ORIGINAL ARTICLE
Heart, Lung and Circulation (2015) 24, 46–54 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2014.06.014
Percutaneous Aspiration Thrombectomy in Treatment of Massive Pulmonary Embolism Hulya Bayiz a, Mert Dumantepe b*, Burak Teymen b, Ibrahim Uyar b a
Department of Pulmonary Medicine, Medical Park Gebze Hospital, Istanbul, Turkey Department of Cardiovascular Surgery, Medical Park Gebze Hospital, Istanbul, Turkey
b
Received 2 May 2014; received in revised form 4 June 2014; accepted 24 June 2014; online published-ahead-of-print 4 July 2014
Background
Pulmonary embolism (PE) associated with haemodynamic instability has exceedingly high mortality. We describe our experience using percutaneous mechanical thrombectomy (PMT) in patients with massive PE and right ventricle dysfunction.
Methods
Sixteen patients (11 males and five females; mean age, 55.7 8.3 years) with massive PE were treated with PMT. A percutaneous Aspiration Device (8 French Aspirex1 aspiration thrombectomy catheter, Straub Medical, Switzerland) was used in all patients. Clinical outcomes, right ventricle and pulmonary artery pressures (PAP), thrombus clearance and complications were evaluated.
Results
Treatment of 16 patients resulted in complete thrombus clearance (90%), in 87.5% of the patients and nearcomplete (50%–90%) clearance in 6.3%. Measurements before and after treatment showed a decrease in PAP (73 11 mm Hg to 34 8 mm Hg, P < .001). The RV/LV ratio decreased from 1.32 0.15 to 0.84 0.13 at follow-up (P < .001). One patient died from refractory shock. No cardiovascular deaths or recurrent PE were documented during clinical follow-up but one patient demonstrated evidence of mild cor pulmonale.
Conclusions
This study demonstrates safety and effectiveness of percutaneous mechanical aspiration thrombectomy in patients with massive PE with a large thrombus burden.
Keywords
Aspiration thrombectomy Catheter-directed therapy Pulmonary artery pressure Pulmonary embolism Right ventricle disfunction.
Introduction Pulmonary embolism (PE) is the third most common cardiovascular disorder after myocardial infarction and stroke and is considered the leading cause of preventable death in hospitalised patients [1,2]. The mortality rate in the first three months following the diagnosis of PE has been shown to range from 15% to 18% [3]. Massive pulmonary embolism (PE) is heralded by sudden onset of dyspnoea, chest discomfort, or syncope, causing clinical deterioration toward cardiovascular collapse. As
the clinical course worsens, systemic arterial hypotension, respiratory failure, and impaired organ perfusion ensue [4]. Right ventricular dysfunction (RVD) and the presence of haemodynamic instability are powerful predictors of the poor prognosis of patients with acute PE [5]. A definitive treatment of RVD secondary to acute PE has not been defined, and the therapeutic controversy about using thrombolytics in patients with RVD but without systemic hypotension still continues [5,6]. Treatment should be more aggressive for this group of patients, with the basic objective of reestablishing patency of the pulmonary circulation and
*Corresponding author at: Address: Merit Life Park Sitesi, B Blok, Kat: 1 Daire: 5, Serifali/Umraniye 34660, I˙STANBUL. Tel.: +90 216 5082702 Mob: +90 532 3771872, Email: [email protected] © 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved.
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Endovascular Treatment of Pulmonary embolism
Figure 1 A, B, C; Computed tomography showed extensive filling defects within the main trunk, right and left main branches, secondary and tertiary branches of the pulmonary arteries representing massive pulmonary embolism (arrows).
preventing further deterioration of right ventricular function and progression to cardiogenic shock [4]. In patients who present with compromised haemodynamics or cardiac function, a variety of treatment options have been utilised to treat acute PE, including surgical embolectomy, intravenous fibrinolysis, catheter directed thrombolysis, and trans catheter mechanical clot fragmentation with or without thrombectomy [7,8]. In recent years, interest has risen in a variety of endovascular strategies based on catheter-based technologies for thrombus removal in patients with massive PE. The goal of the catheter directed procedure is to reduce pulmonary vascular resistance and right ventricular afterload and to increase cardiac output and systemic arterial pressure. PMT has been developed over the past years as a reliable alternative method to treat patients with acute PE and RVD [9]. The primary objective of this study was to evaluate the clinical efficacy of PMT in patients with massive PE. Our secondary objective was to objectively measure the difference in clot burden as assessed by the Miller Score [10]. Following CT-angiography, before and after intervention, as well as to compare the difference in preprocedure and 24-48 hours post-procedure right ventricle and PAP.
Materials and Methods Study Population Consecutive patients with PE, initially diagnosed by either computer tomography, or echocardiography, and transferred from emergency and medical divisions to our catheterisation laboratory for pulmonary angiography from April 2012 to February 2014, were retrospectively evaluated. Twenty-nine patients were referred to the cardiac catheterisation laboratory with a diagnosis of PE, of whom 16 patients met the criteria for massive PE based on the angiographic evidence of a thrombus image in a main pulmonary branch or in two or more lobar branches, and one or more criteria of RVD, the subject of this report. The criteria applied for the diagnosis of RVD were a diastolic diameter of the right ventricle >30 mm, a right ventricular diastolic diameter/left ventricular diastolic
diameter ratio > 1, paradoxical septal movement, hypokinesia of the right ventricular free wall, loss of inspiratory collapse of the inferior vena cava (IVC), and tricuspid regurgitation at a velocity > 2.5 m/s in the absence of inspiratory collapse of the IVC or > 2.8 m/s. [5]. A compromise of the central pulmonary arteries or of two or more lobar arteries by multi-detector contrast-enhanced computed tomography (CT) and confirmed by pulmonary angiography during the procedure was defined as massive PE [11,12] (Fig. 1). The clinical definition of massive PE was established in the presence of cardiogenic shock or hypotension, the latter defined as systemic systolic blood pressure (sSBP) < 90 mm Hg, or a pressure drop > 40 mm Hg for > 15 min not caused by arrhythmia, hypovolaemia, or sepsis. At our centre, PMT was used in patients with massive PE with Miller scores indicative of severe pulmonary vascular bed involvement. PMT was performed in patients with contraindications to or failure of fibrinolysis or with comorbidities resulting in a potentially higher risk of bleeding in case of fibrinolytic administration. Informed consent for participation in the study was obtained according to the guidelines of our institutional review board and the local ethics committee, which approved the study. Patient medical records were reviewed and evaluated for relevant clinical information including: demographics, risk factors for thromboembolism, comorbidities, symptomatic improvement or resolution after treatment, RV pressure and PAP, thrombus clearance, hospital length of stay, survival to discharge and complications.
