Mechanical Thrombectomy for Acute Pulmonary Ischemia

Abstract

Acute pulmonary embolism (PE) is a restrictive pulmonary vascular compromise with devastating complications depending on size and location. Massive and sub-massive classifications reflect hemodynamic compromise and cardiac dysfunction due to right ventricular strain, respectively. In addition to cardiac dysfunction, pulmonary ischemia and infarction play a key clinical factor. Mainstay management is with anticoagulation to prevent further clot propagation. Recent technological advances have revolutionized treatment modalities. Mechanical thrombectomy, catheter-based clot retrieval, is an effective way to eliminate emboli, restore cardiopulmonary function, and prevent ischemic injury. One such device, the FlowTriever System, has emerged as a way interventionalists can proceed with embolectomy and provide high level, life-saving care for acutely decompensated patients.

1. Introduction

Respiratory compromise due to embolization is one of the leading causes of death among hospitalized patients, a condition known as acute pulmonary embolism (PE). In the United States alone, for every 100,000 individuals, about 70 people will experience pulmonary embolism each calendar year [1].

Simply put, acute pulmonary embolism is a restriction of arterial blood flow in the lung that can be detrimental when misdiagnosed. When the cause of obstruction is blood itself, it is known as venous thromboembolism (VTE). This being the most common cause of pulmonary embolism. It is apropos to mention that blood flow is not the only substance that can cause mechanical lung obstructions. Other substances include, but not limited to fat (traumatic bone fracture, especially of long bones, leads to bone marrow/fat freely circulating systemically), amniotic fluid (as a complication of labor), air (a complication of central venous access), septic embolism (heart valve damage by micro-organism) or even tumor cells metastasizing. The broad array of materials that can lead to this obstructive shock makes it imperative for a clinician to put the clinical picture with the patient’s symptoms to make the diagnosis early. Failure to do so in a timely manner can lead to catastrophic cardiopulmonary compromise and even death.

When PE is caused by venous thromboembolism, greater than 50% of patients will have some clot burden in their lower extremities or a deep vein thrombosis (DVT). The culprit vessels being the femoral and popliteal veins. Some patients may present with symptoms of DVT without PE. Therefore, a thorough investigation is warranted to diagnose, treat and prevent future propagation.

2. Pathophysiology of acute pulmonary embolism

Acute pulmonary embolism is a mechanical obstruction of the blood flow to the lung vasculature and the functional unit involved in respiration, the parenchyma. The parenchyma being starved of oxygen leads to an inflammatory response and cellular death made evident by respiratory compromise and the compensatory respiratory alkalosis on patient presentation. It is imperative to note that both PE and DVT share a spectrum in the realm of VTE. The main difference between these two disease states lies in the location. The main mechanism that leads to PE and DVT, known as the Virchow’s triad, comprises of endothelial injury, venous statis and a hypercoagulable state.

Endothelial injury refers to damage to the vasculature which can lead to an inflammatory response in an attempt to heal with thrombus formation. Most commonly, this occurs in acute trauma, previous history of trauma or prior surgery. Venous stasis, which comprises of a no flow state of blood, can lead to thrombus formation as blood has an affinity to coagulate when not freely flowing. Venous stasis is mostly seen as a complication from immobility (postoperative states) or in patients with major strokes. Lastly, a hypercoagulable state can be a complication of disease states, such as active cancer, medications such as hormonal replacement therapy or oral contraceptives, and finally genetic mutations, most common being factor V Leiden. Other genetic mutations include: protein C and S deficiency, prothrombin gene mutation, antithrombin III deficiency.

Hemodynamically, there are many alterations that occur in the presence of an acute PE that is related to the size of the embolus, the duration of blood flow obstruction as well as the patient’s cardiopulmonary history. Large PEs tend to obstruct the main pulmonary artery along with its branches while smaller PEs are culprits of the smaller peripheral vessels. The obstructive burden coupled with neurohormonal release contribute to hemodynamic compromise and ischemic propagation is presence of neurohormonal release that progress propagate ongoing damage. Common neurohormones present include serotonin, thrombin and histamine [2].

