Percutaneous Pulmonary Embolectomy: Indications, Techniques and Outcomes

VASCULAR DISEASE MANAGEMENT. 2010;7(11):E223-E229

Introduction

Venous thromboembolic disease remains the third most common cardiovascular disease and one of the leading causes of sudden death in the United States. The true incidence of pulmonary embolism (PE) is unknown, but based on historic projections, it is estimated that more than 600,000 cases of PE occur every year in the United States.¹ Approximately 10% of patients with PE do not survive their initial event. Of those who do survive, approximately 70% fail to have the diagnosis made and experience a mortality rate of 30%. If the diagnosis of PE is made promptly and appropriate therapy initiated, the mortality rate can be reduced to less than 10%.^1–3 Once the diagnosis of acute PE is made, treatment should be initiated as soon as possible. The therapeutic options that are available should be tailored to each patient and clinical scenario.

Endovascular Interventions

Indications. When obstruction of 70% of the pulmonary arterial circulation occurs, the right ventricle needs to be able to generate a systolic pressure in excess of 50 mmHg and a mean pulmonary artery pressure greater than 40 mmHg in order to maintain pulmonary perfusion. A previously normal right ventricle is incapable of generating a systolic pressure exceeding 50 mmHg, so any incremental embolic obstruction to the vasculature beyond this point results in right ventricular failure.⁴ The degree of obstruction of the pulmonary arterial circulation required to cause a change in pulmonary arterial hemodynamics also depends upon the amount of underlying cardiopulmonary disease prior to an embolic event. Therefore, a patient with massive PE obstructing the majority of the pulmonary circulation or a submassive PE superposed on underlying cardiopulmonary disease may present with right ventricular dysfunction or compromised hemodynamics. In this subset of patients, anticoagulation therapy alone may not be adequate therapy, and more aggressive intervention with thrombolysis and/or pulmonary embolectomy and clot fragmentation techniques should be considered. The most validated risk-assessment tool for patients with acute PE is echocardiography. Right ventricular hypokinesis on echocardiography predicts a doubling of mortality within the next 30 days, even among initially normotensive patients.⁵ Right ventricular enlargement on chest computed tomography (CT) also portends a greater likelihood of death or major in-hospital complication.⁶ Accepted indications for catheter-directed therapy for acute PE include :1) hemodynamic instability, defined as a systolic blood pressure (SBP) 40 mmHg, or ongoing administration of catecholamines for treatment of systemic arterial hypotension; 2) subtotal or total embolic occlusion of the left and/or right main pulmonary artery by chest CT or by conventional pulmonary angiography; 3) echocardiographic findings indicating right ventricular afterload stress with or without pulmonary hypertension; and 4) clinically severe acute PE with a contraindication to anticoagulation or systemic thrombolytic therapy. Surgical embolectomy rather than percutaneous catheter thrombectomy should be considered in the presence of free-floating cardiac thrombi or in patients with paradoxical embolism from a large atrial septal defect.^7,8

Intravenous Thrombolytic Therapy

The Consensus Development Conference recommended that 2-hour bolus intravenous (IV) thrombolytic therapy be considered in any patient who has a perfusion defect involving the equivalent of one or more lobes and hemodynamic compromise.^9,10 Despite the numerous randomized trials demonstrating faster improvement in pulmonary perfusion and hemodynamics and better lung-diffusing capacities and pulmonary capillary blood volumes in patients receiving thrombolytic therapy, when symptoms and mortality rates at 6 and 12 months are analyzed, there is no statistical benefit in outcomes between patients who received IV thrombolytic versus heparin therapy.^11,12