Treatment Procedure Common femoral venous access was established by placement of a vascular sheath (8F, 10 cm;Terumo Medical Corporation, Elkton, Maryland). The main pulmonary artery was catheterised using a 6-F angled pigtail diagnostic catheter (Cordis Corporation, Miami Lakes, Florida). In all cases, we utilised a 65-cm-long introducer (8F) that was placed selectively in either of the two main pulmonary arteries for selective angiography, and as a conduit to manipulate the pigtail catheter. Intraluminal PAP was measured by direct catheter transduction after a satisfactory pulmonary artery waveform was observed. Digital subtraction angiography was performed in two bilateral anterior oblique
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H. Bayiz et al.
echocardiogram was repeated 24 h to 48 h following intervention. Fig. 3.
Definitions and Endpoints Figure 2 Aspirex 8 Fr thrombectomy device is used in combination with a 0.018 inch hydrophilic guidewire. (Reprinted with permission by Straub Medical, Wangs, Switzerland.).
projections with the catheter positioned in the main pulmonary artery. Once the location of a pulmonary arterial thrombus was identified angiographically, the angiographic catheters were exchanged for a 0.018-inch guidewire (Glidewire, Terumo, Somerset, NJ). We used an 8 French mechanical thrombus aspiration device (Aspirex; Straub Medical; Wangs, Switzerland) (Fig. 2). This catheter consists of a high-speed rotating spiral located in the body of the catheter that creates negative pressure through an L-shape aspiration system that macerates the thrombus and removes it by aspiration. The device is connected to a motor that generates a rotation speed of 40,000 revolutions per minute. The catheter is introduced over a 0.018-inch guide wire to the site of proximal occlusion of the pulmonary artery or with the greatest thrombus content. The procedure was considered clinically successful when arterial oxygen saturation (SaO2) was improved and sSBP levels increased after fragmentation and/or aspiration, in the absence of major complications such as a perforation of the pulmonary artery or cardiac structures, tamponade, cerebral vascular accident, or death. Patients were then treated with unfractionated heparin, and subsequently switched to oral anticoagulation with warfarin unless contraindicated. Vena cava filters were also deployed at the operator’s discretion to prevent further thromboembolic episodes, according to the results of lower limb venous Duplex ultrasound scan. Transthoracic
Technical success was defined as successful placement of the devices and initiation of the aspiration thrombectomy. Digital subtraction pulmonary angiograms obtained at baseline and after PMT of the pulmonary arteries were reviewed by two cardiovascular surgeons and two cardiologists. Treatment success was assessed by the extent of angiographic reduction in thrombus burden, determined as: complete (> 90% clearance), near complete (50%–90% clearance), or partial (< 50% clearance). The change from baseline to follow-up of the right-to-left ventricular dimension ratio (RV/LV ratio) was obtained from reconstructed CT four-chamber views. The change from baseline to follow-up CTA pulmonary artery clot burden was assessed by the Miller Score [10]. The obstruction index was calculated based on the following formula: seven major branches were identified in the left pulmonary artery (two in the upper lobe, two in the lingual, and three in the lower lobe), and nine major segmental branches were identified in the right pulmonary artery (three in the upper lobe, two in the middle lobe, and four in the lower lobe). The presence of filling defects (emboli) in any of these branches was scored as 1 point per each segment involved, thus leading to an overall obstruction score ranging from 0 (best) to 16 (worst). The perfusion index, which refers to the effect of embolism on pulmonary artery flow, was scored as follows: each lung was divided into three zones (upper, middle, and lower) and the flow in each zone was assessed as absent (3 points), severely reduced (2 points), mildly reduced (1 point), or normal (0 points), thus leading to an overall perfusion score ranging from 0 (best) to 18 (worst). The Miller Score (MS) was computed as the sum in each patient of obstruction and perfusion indexes, ranging from 0 (best) to 34 (worst). A diagnosis of massive PE was confirmed with an MS > 17 [10]. Pre- and
Figure 3 A. Selective pulmonary angiography shows a large obstructive PE in the right main pulmonary artery. B. An 8-French Aspirex thrombectomy catheter was used C. Post treatment angiography shows complete resolution of clot burden and normal perfusion of the right lung.
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Endovascular Treatment of Pulmonary embolism
post-intervention MS and relative MS improvement, defined as the pre-MS minus the post-MS divided by the pre-MS, were calculated for each patient. The haemodynamic status of the patient was evaluated with the shock index obtained by dividing heart rate by sSBP [13]. Other variables that were analysed to evaluate the effect of therapy were the Pao2, Sao2, PAP, right atrial pressure, and mean systemic BP before and after treatment. Haemodynamic measurements were obtained before diagnostic angiography was performed and after PMT.
