Percutaneous Interventions for Acute Pulmonary Embolism

Chapter 86

Percutaneous Interventions for Acute Pulmonary Embolism

William T. Kuo

Venous thromboembolism (VTE) is a global health problem that encompasses acute deep venous thrombosis (DVT) and acute pulmonary embolism (PE). Although the true incidence of PE is unknown, it is recognized as a significant cause of morbidity and mortality in hospitalized patients.1 In the United States alone, it is estimated there are between 500,000 and 600,000 cases per year,2 and approximately 300,000 people die every year from acute PE.3 Indeed, acute PE is believed to be the third most common cause of death among hospitalized patients.4

Common risk factors for acute PE are related to underlying genetic conditions (e.g., factor V Leiden mutation, prothrombin 20210A mutation, and multiple other thrombophilias), acquired conditions (e.g., cancer, immobilization, trauma, surgery, prior DVT), and acquired hypercoagulable states (e.g., oral contraceptive use, nephrotic syndrome, antiphospholipid syndrome, disseminated intravascular coagulation, hyperestrogenic states, obesity).

There are three basic categories of acute PE: (1) simple PE with no associated heart strain and no hypotension, (2) submassive PE with associated right heart strain, (3) massive PE with associated right heart strain and hemodynamic shock. Patients with simple acute PE require treatment with therapeutic anticoagulation alone. Patients with submassive PE may require treatment escalation beyond anticoagulation; and patients with massive PE certainly require treatment escalation beyond anticoagulation alone.5 The immediate mortality rate related to simple PE is less than 8% when the condition is recognized and treated with anticoagulation.1,6,7 However, patients with submassive PE have a higher cumulative mortality rate, reaching approximately 20% over a 90-day period.8 Patients with massive PE have the highest mortality rate, which can exceed 58%, including a high risk of sudden death.9

The pathophysiology of PE consists of direct physical obstruction of the pulmonary arteries, hypoxemic vasoconstriction, and release of potent pulmonary arterial vasoconstrictors that further increase pulmonary vascular resistance and right ventricular (RV) afterload. Acute RV pressure overload may result in RV hypokinesis and dilation, tricuspid regurgitation, and ultimately RV failure. RV pressure overload may also result in increased wall stress and ischemia by increasing myocardial oxygen demand while simultaneously limiting its supply. Ultimately, cardiac failure due to acute PE results from a combination of the increased wall stress and cardiac ischemia that compromise RV function and impair left ventricular (LV) output, resulting in life-threatening hemodynamic shock.9 Depending on underlying cardiopulmonary reserve, patients with acute massive PE may deteriorate over the course of several hours to days and develop systemic arterial hypotension, cardiogenic shock, and cardiac arrest. Owing to the risk of sudden death, these critically ill patients with massive PE should be quickly identified as candidates for rapid endovascular treatment as a lifesaving procedure.5


Because of the high mortality associated with acute massive PE, successful management requires prompt risk stratification and decisive early intervention (Table 86-1). Confirmation of hemodynamic shock attributed to central obstructing embolus should be present to justify treatment escalation beyond anticoagulation. The American College of Chest Physicians has recommended that percutaneous catheter-directed therapy (CDT) be considered in acute massive PE patients who are unable to receive systemic thrombolytic therapy because of bleeding risk.10 In addition, global meta-analytic data has demonstrated that percutaneous CDT can be considered as a first-line treatment option in lieu of intravenous (IV) tissue plasminogen activator (tPA) for patients with massive PE.11

Pulmonary angiography was once considered the gold standard for diagnosing PE, but it has largely been replaced by the wide availability of cross-sectional imaging. Historically, many types of imaging studies have been used in diagnosing acute pulmonary embolism, including ventilation/perfusion (V/Q) scanning, magnetic resonance angiography (MRA), and computed tomographic angiography (CTA). CTA is the preferred modality and has proven to be advantageous thanks to its wide availability, superior speed, characterization of nonvascular structures, and detection of venous thrombosis. CTA has the greatest sensitivity and specificity for detecting emboli in the main, lobar, or segmental pulmonary arteries. Systematic reviews and randomized trials suggest that outpatients with suspected pulmonary embolism and negative CTA studies have excellent outcomes without therapy.12

If a patient has either acute or chronic renal insufficiency and contrast administration is undesirable, echocardiography may be used to evaluate for right heart dysfunction as an indication for underlying acute PE. The echocardiogram can be performed at bedside, and the study may reveal findings that strongly support hemodynamically significant pulmonary embolism,13 offering the potential to guide treatment escalation to thrombolytic and/or endovascular therapy. Large emboli moving from the heart to the lungs are occasionally confirmed with this technique. In addition, intravascular ultrasonography has also been used at the bedside to visualize central pulmonary emboli.14

