraindicated; patients should be switched to warfarin with target INR 2.0-3.0. 4, 6
UFH is the only parenteral anticoagulant recommended when CrCl <30 mL/min, because LMWH and fondaparinux accumulate. 4
Incidental PE
Incidental or subsegmental PE should be anticoagulated unless contraindicated; recurrence risk equals that of symptomatic PE. 7
Outpatient management is appropriate for low-risk incidental PE. 7
Follow-Up and CTEPH Screening
All patients must be re-evaluated at 3-6 months after acute PE to assess for chronic complications and decide on continued anticoagulation. 7, 4
Implement an integrated care model to ensure optimal transition from hospital to ambulatory care. 4
If persistent or new-onset dyspnea or functional limitation is present at 3-6 months, perform V/Q scintigraphy to detect mismatched perfusion defects suggestive of chronic thromboembolic pulmonary hypertension (CTEPH). 7, 4
Refer symptomatic patients with persistent perfusion defects to a specialized CTEPH center, incorporating echocardiography, natriuretic peptide levels, and/or cardiopulmonary exercise testing. 7, 4
Schedule regular follow-up visits at yearly intervals for patients on extended anticoagulation to reassess drug tolerance, adherence, hepatic/renal function, and bleeding risk. 7, 4
Critical Pitfalls to Avoid
Never delay anticoagulation in high- or intermediate-probability PE while awaiting imaging confirmation. 7, 4
Never measure D-dimer in high-clinical-probability patients; proceed directly to CTPA. 7, 4
Never use NOACs in severe renal impairment (CrCl <25-30 mL/min) or antiphospholipid antibody syndrome; warfarin is mandatory. 7, 4
Never withhold thrombolysis in massive PE solely because of relative contraindications; the mortality risk of untreated PE outweighs bleeding risk. 7
Never lose patients to follow-up after acute PE; routine reassessment at 3-6 months is essential for detecting CTEPH and guiding anticoagulation duration. 7, 4
Never ignore persistent dyspnea, as it may indicate CTEPH requiring specialized evaluation. 4