Statistical Analysis Statistical analysis was performed with Graphpad Instat software (version 3 for Mac; version 11.5, GraphPad Software Inc.). Discrete variables are reported as numbers with percentages and continuous data as mean and standard deviation. The change from baseline to follow-up of both the sub annular RV/LV ratio and of the Miller Score was assessed using one-way, repeated measures analysis or variance for respiratory parameters using ANOVA. A P value < 0.05 was considered statistically significant.
Results Demographics and Procedural Details During the study period, 16 patients who underwent PMT for massive PE were included in the study. The average age of the patients was 55.7 years (range: 38-69), and 11 were men. All patients were treated with heparin once the diagnosis was considered, and all underwent computed tomography (CT) angiography to confirm the diagnosis before the interventional team was consulted. All patients underwent transthoracic echocardiography, which in five cases was performed before CT angiography. Baseline characteristics of the patients are described in Table 1. Most patients (68.7%, n = 11) underwent treatment for bilateral PE, and the remaining patients (31.3%, or n = 5) required unilateral treatment. The most frequent risk factors were prior deep vein thrombosis (56.2%) and obesity (43.7%). Among the clinical manifestations, most patients presented dyspnoea (93.7%), chest pain (81.3%), and cough (62.5%). sSBP level was 85.6 9.8 mm Hg, with 56.2% of patients having sSBP < 90 mm Hg prior to the procedure; mean heart rate was 118.3 10.5 beats/min with preserved left ventricular function (left ventricular ejection fraction, 58.9 5.5%). Echocardiographic evaluation demonstrated right ventricular hypokinesia and dilatation in all patients. A right ventricular diastolic dimension/left ventricular diastolic dimension ratio (RV/LV ratio) > 1 was documented in 68.7% of patients with paradoxical septal movement in 87.5% of the cases. Twelve patients were receiving inotropic support prior to treatment, and nine required mechanical ventilation. Inotropic support was started with 8 mcg/kg/min Dopamine for patient with presenting pre shock, if hypotension or right ventricle failure persists or patient presenting with shock; 0.03 mcg/kg/min Epinephrine was initiated.
Table 1 Baseline Clinical and Demographic Data. N = 16
n (%)
Age: mean (years) Male
55.7 8.3 11 (68.7)
Risk factors for pulmonary embolism Current smoking
12 (75)
Obesity
9 (56.2)
Malignancy
3 (18.7)
Trauma/fractures
2 (12.5)
Recent ( 1)
14(87.5)
Right ventricular hypokinesia
6 (37.5)
Abnormal interventricular septal motion
7 (43.7)
Vena cava dilation Tricuspid regurgitation
5 (31.3) 9 (56.3)
Troponin I > 0.01 ng/mL at presentation
11 (68.7)
D-Dimer > 500 ng/mL at presentation
16 (100)
Deep vein thrombosis
13 (81.3)
LV: Left Ventricle, RV: Right Ventricle.
The administration of vasoactive drugs and volume infusion were maintained constant during the procedure.
Endpoint Analysis Based on pulmonary angiography performed before and after the procedure, treatment of 16 patients resulted in complete thrombus clearance (90%) in 87.5% of the patients and near-complete (50%–90%) clearance in 6.3% (Table 2). The CTA pulmonary clot burden as assessed by the modified Miller Score was significantly reduced from 22.7 3.8 to 11.3 4.4 with significant reduction of both the obstruction and the perfusion indices observed (P < .001) (Fig. 4). Haemodynamic parameters prior to and following the procedure are shown in Table 3. After PMT, a significant increase of both mSBP and Sao2 was observed (75.4 6.2 mm Hg vs 93.6 5.9 mm Hg, p < 0.001; and 81.3 2.2% vs 95.2 3.4%, p < 0.001), as was a significant decrease in the shock index (1.36 0.19 vs, 0.64 0.27, p < 0.0001). Measurements before and after treatment showed a significant decrease in PAP by direct catheterisation (P < .001),
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H. Bayiz et al.
Table 2 Treatment Outcome and Adverse events. n (%) No. of patients No. of PE lesions
16 26
Complete thrombolysis (>90%)
14 (87.5%)
Near-complete thrombolysis (50-90%)
1 (6.25%)
Partial thrombolysis ( 40 mm Hg), cardiogenic shock, cardiopulmonary resuscitation, right ventricular dysfunction, precapillary pulmonary hypertension (mPAP > 20 mm Hg in the presence of normal pulmonary capillary wedge pressure), an alveolararterial oxygen difference > 50 mm Hg, and clinically serious PE with contraindications for thrombolytic treatment [4,9]. In our series, RVD and a severe pulmonary vascular compromise (preprocedure Miller score of 22.7 3.8) was documented in all cases. The majority of our patients (81.3%) who were submitted to PMT were in a high-risk class for systemic thrombolysis (pregnancy, recent surgery and trauma, failed thrombolysis, and age > 70 years). The overall major complication rate was 6%, with a complete thrombus clearance in 87.5% of the patients. The mortality rate attributed directly to pulmonary embolism was 6.3% (n = 1). We consider that the satisfactory evolution of our patients in the early phase is attributable to a reversion of RVD, shown in the improvement of oxygenation and cardiopulmonary haemodynamic parameters. The mortality rate of our series is less than that reported in the meta-analysis published by Kreit [6] (9.8%) and Fava [31] (10.5%). In the our study, a 46% reduction in the mean pulmonary artery pressure, indicating a reduced RV overload, was obtained with PMT. Evidence supports a corroborative relationship between reduction of PAP and resolution of RV dysfunction [32]. Engelhardt et al. demonstrated significant reduction of both RV/LV ratio from 1.33 to 1.00 and Miller Score after CDT in a patient population that exhibited a risk profile comparable to the risk profile in the current study [30]. At the time of follow up (14.7 4.4 months), a 75 year-old female patient, presented to the ER five months after her discharge with a recurrent PE, due to noncompliance to his anticoagulation regimen. Minimum rate of recurrence could probably be related to the use of a filter device in the IVC in most of our patients. Two recently published meta-analyses [33,34] documented a clinical success rate of 71%, with different PMT techniques, which was improved to 90% with local catheter directed thrombolysis. Reported complications are right ventricle perforation, tricuspid insufficiency, significant bleeding at the site of vascular access (2%), mechanical
Endovascular Treatment of Pulmonary embolism