Hypoxic vasoconstriction, a reflex response to acute PE, leads to increase in mean arterial pulmonary pressure. This increase is significantly high in patients with history of pulmonary hypertension. Increased pulmonary artery pressure contributes to increased right ventricular (RV) afterload causing right ventricular enlargement and a leftward bulging of the interventricular septum commonly found on echocardiography. Cardiac arrest is hence from the vascular compromise from increased pressure on the right coronary artery, causing myocardial ischemia.

Acute PE impairs efficient gas exchange. Hypoxemia and increase in the alveolar-arterial oxygen tension gradient are the most common gas exchange abnormalities. Total dead space increases. Ventilation and perfusion become mismatched, with blood flow from obstructed pulmonary arteries redirected to other gas exchange units [2]. The obstruction of blood flow in the pulmonary arteries leads to a redistribution of blood flow causing some alveoli to have low ratios of ventilation to perfusion, whereas others have excessively high ratios of ventilation to perfusion [2].

3. Clinical manifestations

Assessment of PE in patients can be challenging as symptoms can be nonspecific. The patient could present with an array of different possibilities but a history of dyspnea, progressive or sudden onset in nature is a common complaint. Other complaints include pleuritic chest pain, cough and hemoptysis mostly in patients with pulmonary infarction. Due to the nonspecific symptoms that acute PE could present with, it is imperative to garner the appropriate risk factors that could lead to the suspicion. Another complaint that should increase the index of suspicion is a patient with dyspnea coupled with recent onset lower extremity tenderness or swelling.

Most patients with PE have tachypnea and tachycardia associated with hypoxemia. Similar findings can occur in disorders such as heart failure, pneumonia, or chronic obstructive pulmonary disease [2]. A good clinical examination is apropos to ascertain any other possible disease pathology that may mimic PE.

4. Diagnosis

The diagnosis of PE relies on a high clinical suspicion along with the patient’s history and physical exam. After suspicion, confirmation with appropriate testing leads to the final diagnosis. Diagnostic tests alone are not the reflex course of action with a high index of suspicion due to the fact that there are many disease states that could present similarly. In patients with a high index of suspicion, the Wells criteria, developed by Wells et al., is a simple clinical model to predict the likelihood of PE. Scoring system has a maximum of 12.5 points, based on 7 variables: 3 points each for clinical evidence of DVT and an alternative diagnosis being less likely than PE, 1.5 points each for heart rate > 100 per minute, immobilization/surgery within 4 weeks, and previous deep vein thrombosis/PE, and 1 point each for hemoptysis or cancer [2, 3]. The pretest probability for PE after utilization of the Wells scoring system categorizes PE into low (score < 2), moderate (score between 2 and 6) or high risk (score > 6). This will then guide a clinician on subsequent tests such as a D-dimer assay, a byproduct of ineffective fibrinolysis released into systemic circulation. D-dimer elevation has high sensitivity for acute PE, as high as 98%, albeit poor sensitivity. Instances such as malignancy, advanced age and chronic inflammatory conditions are all reasons for an elevated d-dimer besides PE. Therefore, the benefit of a d-dimer assay lies in its high negative predictive value and its ability to effectively reduce further diagnostic testing in patients with an already low to moderate pretest probability with Wells scoring [4, 5].

Imaging studies in patients with acute PE in recent times have been with computed tomography pulmonary angiography (CT-PA). The benefit of CT-PA is direct thrombi visualization in the pulmonary arteries and effectively ruling out patients without PE [2]. The use of radiocontrast dye should be taken into consideration in patients with a suspicion of PE, but in patients with decompensation coupled with a high index of suspicion, the benefits of imaging clearly outweigh the risk. Furthermore, CT-PA with evidence of thrombus in the pulmonary arteries up to the segmental level provides strong evidence of PE. When negative, it does exclude PE but the presence of PE in the subsegmental regions, sometimes missed by CT-PA, does not alter patient outcome as these patients have at least as good an outcome as patients with a negative lung scan [2, 6].

There are indeed other modalities for investigation of acute PE, though by far a CT-PA has emerged as the more favorable option. Other modalities include a ventilation-perfusion (V/Q) scan, a two-part exam with a ventilation phase and perfusion phase. Diagnosis of PE based on a V/Q scan is made when PE-associated lung areas fail to enhance on the perfusion phase using technetium-labeled albumin macroaggregates. Magnetic resonance imaging (MRI) with gadolinium-enhancement has been shown to have similar efficacy to that of CT-PA.