Although the diagnosis of submassive PE follows a similar workup to evaluating massive PE, these patients do not present with systemic arterial hypotension, and particular attention must be paid to detecting the presence of right heart strain, which clinches the diagnosis of submassive PE. Identifying right heart strain allows risk stratification for possible treatment escalation beyond anticoagulation in normotensive PE patients.5 Echocardiography is the best imaging study to detect RV dysfunction in the setting of acute PE. Characteristic echocardiographic findings in patients with submassive PE include RV hypokinesis and dilatation, interventricular septal flattening and paradoxical motion toward the LV, abnormal transmitral Doppler flow profile, tricuspid regurgitation, pulmonary hypertension as identified by a peak tricuspid regurgitant jet velocity over 2.6 m/s, and loss of inspiratory collapse of the inferior vena cava (IVC).15 An RV-to-LV end-diastolic diameter ratio of 0.9 or greater, assessed in the left parasternal long-axis or subcostal view, is an independent predictor of hospital mortality.16 Detection of RV enlargement by chest CTA is especially convenient for diagnosis of submassive PE, because it uses data acquired during the initial diagnostic scan. Submassive PE can be diagnosed when RV enlargement on chest CT, defined by an RV-to-LV diameter ratio greater than 0.9, is observed17; RV enlargement on chest CTA also predicts increased 30-day mortality in patients with acute PE.17,18 Even if shock and death do not ensue, survivors of acute submassive PE remain at risk for developing chronic PE and thromboembolic pulmonary hypertension.19

Additionally, monitoring cardiac troponin T (cTnT) identifies the high-risk group of normotensive patients with submassive PE.20 A persistent increased cTnT level (>0.01 ng/mL) in PE patients with right heart strain predicts a significant risk of a complicated clinical course and fatal outcome, and these patients therefore require more aggressive treatment.20 Identifying submassive PE for treatment escalation is important because these normotensive PE patients demonstrate increased short-term mortality and high risk of adverse outcomes when the degree of heart strain results in elevations in levels of cardiac troponins and brain-type natriuretic peptide.21,22 The optimal protocol for treatment of acute submassive PE is still in evolution, but a proposed algorithm for managing submassive PE has been published23 describing treatment escalation beyond anticoagulation (Fig. 86-1).

Based on the history, angiographic findings, and outcomes of patients undergoing CDT for acute PE, three groups of patients have been identified24:


Because of the risk of major hemorrhage, aggressive anticoagulation, systemic thrombolysis, and local catheter-directed thrombolysis may be contraindicated in patients with recent major general or intracranial surgery. In such cases, mechanical methods of percutaneous catheter-directed thrombectomy, fragmentation, and/or aspiration should be considered without pharmacologic agents. Since pulmonary hypertension is a relative contraindication to pulmonary angiography, the degree of pulmonary hypertension and underlying cardiopulmonary reserve are important considerations prior to performing pulmonary angiography. These factors must be used to determine a safe rate and volume of contrast injection into the pulmonary circulation. For instance, when systolic pulmonary artery pressure (PAP) exceeds 55 mmHg, or right ventricular end diastolic pressure (RVEDP) is greater than 20 mmHg, the mortality associated with pulmonary angiography using large-volume power injection has been reported to be as high as 3%.2,3 Therefore, such patients with massive PE should only receive a limited rate of power injection, controlled by hand. In the submassive PE patient, a selective contrast injection into the main left or right PA should not exceed a 20-mL volume at a rate of 10 mL/s. Lower injection parameters by hand may be considered depending on degree of heart failure, as determined by the operator’s judgment, to achieve adequate vessel opacification without endangering the patient. Pulmonary angiography can be used to calculate the degree of pulmonary obstruction before and after treatment, using the calculated Miller Index (Fig. 86-2). Finally, in PE patients with contraindications to anticoagulation and/or thrombolytic agents, placement of an IVC filter should be considered for prophylaxis of recurrent PE.


Modern CDT for massive PE has been defined according to the following criteria: use of low-profile catheters and devices (≤10F), catheter-directed mechanical fragmentation and/or aspiration of emboli, and intraclot thrombolytic injection if a local drug is infused.11 Therefore, a variety of devices can be successfully used to treat PE, so long as they meet criteria for modern CDT (Table 86-2).