Catheter-Directed Thrombolysis

Catheter-directed thrombolytic therapy with intrapulmonary administration of a thrombolytic agent has been described by several investigators with encouraging results.^13,14 Catheter-directed techniques aim to accelerate clot lysis and achieve rapid reperfusion of the pulmonary arteries and lung parenchyma. In one study, 13 patients were treated with urokinase (Abbott Laboratories) for angiographically proven PE within 14 days of major surgery.¹³ Follow-up pulmonary angiography at 24 hours revealed that 98% of the clots had completely disappeared from the pulmonary vasculature. No deaths or bleeding complications occurred. In another series, 16 patients with massive PE were given a bolus of urokinase directly into the clot followed by infusion into the right atrium.¹⁴ Cardiac output, total pulmonary vascular resistance, and mean pulmonary artery pressures all improved following the thrombolytic therapy. One patient did suffer a severe bleeding complication. In 1988, Verstraete et al¹⁵ published the results of a multicenter comparative study of IV versus intrapulmonary infusion of rt-PA (100 mg over a 7-hour period) (Alteplase, Genetech) for the treatment of acute massive PE. The findings of this study suggested that the intrapulmonary infusion of rt-PA does not offer significant benefit compared to IV administration. However, this study did not use the standard catheter-directed technique currently used by most interventionalists, which includes embedding the infusion catheter directly into the thrombus, while attempting to fragment the clot.

Percutaneous Embolectomy

The published experience with the use of these devices is limited to small case series and case reports from single institutions. In addition, many of the catheter-directed studies for the treatment of acute PE described the use of a combination of techniques, where local or systemic thrombolytics were applied in a very heterogeneous patient population, which makes it difficult to compare the efficacy and outcomes related to the use of these devices. Given these limitations, the summary of the results from these series reveals an overall clinical success rate with catheter-directed therapy for acute PE of > 80%, with clinical success being defined as immediate hemodynamic improvement. The reported mortality rates range from 0–25%, again reflecting the wide variations in the patients being treated. The ideal device should be: 1) easy to use and position within in the pulmonary artery clots; 2) highly maneuverable to allow rapid right heart passage and advancement into major pulmonary arteries; 3) able to promote complete removal of clots or fragmentation of clots into very small particles; and 4) low profile and safe to use in the pulmonary circulation.^7,8 A review of the most commonly used devices is detailed below. None of the currently available devices described below are FDA-approved for application in the pulmonary arterial system and their use for acute PE represents an off-label use of these devices. Ideally, the procedure should be performed with a guide catheter/sheath positioned in the main pulmonary artery to minimize trauma to the heart and the induction of arrythmias during catheter manipulations and exchanges. The diagnostic pulmonary arterial catheter is removed over a 0.035 inch stiff J-tipped guidewire (Rosen Wire, Angiodynamics), maintaining access in the pulmonary artery. An appropriate diameter (6–12 Fr) and length (65–80 cm) introducer sheath (Flexor Sheath, Cook Medical) is inserted via the femoral vein and positioned in the main pulmonary artery. The sidearm of the sheath is connected to a heparinized saline flush (4,000 IU heparin/1,000 cc normal saline), which is infused at 15 cc/hr. Alternatively, a guide catheter (Envoy, Cordis Corporation) can be used through a short sheath in a similar fashion. A sidearm adaptor can be placed on the back of the guide catheter to allow infusion of a heparinized saline flush. Catheter-directed thrombolyis or thrombectomy/embolectomy can then be performed by advancing the appropriate catheter or device through the guide catheter/sheath into the thrombus.