haemolysis, and blood loss, while the mortality rates range from 0 to 25% [33,34]. The Aspirex device, with its ability to macerate and remove the thrombus from the pulmonary circulation, has proven to be effective in experimental models to revert cardiogenic shock secondary to PE [35]. No patient of our series presented major bleeding at the puncture site, minor bleeding and haematoma was documented in only one patient, without further complications. The use of the Aspirex device was not associated with macroembolisation; nevertheless, a transitory deterioration of oxygenation was observed in one case that was very likely related to microembolisation without conditioning further haemodynamic instability. Clinically evident haemolysis was not documented, and was probably due to the property of the device to prevent thrombus recirculation; only one of our patients required blood transfusion. The main limitations of our study were the small patient population and the retrospective nature of the study. Future prospective studies with larger patient populations may be needed. Although we had a small number of patients, we were able to evaluate and show a significant improvement in cardiac function, providing us with important physiological information after treatment. Our practice has evolved to using PMT in patients who are unstable or deemed to be at increased risk of haemodynamic compromise, and who are judged to have contraindications to systemic thrombolysis. In our small series, we found a marked improvement in haemodynamic parameters using the Aspirex. Our retrospective study demonstrates successful treatment of patients with massive PE using percutaneous aspiration thrombectomy. The results show a reduction of PAP, a high percentage of thrombus clearance, improvement in respiratory parameters and a decrease in the Miller Score rating. The Aspirex was found to be safe and was not associated with damage to cardiac structures although experience with its use in a larger number of patients is required for a better assessment of its safety characteristics. Excluding the one patient who died, all patients experienced symptomatic relief and clinical improvement. PMT is a promising modality used for PE and shows safe, reproducible results.
Disclosure statement All authors declare that there is no conflict of interest to be disclosed.
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[5] Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of haemodynamically significant pulmonary embolism. Chest 2002;121:877–905. [6] Kreit JW. The impact of right ventricular dysfunction on the prognosis and therapy of normotensive patients with pulmonary embolism. Chest 2004;125. 1539–1454. [7] Zeni Jr PT, Blank BG, Peeler DW. Use of rheolytic thrombectomy in treatment of acute massive pulmonary embolism. Journal of Vascular and Interventional Radiology 2003;14(12):1511–5. [8] Banovac F, Buckley DC, Kuo WT, Lough DM, Martin LG, Millward SF, et al. Reporting standards for endovascular treatment of pulmonary embolism. Journal of Vascular and Interventional Radiology 2010;21 (1):44–53. [9] Greenfield LJ. Pulmonary embolism: diagnosis and management. Curr Probl Surg 1976;13(Apr (4)):1–52. [10] Miller GAH, Sutton GC, Kerr IH, Gibson RV, Honey M. Comparison of streptokinase and heparin in treatment of isolated acute massive pulmonary embolism. BMJ 1971;2:681–4. [11] Engelke C, Prokop M. Pulmonary vascular imaging using computed tomography. In: Lanzer P, Topol EJ, editors. Panvascular medicine.. Berlin, Germany: Springer Verlag; 2002466–96. [12] Kucher N, Goldhaber SZ. Pulmonary angiography. In: Baim DS, editor. Grossman’s cardiac catheterization, angiography, and intervention. Philadelphia, PA: Lippincott Williams & Wilkins; 2006234–53. [13] Caprini JA. Risk assessment as a guide for the prevention of the many faces of venous thromboembolism. Am J Surg 2010;199:3–10. [14] Menaker J, Stein DM, Scalea TM. Pulmonary embolism after injury: More common than we think? J Trauma 2009;67:1244–9. [15] Donze J, Le Gal G, Fine MJ, Roy PM, Sanchez O, Verschuren F, et al. Prospective validation of the Pulmonary Embolism Severity Index. A clinical prognostic model for pulmonary embolism. Thromb Haemost 2008;100:943–8. [16] Jimenez D, Yusen RD. Prognostic models for selecting patients with acute pulmonary embolism for initial outpatient therapy. Curr Opin Pulm Med 2008;14:414–21. [17] Konstantinides S. Should thrombolytic therapy be used in patients with pulmonary embolism? Am J Cardiovasc Drugs 2004;4:69–74. [18] Bova C, Pesavento R, Marchiori A, Marchiori A, Palla A, Enea I, et al. Risk stratification and outcomes in hemodynamically stable patients with acute pulmonary embolism: A prospective, multicentre, cohort study with three months of follow-up. J Thromb Haemost 2009;7:938–44. [19] 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 mm Hg or higher. Arch Intern Med 2005; 165:1777–81. [20] Sanchez O, Trinquart L, Colombet I, Colombet I, Durieux P, Huisman MV, et al. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: A systematic review. Eur Heart J 2008;29:1569–77. [21] Hamilton-Craig CR, McNeil K, Dunning J, Walters DL, Slaughter R, Kermeen F. Treatment options and strategies for acute severe pulmonary embolism. Intern Med J 2008;38:657–67. [22] Kuo WT, van den Bosch MA, Hofmann LV, Louie JD, Kothary N, Sze DY. Catheter-directed embolectomy, fragmentation, and thrombolysis for the treatment of massive pulmonary embolism after failure of systemic thrombolysis. Chest 2008;134:250–4. [23] Siablis D, Karnabatidis D, Katsanos K, Kagadis GC, Zabakis P, Hahalis G. AngioJet rheolytic thrombectomy versus local intrapulmonary thrombolysis in massive pulmonary embolism: a retrospective data analysis. J Endovasc Ther 2005;12:206–14. [24] Konstantinides S, Geibel A, Olschewski M, Heinrich F, Grosser K, Rauber K, et al. Association between thrombolytic treatment and the prognosis of hemodynamically stable patients with major pulmonary embolism: results of a multicenter registry. Circulation 1997;96:882–8. [25] Hamel E, Pacouret G, Vincentelli D, Forissier JF, Peycher P, Pottier JM, et al. Thrombolysis or heparin therapy in massive pulmonary embolism with right ventricular dilation: results from a 128-patient monocenter registry. Chest 2001;120:120–5. [26] Meneveau N, Ming LP, Seronde MF, Mersin N, Schiele F, Caulfield F, et al. In-hospital and long-term outcome after sub-massive and massive pulmonary embolism submitted to thrombolytic therapy. Eur Heart J 2003;24:1447–54. [27] Torbicki A, van Beek EJR, Charbonnier B, Meyer G, Morpurgo M, Palla A, et al. Task force report on pulmonary embolism, European Society of Cardiology: guidelines on diagnosis and management of acute pulmonary embolism. Eur Heart J 2000;21:1301–36.