TABLE 86-2

Catheter-Directed Therapy for Massive Pulmonary Embolism in 594 Patients

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Dec 23, 2015 | Posted by in INTERVENTIONAL RADIOLOGY | Comments Off on Percutaneous Interventions for Acute Pulmonary Embolism
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Author, Year (Reference) Country Patients, n Sex-n Age: Mean, Range Technique-n Local Intraclot Lytic During CDT-n Local Intraclot Lytic, Extended Infusion-n Minor Cxs Major Cxs Clinical Success (%)
Prospective Studies
Schmitz-Rode et al. 199848 Germany 10 M-6, F-4 54 (36-70) PF-10 8 1 0 0 8/10 (80)
Schmitz-Rode et al. 200049 Germany 20 M-10, F-10 59 (48-60) PF-20 0 0 1 0 16/20 (80)
Muller-Hulsbeck et al. 200150 Germany 9 M-4, F-5 55 (27-85) ATD-9 0 5 0 0 9/9 (100)
Prokubovsky et al. 200351 Russia 20 na 51 (32-75) PF-20 0 16 0 0 14/20 (70)
Tajima et al. 200452 Japan 25 M-8, F-17 61 (35-77) PF & AT-25 25 21 0 0 25/25 (100)
Barbosa et al. 200853 Brazil 10 M-7, F-3 57 (39-75) PF-10, (ATD-na) 0 0 0 0 9/10 (90)
Retrospective Studies
Brady et al. 199154 England 3 M-0, F-3 36 (18-71) PF-1, MC-2 2 2 0 0 3/3 (100)
Rafique et al. 199255 South Africa 5 M-1, F-4 35 (21-47) MC-5 5 5 1 0 5/5 (100)
Uflacker et al. 199624 U.S.A. 5 M-4, F-1 45 (25-64) ATD-5 1 1 0 1 3/5 (60)
Fava et al. 199732 Chile 16 M-8, F-8 49 (20-68) PF-16, (BA-na) 16 16 3 0 14/16 (88)
Stock et al. 199756 Switzerland 5 M-3, F-2 50 (21-80) PF & BA-5 5 5 0 2 5/5 (100)
Basche et al. 199757 Germany 15 na na (21-73) PF & BA-2, BA-13 na na 0 0 12/15 (80)
Hiramatsu et al. 199958 Japan 8 M-4, F-4 58 (42-87) AT & WD-8 0 8 0 0 7/8 (88)
Wong et al. 199959 England 4 M-2, F-2 33 (18-46) PF-1,PF & G-1, G-2 0 4 0 1 3/4 (75)
Murphy et al. 199960 Ireland 4 M-2, F-2 60 (46-66) MC & WD-4 4 4 0 0 4/4 (100)
Voigtlander 199961 Germany 5 M-4, F-1 57 (25-72) RT-5 0 0 4 0 3/5 (60)
Fava et al. 200062 Chile 11 M-3, F-8 61 (37-79) Hy-11 0 4 0 0 10/11 (91)
Egge et al. 200263 Norway 3 M-2, F-1 49 (40-54) PF-3 3 3 0 0 3/3 (100)
De Gregorio et al. 200233 Spain 59 M-25, F-34 56 (22-85) PF-52, PF & BA-4, PF & DB -3 59 57 8 0 56/59 (95)
Zeni et al. 200336 U.S.A. 16 M-9, F-8 52 (30-86) RT-16 0 10 2 1 14/16 (88)
Reekers et al. 200364 Netherlands 7 M-2, F-6 46 (28-76) Hy-6, Oa-1 7 0 0 0 6/7 (86)
Tajima et al. 200465 Japan 15 M-4, F-11 60 (27-79) AT-15 9 0 0 0 15/15 (100)
Fava et al. 200566 Chile 7 M-3, F-4 56 (30-79) Hy-4, Oa-3 3 3 1 1 6/7/ (86)
Siablis et al. 200537 Greece 6 M-4, F-2 59 (42-76) RT-6 4 0 2 0 5/6 (83)
Yoshida et al. 200667 Japan 8 M-4, F-4 61 (47-75) PF & AT-8 na na 0 1 7/8 (88)
Li J-J et al. 200668 China 15 M-11, F-4 56 (19-73) PF & ATD-13, PF & Hy-1, PF & Oa-1 6 0 0 0 15/15 (100)
Pieri and Agresti. 200769 Italy 164 na 68 (35-78) PF-164 164 164 0 0 138/164 (84)
Chauhan et al. 200770 U.S.A. 6 M-2 F-4 64 (49-78) RT-6 2 0 5 2 4/6 (67)
Krajina 200771 Czech Rep 5 M-1, F-4 67 (52-80) PF-3, PF & AT-2 3 0 0 0 2/5 (40)
Yang 200772 China 19 M-13, F-6 62 (22-87) PF-10, PF & AT-5, PF+SR-4 19 na 0 0 18/19 (95)
Margheri 200873 Italy 20 M-12, F-8 66 (32-85)