Thrombectomy and Embolectomy Devices

The Greenfield device (Boston Scientific Corporation) is a 10 Fr braided catheter designed for pulmonary artery embolectomy. The device is somewhat bulky, requires familiarity with the control handle, and is designed for insertion via a surgical venotomy since it requires insertion through a 22 Fr sheath, although it was used percutaneously. The device was not widely used, so it is no longer manufactured. The Amplatz Thrombectomy Device (ATD) (ev3, Inc.) consists of a 120 cm long, 8 Fr polyurethane catheter with an impeller mounted on a drive shaft inside a metal cap 5 mm in length. The metal cap has three sideports which are used for recirculation of clot particles.¹⁶ A multipurpose 10 Fr guide catheter positioned into the clot provides some ability to guide the direction of the ATD. The ATD is advanced to the end of the guide catheter and the guide catheter is retracted to expose the ATD. Advancing the ATD outside the guide catheter should be done with care since it is rigid, non-steerable, and could traumatize the pulmonary artery. Initial experience with the ATD device showed clinical improvement in a limited group of patients, with reduction of the respiratory symptoms and improvement of hypotension.^16,17 Transient hemoptysis and arrythmias have been described as complications associated with the use of the ATD device. Hemolysis also commonly occurs with the use of the ATD device, but there are no reported cases of associated renal failure. The use of ATD has been limited recently due to its bulkiness and lack of steerability. The 11 Fr Aspirex catheter thrombectomy device (Straub Medical) was specifically designed and developed for percutaneous interventional treatment of acute PE in arteries ranging from 6–14 mm in caliber. The central part of the catheter system is a high-speed rotational coil (40,000 revolutions per minute) within the catheter body that creates negative pressure through an L-shaped aspiration port at the catheter tip. The rotating coil macerates aspirated thrombus and removes thrombus fragments via an auger-like action. The distal part of the catheter has enhanced flexibility, which facilitates its passage through the right side of the heart into the pulmonary arteries. A recent study on the use of this device in 11 patients reported a clinical success rate of 88%.18 A cohort study is currently being performed in Europe to investigate the effectiveness and safety of the Aspirex device in patients with acute, massive PE and a contraindication for thrombolysis.⁷

Thrombus Fragmentation Catheters and Balloons

The theoretical advantage of the fragmentation technique is that the central pulmonary artery volume is roughly 50% of the volume of the branch pulmonary arterial segments. Therefore, by achieving immediate redistribution of the occlusive thrombus from the central main pulmonary artery to the more peripheral pulmonary artery branches, the afterload on the right ventricle is immediately reduced. In addition, following clot fragmentation, a greater surface area of the thrombus is exposed to allow greater activation of clot-bound plasminogen to plasmin by the infused lytic agents if thrombolysis is used in combination with the fragmentation technique.

Balloon catheters. Balloon angioplasty (6–16 mm in diameter) for fragmentation of large central pulmonary emboli has been used in association with local thrombolytic infusion with encouraging results. Recovery rates, as measured by pulmonary artery pressures, blood oxygen values, and clinical outcomes, of 87.5% have been reported with the use of this technique.¹⁹

Angiographic and pigtails catheters. Various angiographic or pigtail catheter devices have been used to fragment centrally located emboli by direct mechanical action. The majority of the reported patients were also treated with local or systemic thrombolysis.^20,21 Therefore, it is unclear whether thrombus fragmentation with a catheter without thrombolysis is effective. The rotatable pigtail catheter is a custom-made 5 Fr pigtail catheter. It is 110 cm in length and has 10 sideholes for contrast injection. The catheter is introduced via a flexible 5.5 Fr sheath. The pigtail catheter is designed to rotate within the sheath with a guidewire exiting through a distal sidehole that is positioned just before the curve of the pigtail begins.⁸ In 20 patients with massive PE, catheter intervention with the pigtail rotational catheter showed a 33% recanalization rate by fragmentation, but the catheter was more effective with adjuvant thrombolytic therapy. The mortality rate in this series was 20%.²²

Suction Embolectomy with Guide Catheters/Sheaths

Manual suction embolectomy has been utilized alone or as an adjunct to other techniques. An 8–16 Fr guiding catheter/sheath is advanced into the thrombus in the main right or left pulmonary artery. A 20–50 ml syringe with a luer-lock connector is then used to apply suction while the catheter is moved slowly to-and-fro over several centimeters within the clot within the pulmonary artery. During advancement of the catheter used to perform suction embolectomy, it is important to be aware of any resistance, which may indicate subintimal passage of the catheter. When blood readily enters the syringe, the clot material has cleared the catheter. The syringe is then removed and its contents are expressed over a gauze-draped basin. If no blood is obtained, it usually means that the suctioned thrombus is totally occluding the catheter and may actually be protruding from the catheter tip. In these situations, it is good to provide suction to the sideport of the sheath with a syringe to allow aspiration of any clot that may shear off the tip of the suction catheter during its removal through the sheath. It may be necessary to re-advance the suction catheter into the pulmonary artery over a guidewire for each successive aspiration. This technique has been described with or without the use of local thrombolytics.^23–25 In a recent study, the clinical success rate was 100% in 15 patients utilizing an 8 Fr guiding catheter. In another study, the survival rate of patients with PE utilizing this technique for removal of clot was 72%. The study also showed that this technique is more efficacious when the procedure is performed within 48 hours from the onset of symptoms of PE.²⁵ A combination of thrombus fragmentation and suction embolectomy techniques with or without thrombolysis have also been described. In this study, use of a modified rotatable pigtail catheter for clot fragmentation was followed by suction embolectomy with or without thrombolytics and compared to catheter-directed thrombolysis alone in a cohort of 18 patients. The study showed shorter hospital stays and higher survival rates when utilizing catheter fragmentation and aspiration with selective use of thrombolytics than when thrombolytics were used alone.²⁶