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[28] Kasper W, Konstantinides S, Geibel A, Olschewski M, Heinrich F, Grosser KD, et al. Management strategies and determinants of outcome in acute major pulmonary embolism: results of a multicenter registry. J Am Coll Cardiol 1997;30:1165–71. [29] Buller HR, Agnelli G, Hull RD, Hyers TM, Prins MH, Raskob GE. Antithrombotic therapy for venous thromboembolic disease: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:401–28. [30] Engelhardt TC, Taylor AJ, Simprini LA, Kucher N. Catheter-directed ultrasound-accelerated thrombolysis for the treatment of acute pulmonary embolism. Thromb Res 2011;128:149–54. [31] Fava M, Loyola S. Applications of percutaneous mechanical thrombectomy in pulmonary embolism. Tech Vasc Interv Radiol 2003;6:53–8.
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[32] Lin PH, Annambhotla S, Bechara CF, Athamneh H, Weakley SM, Kobayashi K. Comparison of percutaneous ultrasound-accelerated thrombolysis versus catheter-directed thrombolysis in patients with acute massive pulmonary embolism. Vascular 2009;17(3):137–47. [33] Kucher N. Catheter embolectomy for acute pulmonary embolism. Chest 2007;132:657–63. [34] Skaf E, Beemath A, Siddiqui T, Janjua M, Patel NR, Stein PD. Catheter-tip embolectomy in the management of acute massive pulmonary embolism. Am J Cardiol 2007;99:415–20. [35] Kucher N, Windecker S, Banz Y, Schmitz-Rode T, Mettler D, Meier B, et al. Percutaneous catheter thrombectomy device for acute pulmonary embolism: in vitro and in vivo testing. Radiology 2005;236:852–8.
Heart, Lung and Circulation (2015) 24, 46–54 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2014.06.014
Percutaneous Aspiration Thrombectomy in Treatment of Massive Pulmonary Embolism Hulya Bayiz a, Mert Dumantepe b*, Burak Teymen b, Ibrahim Uyar b a
Department of Pulmonary Medicine, Medical Park Gebze Hospital, Istanbul, Turkey Department of Cardiovascular Surgery, Medical Park Gebze Hospital, Istanbul, Turkey
b
Received 2 May 2014; received in revised form 4 June 2014; accepted 24 June 2014; online published-ahead-of-print 4 July 2014
Background
Pulmonary embolism (PE) associated with haemodynamic instability has exceedingly high mortality. We describe our experience using percutaneous mechanical thrombectomy (PMT) in patients with massive PE and right ventricle dysfunction.
Methods
Sixteen patients (11 males and five females; mean age, 55.7 8.3 years) with massive PE were treated with PMT. A percutaneous Aspiration Device (8 French Aspirex1 aspiration thrombectomy catheter, Straub Medical, Switzerland) was used in all patients. Clinical outcomes, right ventricle and pulmonary artery pressures (PAP), thrombus clearance and complications were evaluated.
Results
Treatment of 16 patients resulted in complete thrombus clearance (90%), in 87.5% of the patients and nearcomplete (50%–90%) clearance in 6.3%. Measurements before and after treatment showed a decrease in PAP (73 11 mm Hg to 34 8 mm Hg, P < .001). The RV/LV ratio decreased from 1.32 0.15 to 0.84 0.13 at follow-up (P < .001). One patient died from refractory shock. No cardiovascular deaths or recurrent PE were documented during clinical follow-up but one patient demonstrated evidence of mild cor pulmonale.
Conclusions
This study demonstrates safety and effectiveness of percutaneous mechanical aspiration thrombectomy in patients with massive PE with a large thrombus burden.
Keywords
Aspiration thrombectomy Catheter-directed therapy Pulmonary artery pressure Pulmonary embolism Right ventricle disfunction.