5. Management of acute pulmonary embolism

Anticoagulation has become the mainstay treatment for acute PE though the degree of severity influences the length of treatment. The severity of acute PE depends on parameters such as hemodynamics, right ventricular dysfunction, presence of troponin and/or brain natriuretic peptide (BNP). Risk stratification using the appropriate criteria not only guides the choice of treatment, but also provides outpatient management options. It is also highly important to know if the patient has any contraindications to anticoagulation prior to initiation of treatment. Massive (high-risk) PE is the presence of hemodynamic compromise, right ventricular dysfunction and increased troponin and/or BNP levels. In such patients, the most common cause of death is not the PE, but the complication of acute right ventricular failure. To mitigate this complication, hemodynamic and respiratory support early is crucial. Due to the dependence of preload in right ventricular failure, both fluid expansion and inotropic agents, such as dobutamine, dopamine and/or norepinephrine, are needed to manage shock [2]. In patients with presence of right ventricular dysfunction and increased troponin and/or BNP levels without hemodynamic compromise, are classified as sub-massive (intermediate-risk) PE with consideration of fibrinolytic therapy if very symptomatic. Lastly, low-risk PE classification is in the group of patients with no hemodynamic compromise, right ventricular dysfunction or increased troponin or BNP levels. In such patients, a consideration of outpatient management is acceptable.

5.1 Anticoagulation

Anticoagulation has become the cornerstone modality of treatment in patients with acute PE. In patients with a very high index of suspicion or massive PE, anticoagulation should be initiated prior to confirmatory test. The most extensively studied anticoagulant in PE is heparin. Heparin, an anti-thrombin III inhibitor, acts mainly by inactivation of factor Xa in the clotting cascade, preventing the conversion of prothrombin to thrombin. Other options include low molecular weight heparin (LMWH), fondaparinux or the direct factor Xa inhibitors, rivaroxaban and apixaban. Dosing for heparin is usually 80 U/kg bolus followed by an infusion at the rate of 18 U/kg per hour with subsequent doses based on aPTT results [4]. Additionally, it is important to monitor platelet count while heparin is administered due to the risk of heparin-induced thrombocytopenia (HIT). After the initial heparinization phase, continued treatment is with an oral direct thrombin inhibitor, factor Xa inhibitor or warfarin.

The duration of treatment of PE is directly related to the precipitating factors that led to the PE. In other words, whether the PE was provoked or unprovoked. Special considerations in terms of treatment modality and duration are made for certain populations such as pregnant females or patients with active cancer. For all other patient populations with who present with a first time PE, the minimum duration of treatment is 3 months. If the PE is provoked and the factors are withdrawn such as a female stopping hormonal treatment, then a 3-month period of oral anticoagulation is sufficient. In patients with an unprovoked or life-threatening PE, indefinite anticoagulation is ideal due to a higher risk of recurrence. There must be a risk and benefit analysis when indefinite anticoagulation is being pursued, especially in patients with a higher bleeding risk [4].

5.2 Thrombolytic therapy

Systemic thrombolytic therapy is an effective therapy in preventing deaths from PE, however it markedly increases bleeding risks, including intracranial and fatal bleeding [7]. The PEITHO (Pulmonary Embolism Thrombolysis Study), which compared tenecteplase with placebo in 1000 PE patients without hypotension but with right ventricular dysfunction, found no clear net benefit from systemic thrombolytic therapy; the reduction in cardiovascular collapse (odds ratio: 0.30) was offset by the increase in major bleeding (odds ratio: 5.2) [8]. Consequently, systemic thrombolytic therapy is usually reserved for PE patients with hypotension. Catheter-directed thrombolysis (CDT) was initially developed for treatment of arterial, dialysis graft, and deep vein thromboses (leg or arm). When used to treat acute PE, a wire is usually passed through the embolus, followed by placement of a multi-sidehole infusion catheter through which a thrombolytic drug is infused over 12–24 h. The delivery of the drug directly into the thrombus is expected to be as effective as systemic therapy but to cause less bleeding because a much lower dose of the drug is used.