Hydrodynamic Thrombectomy Devices

Although none of the currently available hydrodynamic or rheolytic catheter devices were designed for the treatment of large arteries, they have been successfully used in an off-label fashion for the treatment of patients with massive PE. The AngioJet Xpeedior (Possis Medical) is a 6 Fr over-the-wire mechanical thrombectomy device and is probably the most efficacious catheter among the currently available hydrodynamic devices. Power saline jets at speeds up to 300 miles per hour are injected in a retrograde fashion using the Bernoulli principle to create a low-pressure zone around the catheter tip causing a Venturi effect and a recirculating vortex. The injected saline is removed in a euvolemic fashion via a suction port on the catheter. The thrombus at the catheter tip is withdrawn into the vortex that is created by the rapidly flowing saline and fragmented into small particles that are, in theory, removed along with the injected fluid through the suction port of the device. Since the AngioJet Xpeedior was not designed to treat vessels larger than 12 mm in diameter, its use in the treatment of central PE located in the large arteries is limited to large-volume central thrombus. The disruption of clot within these large arteries with this device is often enough to result in pulmonary perfusion that is sufficient enough to improve the hemodynamics and clinical outcomes in these patients.^7,27–30 In one study, 14 patients were treated with this device. Adjunctive local thrombolysis was performed in 5 patients. Clinical success was obtained in 86% of patients. Procedural mortality occurred in 1 patient who presented in cardiogenic shock, and non-fatal hemoptysis also occurred in 1 patient.²⁹ In another study, 51 patients were treated with the Angiojet device, 21% of whom also received local thrombolytic therapy. The in-hospital mortality rate was 15%.³⁰ The use of this device close to the heart is commonly associated with bradyarrhythmias, including transient asystole, which can cause significant symptoms and hinder its use in some patients. Most typically, the bradyarrythmias will stop within 10 seconds of deactivating the device. In addition, activation of the device for short bursts (i.e., Complications of Catheter-Directed Interventions Complications of catheter-directed interventions for acute PE include perforation or dissection of cardiovascular structures, pericardial tamponade, pulmonary hemorrhage, distal thrombus embolization, and death.^7,31 Other potential complications include chest pain, hemoptysis, blood loss, arrhythmias, contrast-induced nephropathy, anaphylactic reaction to iodine contrast, hemolysis, and vascular access complications such as hematoma, access-site thrombosis, arterial puncture, pseudoaneurysm, or arterio-venous (AV) fistula. To minimize the risk of vascular perforation or dissection, mechanical thrombectomy should be performed only in the main and lobar pulmonary arteries, not in the segmental pulmonary arteries. The procedure should be performed with a guiding catheter/sheath positioned in the main pulmonary to minimize trauma to the heart and the induction of arrythmias during catheter manipulations and exchanges. The procedure should be terminated as soon as hemodynamic improvement is achieved, regardless of the angiographic result.^7,8 Fewer hemorrhagic complications should be seen with catheter-directed thrombolysis than with bolus IV infusion, but no randomized control data have demonstrated this difference. However, the rate of major bleeding with catheter-directed infusion of rt-PA has been reported to be 6%, as compared with 27% and 12%, respectively, for peripherally infused urokinase in Phases I and II of the UPET study.8 In a recent meta-analysis, 594 patients from 35 studies were analyzed. The clinical success rate of catheter-directed interventions was 86.5%. The risks of minor and major procedural complications as defined by the Society of Interventional Radiology’s clinical practice guidelines³² were 7.9% and 2.4 %, respectively.³³