Introduction Pulmonary embolism (PE) is the third most common cardiovascular disorder after myocardial infarction and stroke and is considered the leading cause of preventable death in hospitalised patients [1,2]. The mortality rate in the first three months following the diagnosis of PE has been shown to range from 15% to 18% [3]. Massive pulmonary embolism (PE) is heralded by sudden onset of dyspnoea, chest discomfort, or syncope, causing clinical deterioration toward cardiovascular collapse. As
the clinical course worsens, systemic arterial hypotension, respiratory failure, and impaired organ perfusion ensue [4]. Right ventricular dysfunction (RVD) and the presence of haemodynamic instability are powerful predictors of the poor prognosis of patients with acute PE [5]. A definitive treatment of RVD secondary to acute PE has not been defined, and the therapeutic controversy about using thrombolytics in patients with RVD but without systemic hypotension still continues [5,6]. Treatment should be more aggressive for this group of patients, with the basic objective of reestablishing patency of the pulmonary circulation and
*Corresponding author at: Address: Merit Life Park Sitesi, B Blok, Kat: 1 Daire: 5, Serifali/Umraniye 34660, I˙STANBUL. Tel.: +90 216 5082702 Mob: +90 532 3771872, Email: [email protected] © 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier Inc. All rights reserved.
47
Endovascular Treatment of Pulmonary embolism
Figure 1 A, B, C; Computed tomography showed extensive filling defects within the main trunk, right and left main branches, secondary and tertiary branches of the pulmonary arteries representing massive pulmonary embolism (arrows).
preventing further deterioration of right ventricular function and progression to cardiogenic shock [4]. In patients who present with compromised haemodynamics or cardiac function, a variety of treatment options have been utilised to treat acute PE, including surgical embolectomy, intravenous fibrinolysis, catheter directed thrombolysis, and trans catheter mechanical clot fragmentation with or without thrombectomy [7,8]. In recent years, interest has risen in a variety of endovascular strategies based on catheter-based technologies for thrombus removal in patients with massive PE. The goal of the catheter directed procedure is to reduce pulmonary vascular resistance and right ventricular afterload and to increase cardiac output and systemic arterial pressure. PMT has been developed over the past years as a reliable alternative method to treat patients with acute PE and RVD [9]. The primary objective of this study was to evaluate the clinical efficacy of PMT in patients with massive PE. Our secondary objective was to objectively measure the difference in clot burden as assessed by the Miller Score [10]. Following CT-angiography, before and after intervention, as well as to compare the difference in preprocedure and 24-48 hours post-procedure right ventricle and PAP.
Materials and Methods Study Population Consecutive patients with PE, initially diagnosed by either computer tomography, or echocardiography, and transferred from emergency and medical divisions to our catheterisation laboratory for pulmonary angiography from April 2012 to February 2014, were retrospectively evaluated. Twenty-nine patients were referred to the cardiac catheterisation laboratory with a diagnosis of PE, of whom 16 patients met the criteria for massive PE based on the angiographic evidence of a thrombus image in a main pulmonary branch or in two or more lobar branches, and one or more criteria of RVD, the subject of this report. The criteria applied for the diagnosis of RVD were a diastolic diameter of the right ventricle >30 mm, a right ventricular diastolic diameter/left ventricular diastolic
diameter ratio > 1, paradoxical septal movement, hypokinesia of the right ventricular free wall, loss of inspiratory collapse of the inferior vena cava (IVC), and tricuspid regurgitation at a velocity > 2.5 m/s in the absence of inspiratory collapse of the IVC or > 2.8 m/s. [5]. A compromise of the central pulmonary arteries or of two or more lobar arteries by multi-detector contrast-enhanced computed tomography (CT) and confirmed by pulmonary angiography during the procedure was defined as massive PE [11,12] (Fig. 1). The clinical definition of massive PE was established in the presence of cardiogenic shock or hypotension, the latter defined as systemic systolic blood pressure (sSBP) < 90 mm Hg, or a pressure drop > 40 mm Hg for > 15 min not caused by arrhythmia, hypovolaemia, or sepsis. At our centre, PMT was used in patients with massive PE with Miller scores indicative of severe pulmonary vascular bed involvement. PMT was performed in patients with contraindications to or failure of fibrinolysis or with comorbidities resulting in a potentially higher risk of bleeding in case of fibrinolytic administration. Informed consent for participation in the study was obtained according to the guidelines of our institutional review board and the local ethics committee, which approved the study. Patient medical records were reviewed and evaluated for relevant clinical information including: demographics, risk factors for thromboembolism, comorbidities, symptomatic improvement or resolution after treatment, RV pressure and PAP, thrombus clearance, hospital length of stay, survival to discharge and complications.
Treatment Procedure Common femoral venous access was established by placement of a vascular sheath (8F, 10 cm;Terumo Medical Corporation, Elkton, Maryland). The main pulmonary artery was catheterised using a 6-F angled pigtail diagnostic catheter (Cordis Corporation, Miami Lakes, Florida). In all cases, we utilised a 65-cm-long introducer (8F) that was placed selectively in either of the two main pulmonary arteries for selective angiography, and as a conduit to manipulate the pigtail catheter. Intraluminal PAP was measured by direct catheter transduction after a satisfactory pulmonary artery waveform was observed. Digital subtraction angiography was performed in two bilateral anterior oblique
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echocardiogram was repeated 24 h to 48 h following intervention. Fig. 3.