SEATTLE II is a single-arm prospective cohort study in which 150 patients with lobar artery or more central PE (31 with and 119 without hypotension) were treated with ultrasound-assisted CDT using a standardized protocol [9]. Tissue plasminogen activator was infused into each treated lung at a rate of 1 mg/h, to a total dose of 24 mg (over 12 h for bilateral lung infusions), and no additional mechanical maneuvers were used to disrupt or aspirate thrombus. When computed tomography pulmonary angiography was repeated after 48 h, the right ventricular to left ventricular ratio was decreased by 27% and thrombus burden was reduced by 30%. Pulmonary artery pressure also decreased by 27% between the start to the end of CDT. These 3 improvements were each highly statistically significant. There were 17 episodes of major bleeding in 15 patients (10%): one was associated with hypotension; all required transfusion; none was intracranial; and none was fatal.

5.3 Mechanical thrombectomy

Acute pulmonary ischemia due to pulmonary embolism results in a cascade of events, from decreasing lung compliance to increasing pulmonary resistance ultimately resulting in RV dysfunction and hemodynamic collapse. Thus, in certain cases more rapid thrombus removal is required, and mechanical techniques are now available.

The FlowTriever System (Figure 1) is a mechanical thrombectomy device indicated for use in the peripheral vasculature and pulmonary arteries (PAs). FlowTriever received U.S. Food and Drug Administration 510(k) clearance for PE in May 2018—the first mechanical thrombectomy device to receive that indication. The FlowTriever System includes Triever aspiration catheters (16-F, 20-F, 24-F) capable of removing large amounts of thrombus via aspiration with a 60 cc syringe. The FlowTriever System also includes FlowTriever catheters with three self-expanding nitinol mesh disks of different sizes designed to aid in extraction, if needed, by engaging and disrupting thrombus. Anticoagulation with heparin is recommended per routine catheterization laboratory practice to prevent thrombosis of the catheter. The aspiration catheter is advanced over a 0.035-inch wire to the level of the right or left PA, just proximal to the occlusive thrombus. Once engaged, the clot is extracted via aspiration through the catheter. The procedure can be repeated several times per side at the discretion of the physician, depending on the amount of clot retrieved and the improvement in distal flow on repeat angiography.

Figure 1.

The FlowTriever® system. The Triever aspiration catheter is shown in purple, and the optional FlowTriever® catheter with nitinol disks is shown emerging from the distal end of the Triever catheter.

The FlowTriever System has been evaluated in several clinical studies both prospectively and retrospectively. The first of these was a prospective multi-center study, the FLARE (FlowTriever Pulmonary Embolectomy Clinical Study) trial, which was the largest systematic evaluation of the effectiveness of mechanical thrombectomy for PE at the time [10]. From April 2016 to October 2017, 106 patients were treated with the FlowTriever System at 18 U.S. sites. Two patients (1.9%) received adjunctive thrombolytics. The mean procedural time was 94 min, and the mean intensive care unit stay was 1.5 days. Forty-three patients (41.3%) did not require any intensive care unit stay. At 48 h post-procedure, average RV/LV ratio reduction was 0.38 (25.1%; p < 0.0001). Four patients (3.8%) experienced 6 major adverse events, with 1 patient (1.0%) experiencing major bleeding. One patient (1.0%) died from undiagnosed breast cancer through 30-day follow-up. The trial concluded that percutaneous mechanical thrombectomy with the FlowTriever System appears safe and effective in patients with acute intermediate-risk PE, achieved significant improvement in RV/LV ratio, and resulted in minimal major bleeding.

Large-bore aspiration mechanical thrombectomy with the FlowTriever System was also evaluated in two retrospective single-arm clinical studies. The first of these [11] was a single-center study of 46 patients with both massive (high-risk) and submassive (intermediate-risk) PE. The authors reported a significant reduction in mean PA pressure from 33.9 ± 8.9 mmHg to 27.0 ± 9.0 mmHg (p < 0.0001) immediately following thrombectomy. The majority of patients experienced intraprocedural reductions in mean PA pressure (88%) and supplemental oxygen requirements (71%). All patients survived to discharge, and there were no procedure-related complications or deaths within the 30 days following discharge. The second retrospective study [12] was a multi-center study of 34 patients with massive and very-high-risk submassive PE. All patients were either hemodynamically unstable, intubated, or normotensive but with low cardiac index (< 1.8 L/min/m²). In this very sick population, cardiac index improved significantly immediately following thrombectomy (2.0 ± 0.1 L/min/m² vs. 2.4 ± 0.1 L/min/m², p = 0.1), as did mean PA pressure (33.2 ± 1.6 mmHg vs. 25.0 ± 1.5 mmHg, p = .01). Two patients deteriorated during the procedure, one who expired and one who was stabilized on ECMO. All other patients survived through a mean follow-up of 205 days. These two retrospective studies provide clinical evidence supporting the safety and effectiveness of mechanical thrombectomy with the FlowTriever System for PE treatment.