Conclusion

Catheter-directed thrombolytic therapy used selectively in conjunction with percutaneous embolectomy and fragmentation techniques in patients with acute PE and hemodynamic instability appears to be useful in rapidly restoring more normal hemodynamics and may prove to be useful in reducing mortality and the sequela of chronic pulmonary hypertension. Several studies have shown that simple catheter techniques aiming at mechanical fragmentation of the clot using angioplasty balloons and pigtail catheters, coupled with either suction embolectomy and/or local thrombolytic administration, have resulted in dramatic improvements in patients with massive, acute PE.^21,33,34

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REFERENCES

1. Dalen JE, Alpert JS. Natural history of pulmonary embolism. Prog Cardiovas Dis 1975;17:259–270.

2. Hermann RE, Davis JH, Holden WD: Pulmonary embolism: A clinical and pathologic study with emphasis on the effect of prophylactic therapy with anticoagulants. Am J Surg 1961;102:19–28.

3. Barritt DW, Jordan SE. Anticoagulant drugs in the treatment of pulmonary embolism: A controlled trial. Lancet 1960;1:1309–1312.

4. Benotti JR, Dalen JE. The natural history of pulmonary embolism. Clin Chest Med 1984;5:403–410.

5. Kucher N, Rossi E, De Rosa M, Goldhaber SZ. Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mmHg or higher. Arch Intern Med 2005;165:1777–1781.

6. Schoepf UJ, Kucher N, Kipfmueller F, et al. Right ventricular enlargement on chest computed tomography: A predictor of early death in acute pulmonary embolism. Circulation 2004;110:3276–3280.

7. Kucher N.Catheter embolectomy for acute pulmonary embolism. Chest 2007;132:657–663.

8. Uflacker R. Interventional therapy for pulmonary embolism. J Vasc Interv Radiol 2001;12:147–164.

9. National Institutes of Health Consensus Panel. Thrombolytic therapy and thrombosis: A National Institutes of Health consensus development conference. Ann Intern Med 1980;93:141–144.

10. Goldhaber SZ. Thrombolysis for pulmonary embolism. Prog Cardiovasc Dis 1991;34:113–134.

11. Anderson DR, Levine MN. Thrombolytic therapy for the treatment of acute plmonary embolism. Can Med Assoc J 1992;146:1317–1324.

12. Konstantinides S, Geibel A, Heusel G, et al. Management Strategies and Prognosis of Pulmonary Embolism-3 trial investigators. Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. N Engl J Med 2002;347:1143-1150.

13. Molina JE, Hunter DW, Yedlick JW, et al. Thrombolytic therapy for post operative pulmonary embolism. Am J Surg 1992;163:375–381.

14. Gonzalez-Juanatey JR, Valdes L, Amaro A, et al. Treatment of massive pulmonary thromboembolism with low intrapulmonary dosages of urokinase: Short-term angiographic and hemodynamic evolution. Chest 1992;102:341–346.

15. Verstraete M, Miller GAH, Bounameaux H, et al. Intravenous and intrapulmonary recombinant tissue-type plasminogen activator in the treatment of acute massive pulmonary embolism. Circulation 1988;77:353–360.

16. Uflacker R, Strange C, Vujic B. Massive pulmonary embolism: Preliminary results of treatment with the Amplatz thrombectomy device. J Vasc Interv Radiol 1996;7:519–528.

17. Muller-Hulsbeck S, Brossmann J, Jahnke T, et al. Mechanical thrombectomy of major and massive pulmonary embolism with use of the Amplatz thrombectomy device. Invest Radiol 2001;36:317–322.

18. Eid-Lidt G, Gaspar J, Sandoval J. Combined clot fragmentation and aspiration in patients with acute pulmonary embolism. Chest 2008;134:45–60.