Definitions and Endpoints Figure 2 Aspirex 8 Fr thrombectomy device is used in combination with a 0.018 inch hydrophilic guidewire. (Reprinted with permission by Straub Medical, Wangs, Switzerland.).
projections with the catheter positioned in the main pulmonary artery. Once the location of a pulmonary arterial thrombus was identified angiographically, the angiographic catheters were exchanged for a 0.018-inch guidewire (Glidewire, Terumo, Somerset, NJ). We used an 8 French mechanical thrombus aspiration device (Aspirex; Straub Medical; Wangs, Switzerland) (Fig. 2). This catheter consists of a high-speed rotating spiral located in the body of the catheter that creates negative pressure through an L-shape aspiration system that macerates the thrombus and removes it by aspiration. The device is connected to a motor that generates a rotation speed of 40,000 revolutions per minute. The catheter is introduced over a 0.018-inch guide wire to the site of proximal occlusion of the pulmonary artery or with the greatest thrombus content. The procedure was considered clinically successful when arterial oxygen saturation (SaO2) was improved and sSBP levels increased after fragmentation and/or aspiration, in the absence of major complications such as a perforation of the pulmonary artery or cardiac structures, tamponade, cerebral vascular accident, or death. Patients were then treated with unfractionated heparin, and subsequently switched to oral anticoagulation with warfarin unless contraindicated. Vena cava filters were also deployed at the operator’s discretion to prevent further thromboembolic episodes, according to the results of lower limb venous Duplex ultrasound scan. Transthoracic
Technical success was defined as successful placement of the devices and initiation of the aspiration thrombectomy. Digital subtraction pulmonary angiograms obtained at baseline and after PMT of the pulmonary arteries were reviewed by two cardiovascular surgeons and two cardiologists. Treatment success was assessed by the extent of angiographic reduction in thrombus burden, determined as: complete (> 90% clearance), near complete (50%–90% clearance), or partial (< 50% clearance). The change from baseline to follow-up of the right-to-left ventricular dimension ratio (RV/LV ratio) was obtained from reconstructed CT four-chamber views. The change from baseline to follow-up CTA pulmonary artery clot burden was assessed by the Miller Score [10]. The obstruction index was calculated based on the following formula: seven major branches were identified in the left pulmonary artery (two in the upper lobe, two in the lingual, and three in the lower lobe), and nine major segmental branches were identified in the right pulmonary artery (three in the upper lobe, two in the middle lobe, and four in the lower lobe). The presence of filling defects (emboli) in any of these branches was scored as 1 point per each segment involved, thus leading to an overall obstruction score ranging from 0 (best) to 16 (worst). The perfusion index, which refers to the effect of embolism on pulmonary artery flow, was scored as follows: each lung was divided into three zones (upper, middle, and lower) and the flow in each zone was assessed as absent (3 points), severely reduced (2 points), mildly reduced (1 point), or normal (0 points), thus leading to an overall perfusion score ranging from 0 (best) to 18 (worst). The Miller Score (MS) was computed as the sum in each patient of obstruction and perfusion indexes, ranging from 0 (best) to 34 (worst). A diagnosis of massive PE was confirmed with an MS > 17 [10]. Pre- and
Figure 3 A. Selective pulmonary angiography shows a large obstructive PE in the right main pulmonary artery. B. An 8-French Aspirex thrombectomy catheter was used C. Post treatment angiography shows complete resolution of clot burden and normal perfusion of the right lung.
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Endovascular Treatment of Pulmonary embolism
post-intervention MS and relative MS improvement, defined as the pre-MS minus the post-MS divided by the pre-MS, were calculated for each patient. The haemodynamic status of the patient was evaluated with the shock index obtained by dividing heart rate by sSBP [13]. Other variables that were analysed to evaluate the effect of therapy were the Pao2, Sao2, PAP, right atrial pressure, and mean systemic BP before and after treatment. Haemodynamic measurements were obtained before diagnostic angiography was performed and after PMT.
Statistical Analysis Statistical analysis was performed with Graphpad Instat software (version 3 for Mac; version 11.5, GraphPad Software Inc.). Discrete variables are reported as numbers with percentages and continuous data as mean and standard deviation. The change from baseline to follow-up of both the sub annular RV/LV ratio and of the Miller Score was assessed using one-way, repeated measures analysis or variance for respiratory parameters using ANOVA. A P value < 0.05 was considered statistically significant.
Results Demographics and Procedural Details During the study period, 16 patients who underwent PMT for massive PE were included in the study. The average age of the patients was 55.7 years (range: 38-69), and 11 were men. All patients were treated with heparin once the diagnosis was considered, and all underwent computed tomography (CT) angiography to confirm the diagnosis before the interventional team was consulted. All patients underwent transthoracic echocardiography, which in five cases was performed before CT angiography. Baseline characteristics of the patients are described in Table 1. Most patients (68.7%, n = 11) underwent treatment for bilateral PE, and the remaining patients (31.3%, or n = 5) required unilateral treatment. The most frequent risk factors were prior deep vein thrombosis (56.2%) and obesity (43.7%). Among the clinical manifestations, most patients presented dyspnoea (93.7%), chest pain (81.3%), and cough (62.5%). sSBP level was 85.6 9.8 mm Hg, with 56.2% of patients having sSBP < 90 mm Hg prior to the procedure; mean heart rate was 118.3 10.5 beats/min with preserved left ventricular function (left ventricular ejection fraction, 58.9 5.5%). Echocardiographic evaluation demonstrated right ventricular hypokinesia and dilatation in all patients. A right ventricular diastolic dimension/left ventricular diastolic dimension ratio (RV/LV ratio) > 1 was documented in 68.7% of patients with paradoxical septal movement in 87.5% of the cases. Twelve patients were receiving inotropic support prior to treatment, and nine required mechanical ventilation. Inotropic support was started with 8 mcg/kg/min Dopamine for patient with presenting pre shock, if hypotension or right ventricle failure persists or patient presenting with shock; 0.03 mcg/kg/min Epinephrine was initiated.
