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Brett S Bernstein
Cardiology Registrar, West Middlesex University Hospital
Invasive Management of Acute Pulmonary Embolism: An Interventional Fellow’s Guide
Setting the Scene
A 65-year-old gentleman with a past medical history of hypercholesterolaemia and stage 3 chronic kidney disease arrives in the Emergency Department with pleuritic chest pain and acute shortness of breath, 12 hours after a flight from South Africa. His heart rate is 100 (sinus rhythm) with a BP of 100/60. He is requiring 4l/min of oxygen to maintain sats of 94%.
Blood tests are not suggestive of infection. Troponin was elevated at 100ng/l and D dimer was 5000ng/l. A bedside echo shows mild right ventricular impairment, and a CTPA confirms a solitary large right pulmonary artery embolism.
Risk Stratification
The above clinical presentation and initial investigations are not uncommon to clinicians working in A&E and on the acute medical take.
Safe, effective, and resource-efficient treatment of pulmonary embolism (PE) is achieved after risk-stratification of the individual patient.
Three common tools for assessing the risk of a patient with a PE are detailed below.
Pulmonary Embolism Severity Index (PESI)1
The PESI score, developed by Aujesky et al. in 2005, uses 11 clinical characteristics to risk stratify patients into five groups (I-V; see below table). Based on 15,531 patients, these 5 groups had their 30 day mortality charted, with Group I patients demonstrating a mortality of 0-1.6%, and Group V patients showing a mortality of 10-24.5%.
| Predictors | Points Assigned |
| Demographic characteristics | |
| Age, per years | Age, in years |
| Male sex | +10 |
| Comorbid illnesses | |
| Cancer | +30 |
| Heart failure | +10 |
| Chronic lung disease
|
+10 |
| Clinical findings | |
| Pulse ⩾ 110/min | +20 |
| Systolic blood pressure < 100 mmHg | +30 |
| Respiratory rate ⩾ 30/min | +20 |
| Temperature < 36°C | +20 |
| Altered mental status | +60 |
| Arterial oxygen saturation < 90% | +20 |
Points assignments correspond with the following risk classes: 0-65 class I, very low risk; 66–85 class II, low risk; 86–105 class III, intermediate risk; 106–125 class IV, high risk; > 125 class V, very high risk1. The PESI score has been extensively validated2,3 and used as the basis for a trial looking at suitability of treatment at home for low risk patients4.
Simplified Pulmonary Embolism Severity Index (sPESI)5
In 2010, Jimenez et al used a Spanish outpatient cohort of 995 patients to derive a simplified PESI score, by discarding variables that did not reach statistical significance in their dataset with respect to 30-day mortality. This was then validated in an external dataset of 7106 patients. The prognostic accuracy of the SPESI score was similar to that of the PESI score (AUC 0.75).
The sPESI score gives one point each for presence of the following variables: Age >80, history of cancer, chronic cardiopulmonary disease, HR ⩾ 110 bpm, SBP <100 mmHg, arterial oxygen saturations < 90%.
Whereas a sPESI score of 0 gives a 30 day mortality risk of 1%, a score of ⩾1 indicates a 30 day mortality risk of 10.9%5. The score has been validated in observational cohort studies2,3.
European Society of Cardiology (ESC) Prognostic Assessment Strategy6
The 2019 ESC guidelines for diagnosis and management of acute PE introduces a separate classification system, visualised below6.
| Early mortality risk | Indicators of risk | |||
| Haemodynamic instability | Clinical parameters of PE severity and/or comorbidity (PESI class III–V or sPESI ≥1) | RV dysfunction on TTE/ CTPA | Elevated troponin | |
| High | + | (+) | + | (+) |
| Intermediate–high | – | + | + | + |
| Intermediate–low | – | + | One (or none) positive
|
|
| Low | – | – | – | Assessment optional; if assessed, negative |
Risk-Based Approach to Treatment
For those in the “high” risk group above, who by definition demonstrate haemodynamic instability, the guidelines suggest urgent systemic thrombolysis (eg alteplase bolus) and close haemodynamic monitoring6. Commonly these patients are commenced on an unfractionated heparin infusion several hours later, before eventually transitioning to a low-molecular weight heparin (LMWH), or indeed a direct oral anticoagulant (DOAC), for their further pharmacological management. Those in the “low” risk group are generally commenced immediately on a DOAC and discharged.
The “intermediate” risk group, by definition without haemodynamic instability, require close monitoring to detect any deterioration. Systemic thrombolysis is generally avoided due to the unacceptable risk of life-threatening complications compared to the expected benefits7. Conventionally, these patients receive 2-3 days of daily LMWH subcutaneous injections before transitioning to a DOAC.
“Intermediate” (and more commonly “intermediate-high”) risk patients who begin to develop haemodynamic instability, and “high” risk patients in whom thrombolysis is contra-indicated, can be considered for catheter-based therapies to treat their PE. Increasingly these decisions are aided by dedicated multi-disciplinary Pulmonary Embolism Response Teams [PERT]8.