19. Fava M, Loyola S, Flores P, Huete I. Mechanical fragmentation and pharmacologic thrombolysis in massive pulmonary embolism. J Vasc Interv Radiol 1997;8:261–266.

20. Schmitz-Rode T, Janssens U, Hanrath P, et al. Fragmentation of massive pulmonary embolism using a pigtail rotation catheter: Possible complication. Eur Radiol 2001;11:2047–2049.

21. De Gregorio MA, Gimeno MJ, Mainar A, et al. Mechanical and enzymatic thrombolysis for massive pulmonary embolism. J Vasc Interv Radiol 2002;13:163–169.

22. Schmitz-Rode T, Janssens U, Schild HH, et al. Fragmentation of massive pulmonary embolism using a pigtail rotation catheter. Chest 1998;114:1427–1436.

23. Lang EV, Barnhart WH, Walton DL, Raab SS. Percutaneous pulmonary thrombectomy. J Vasc Interv Radiol 1997;8:427–432.

24. Tajima H, Murata S, Kumazaki T, et al. Manual aspiration thrombectomy with a standard PTCA guiding catheter for treatment of acute massive pulmonary thromboembolism. Radiat Med 2004;22:168–172.

25. Timsit JF, Reynaud P, Meyer G, et al. Pulmonary embolectomy by catheter device in massive pulmonary embolism. Chest 1991;100:655–658.

26. Yoshida M, Inoue I, Kawagoe T, et al. Novel percutaneous catheter thrombectomy in acute massive pulmonary embolism: Rotational bidirectional thrombectomy (ROBOT). Catheter Cardiovasc Interv 2006;68:112–117.

27. Siablis D, Karnabatidis D, Katsanos K, et al. AngioJet rheolytic thrombectomy versus local intrapulmonary thrombolysis in massive pulmonary embolism: A retrospective data analysis. J Endovasc Ther 2005;12:206–214.

28. Zeni PT, Blank BG, Peeler DW. Use of rheolytic thrombectomy in treatment of acute massive pulmonary embolism. J Vasc Interv Radiol 2003;14:1511–1515.

29. Chauhan MS, Kawamura A. Percutaneous rheolytic thrombectomy for large pulmonary embolism: A promising treatment option. Catheter Cardiovasc Interv 2007;70:123–130.

30. Chechi T, Vecchio S, Spaziani G, et al. Rheolytic thrombectomy in patients with massive and submassive acute pulmonary embolism. Catheter Cardiovasc Interv 2009;73:506–513.

31. Skaf E, Beemath, A, Siddiqui, T, et al Catheter-tip embolectomy in the management of acute massive pulmonary embolism. Am J Cardiol 2007;99:415–420.

32. Sacks D, McClenny TE, Cardella JF, Lewis CA. Society of interventional radiology clinical practice guidelines. J Vasc Interv Radiol 2003;14:199–202.

33. Kuo WT, Gould MK, van den Bosch AAJ, et al. Catheter-directed therapy for the treatment of massive pulmonary embolism: Systematic review and meta-analysis of modern techniques. J Vasc Interv Radiol 2009;20:1431–1440.

34. Kuo WT, van den Bosch MA, Hofmann LV, et al. Catheter-directed embolectomy, fragmentation, and thrombolysis for the treatment of massive pulmonary embolism after failure of systemic thrombolysis. Chest 2008;134;250–254.

From the Department of Radiology, University of Virginia Health System, Charlottesville, Virginia. Relevant disclosures: Dr. Angle: consultant to Terumo Corp.; Dr. Matsumoto: on the board of Bolton Medical; consultant to Boston Scientific, Bard Peripheral Vascular, and Endologix; received grants from Cook, Inc., W.L. Gore, Medtronic, NIH; honoraria from Endologix, Medtronic, and W.L. Gore. Manuscript submitted February 22, 2010, provisional acceptance given May 17, 2010, final version accepted June 28, 2010. Address for correspondence: Saher S. Sabri, MD, Department of Radiology, University of Virginia Health System, 1215 Lee Street, Charlottesville, VA 22908. E-mail: ss2bp@virginia.edu