Table 1 Baseline Clinical and Demographic Data. N = 16
n (%)
Age: mean (years) Male
55.7 8.3 11 (68.7)
Risk factors for pulmonary embolism Current smoking
12 (75)
Obesity
9 (56.2)
Malignancy
3 (18.7)
Trauma/fractures
2 (12.5)
Recent ( 1)
14(87.5)
Right ventricular hypokinesia
6 (37.5)
Abnormal interventricular septal motion
7 (43.7)
Vena cava dilation Tricuspid regurgitation
5 (31.3) 9 (56.3)
Troponin I > 0.01 ng/mL at presentation
11 (68.7)
D-Dimer > 500 ng/mL at presentation
16 (100)
Deep vein thrombosis
13 (81.3)
LV: Left Ventricle, RV: Right Ventricle.
The administration of vasoactive drugs and volume infusion were maintained constant during the procedure.
Endpoint Analysis Based on pulmonary angiography performed before and after the procedure, treatment of 16 patients resulted in complete thrombus clearance (90%) in 87.5% of the patients and near-complete (50%–90%) clearance in 6.3% (Table 2). The CTA pulmonary clot burden as assessed by the modified Miller Score was significantly reduced from 22.7 3.8 to 11.3 4.4 with significant reduction of both the obstruction and the perfusion indices observed (P < .001) (Fig. 4). Haemodynamic parameters prior to and following the procedure are shown in Table 3. After PMT, a significant increase of both mSBP and Sao2 was observed (75.4 6.2 mm Hg vs 93.6 5.9 mm Hg, p < 0.001; and 81.3 2.2% vs 95.2 3.4%, p < 0.001), as was a significant decrease in the shock index (1.36 0.19 vs, 0.64 0.27, p < 0.0001). Measurements before and after treatment showed a significant decrease in PAP by direct catheterisation (P < .001),
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Table 2 Treatment Outcome and Adverse events. n (%) No. of patients No. of PE lesions
16 26
Complete thrombolysis (>90%)
14 (87.5%)
Near-complete thrombolysis (50-90%)
1 (6.25%)
Partial thrombolysis ( 40 mm Hg), cardiogenic shock, cardiopulmonary resuscitation, right ventricular dysfunction, precapillary pulmonary hypertension (mPAP > 20 mm Hg in the presence of normal pulmonary capillary wedge pressure), an alveolararterial oxygen difference > 50 mm Hg, and clinically serious PE with contraindications for thrombolytic treatment [4,9]. In our series, RVD and a severe pulmonary vascular compromise (preprocedure Miller score of 22.7 3.8) was documented in all cases. The majority of our patients (81.3%) who were submitted to PMT were in a high-risk class for systemic thrombolysis (pregnancy, recent surgery and trauma, failed thrombolysis, and age > 70 years). The overall major complication rate was 6%, with a complete thrombus clearance in 87.5% of the patients. The mortality rate attributed directly to pulmonary embolism was 6.3% (n = 1). We consider that the satisfactory evolution of our patients in the early phase is attributable to a reversion of RVD, shown in the improvement of oxygenation and cardiopulmonary haemodynamic parameters. The mortality rate of our series is less than that reported in the meta-analysis published by Kreit [6] (9.8%) and Fava [31] (10.5%). In the our study, a 46% reduction in the mean pulmonary artery pressure, indicating a reduced RV overload, was obtained with PMT. Evidence supports a corroborative relationship between reduction of PAP and resolution of RV dysfunction [32]. Engelhardt et al. demonstrated significant reduction of both RV/LV ratio from 1.33 to 1.00 and Miller Score after CDT in a patient population that exhibited a risk profile comparable to the risk profile in the current study [30]. At the time of follow up (14.7 4.4 months), a 75 year-old female patient, presented to the ER five months after her discharge with a recurrent PE, due to noncompliance to his anticoagulation regimen. Minimum rate of recurrence could probably be related to the use of a filter device in the IVC in most of our patients. Two recently published meta-analyses [33,34] documented a clinical success rate of 71%, with different PMT techniques, which was improved to 90% with local catheter directed thrombolysis. Reported complications are right ventricle perforation, tricuspid insufficiency, significant bleeding at the site of vascular access (2%), mechanical
Endovascular Treatment of Pulmonary embolism
haemolysis, and blood loss, while the mortality rates range from 0 to 25% [33,34]. The Aspirex device, with its ability to macerate and remove the thrombus from the pulmonary circulation, has proven to be effective in experimental models to revert cardiogenic shock secondary to PE [35]. No patient of our series presented major bleeding at the puncture site, minor bleeding and haematoma was documented in only one patient, without further complications. The use of the Aspirex device was not associated with macroembolisation; nevertheless, a transitory deterioration of oxygenation was observed in one case that was very likely related to microembolisation without conditioning further haemodynamic instability. Clinically evident haemolysis was not documented, and was probably due to the property of the device to prevent thrombus recirculation; only one of our patients required blood transfusion. The main limitations of our study were the small patient population and the retrospective nature of the study. Future prospective studies with larger patient populations may be needed. Although we had a small number of patients, we were able to evaluate and show a significant improvement in cardiac function, providing us with important physiological information after treatment. Our practice has evolved to using PMT in patients who are unstable or deemed to be at increased risk of haemodynamic compromise, and who are judged to have contraindications to systemic thrombolysis. In our small series, we found a marked improvement in haemodynamic parameters using the Aspirex. Our retrospective study demonstrates successful treatment of patients with massive PE using percutaneous aspiration thrombectomy. The results show a reduction of PAP, a high percentage of thrombus clearance, improvement in respiratory parameters and a decrease in the Miller Score rating. The Aspirex was found to be safe and was not associated with damage to cardiac structures although experience with its use in a larger number of patients is required for a better assessment of its safety characteristics. Excluding the one patient who died, all patients experienced symptomatic relief and clinical improvement. PMT is a promising modality used for PE and shows safe, reproducible results.
Disclosure statement All authors declare that there is no conflict of interest to be disclosed.
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