Catheter-Based Therapies
The following table, based on a supplementary figure from the ESC 2019 guidelines6, details the currently available catheter directed therapies.
| Catheter interventions with thrombolysis | Catheter interventions without thrombolysis | ||
| Technique | Device examples | Technique | Device examples |
| Catheter-directed thrombolysis | UniFuse (AngioDynamics, Latham, NY) Cragg-McNamara (ev3 Endovascular, Plymouth, MN), 4–5 F infusion catheters with 10–20 cm infusion length |
Aspiration thrombectomy | Aspirex 8 F or 10 F catheter (Straub Medical, Switzerland): rotational thrombectomy AngioVac suction cannula (AngioDynamics, Latham, NY): veno-venous bypass system with 26 F access for inflow and 16–20 F access for outflow Indigo Mechanical Thrombectomy System (Penumbra, Alameda, CA): 8 F vacuum-assisted aspiration with mechanical clot engagement Sheath with detachable haemostatic valve 8–9 F (Argon Medical Devices, Athens, TX), multi-purpose guide catheter (8–9 F), aspiration syringe (60 mL) |
| Ultrasound-assisted catheter-directed thrombolysis | EkoSonic 5.2, 12 cm treatment zone device (EKOS, Bothell, WA) | Mechanical thrombectomy | FlowTriever (Inari Medical, Irvine, CA): 20 F device with three self-expanding nitinol discs entrapping the thrombus with simultaneous aspiration |
| Rheolytic thrombectomy plus catheter-directed thrombolysis | AngioJet 6 F PE thrombectomy with Power Pulse thrombolysis (Boston Scientific, Minneapolis, MN) | Rheolytic thrombectomy | AngioJet 6 F PE catheter (Boston Scientific, Minneapolis, MN) |
| Combined techniques | For example, pigtail fragmentation (5 F) plus AngioJet 6 F PE thrombectomy with Power Pulse thrombolysis | Thrombus fragmentation Combined techniques |
Pigtail catheter (5–6 F) or peripheral balloon catheters (6–7 F, balloon diameter 5–10 mm) Pigtail fragmentation (5 F) plus thrombectomy with Aspirex 8/10 F |
In the UK, where available, these interventions are carried out by both interventional cardiologists and interventional radiologists.
With respect to catheter interventions with thrombolysis, the most commonly used technique in the UK is the ultrasound-assisted catheter directed thrombolysis (EKOS). In most cases two catheters are used (one for each lung) necessitating bilateral 8Fr femoral venous access. For each lung, an exchange length guidewire is advanced across the obstructing embolus in the pulmonary artery, before the infusion catheter is backloaded and advanced so that the tip is 1cm beyond the embolus. The guidewire is then removed and the ultrasonic core is advanced into the pulmonary artery through the infusion catheter. The infusion catheter is connected to an infusion pump containing a low-dose thrombolytic agent (eg alteplase), and an infusion pump containing saline is connected to the ultrasonic core for cooling. As such, there is simultaneous mechanical disruption of the clot as well as pharmacological breakdown.
The catheters are sutured in situ and the infusions are commenced; monitoring should take place on a coronary care unit or high dependency unit. The catheters are left to infuse for 12-24 hours and can then be removed without fluoroscopic guidance.
Kucher et al (2014)9 demonstrated that patients randomly assigned to catheter-directed thrombolysis showed a greater reduction in RV/LV ratio at 24h compared to conventional heparin-based treatment, without an increase in bleeding complications. Prospective studies10,11 and a registry12 have demonstrated improvement in right ventricular function and pulmonary artery pressures with this technique.
With respect to catheter-based thrombectomy without thrombolysis, both aspiration and mechanical thrombectomy are available at various UK centres (Flowtriever, Penumbra). Large bore femoral venous access is gained and the pulmonary emboli are entrapped / aspirated as able. With this technique the lungs can be tackled sequentially and no catheter is left in situ after the procedure.
The PEERLESS study13, which reported in 2025, directly compared large bore mechanical thrombectomy (LBMT) to catheter directed thrombolysis for the treatment of “intermediate” risk pulmonary embolism with respect to a primary end point of a hierarchal win ratio composite of all-cause mortality, intracranial haemorrhage, major bleeding, clinical deterioration and/or escalation to bailout, postprocedural intensive care unit admission and length of stay (assessed at the sooner of hospital discharge or 7 days after the procedure). 550 patients were enrolled. The study demonstrated that patients who underwent LBMT were at significantly decreased risk of developing the primary end point composite, without any difference in bleeding risk.
Computer Assisted Vacuum Thrombectomy [CAVT] has recently been shown be effective in reducing the RV/LV ratio and speed to normalisation of haemodynamics when compared to anticoagulation alone in intermediate-high risk patients with PE in the landmark STORM-PE trial14.
Future Work
Over the next 10 years, it is likely that catheter-based therapies will expand in both directions – showing suitability for some “high” risk patients who had conventionally been treated with thrombolysis, while also allowing selected “intermediate-low” risk patients to achieve quicker control of symptoms compared to anticoagulation alone.
As this happens, cardiac catheterisation labs are likely to be the fertile ground for this expansion of services, and interventional fellows will benefit from increased exposure to and familiarity with the techniques described herein.
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