More recently, the FlowTriever System was studied in a nonrandomized two-arm retrospective analysis versus routine care [13]. This single-center study compared outcomes for 28 patients who underwent mechanical thrombectomy with the FlowTriever System to those for 30 patients who received routine care, which consisted of anticoagulation alone, anticoagulation with CDT, or systemic thrombolysis. In-hospital mortality was significantly lower for patients undergoing mechanical thrombectomy versus routine care (3.6% vs. 23.3%, p < 0.05). Furthermore, the average intensive care unit length of stay was also significantly shorter for patients undergoing mechanical thrombectomy (2.1 ± 1.2 days vs. 6.1 ± 8.6 days, p < 0.05). Total hospital length of stay and 30-day readmission rates were similar between the two groups. This study provides initial comparative data suggesting that mechanical thrombectomy can improve in-hospital mortality and decrease ICU length of stay for PE patients with elevated risk profiles.

5.4 Technical aspects of mechanical thrombectomy

1. Pre procedure planning

   1. Patient Information

      1. Prior to any pulmonary embolism procedure several patient conditions must be made clear. Several questions that all operators should ask include, what are the current hemodynamics and does that patient require vasopressor support? What is the current respiratory status (Ie O2 supplementation or on mechanical ventilation)? What is the bleeding risk and can the patient be anticoagulated? During our procedure we maintain and actual clotting time (ACT) of >250 secs.

   2. Pre case Imaging

      1. CT is the most rapid and common imaging tool used. Specific items to look for include, location and size of clot, RV/LV Ratio, and pulmonary infarct.

      2. Echocardiography will not only show LV and RV size but RV systolic function.

   3. Additional things to consider:

      1. History or current DVT

      2. IVC Filter in Place

      3. Clot in Transit (is TEE or TTE available urgently)

      4. Recent Surgery/Extended immobile time (travel)

      5. Cancer History

      6. History of PE

      7. Infarct consideration (reperfusion injury/elevated wire perforation risk)

   4. Anesthesia:

      1. Conscious sedation is recommended. General Anesthesia has a risk of worsening hypotension and reducing preload to the RV. If systemic pressure is tenuous, a rapid reduction in RV filling can result in immediate hemodynamic collapse.

2. Patient Selection

   1. Avoidance of thrombolytics

      1. There are several advantages to the decision making for who would benefit from thrombolytic therapy for pulmonary embolism. The immediate decision is to determine who is at highest risk and thus has the largest to gain. Any patient with right ventricular (RV) dysfunction, we feel should be considered for thrombolytic therapy. Patients with an elevated RV: LV ratio; greater than 0.9, elevated pro-bnp, elevated troponins, and hemodynamics suggestive of reduced cardiac output, should be considered for thrombolytic therapy.

      2. Patients need to be able to lay either supine or prone for a minimum of 30 minutes, thus taking oxygen requirements and body habitus into consideration.

      3. Any patient with a relative contraindication to thrombolytic therapy, or felt to be at elevated risk, immediately should be considered for thrombotic intervention.

3. Access

   1. US guidance

      1. Access to venous circulation, when using large bore sheaths should always be performed with ultrasound guidance. It is advantageous in the venous system to evaluate for upper or lower extremity deep venous thrombosis, prior to starting the procedure, as well as avoidance of an arterial puncture.

   2. Femoral

      1. The most common access site for pulmonary thrombectomy is the common femoral vein

   3. Jugular

      1. When an alternative access is required another option is the internal jugular vein.

4. Pulmonary angiogram

   1. Difficulties

      1. Image quality tends to be the dis-advantage. Morbid obesity, patient movement, as well as variations in imaging acquisition (ie dye load, manual vs. power injection), can result in wide range of image quality.

5. Aspiration thrombectomy catheters

   1. Inari Medical

      1. Twenty-four french aspiration guide catheter that navigates through the right heart and delivers the catheter directly into the pulmonary artery. Aspiration is performed by a manual pull. The large bore catheter maximizes aspiration and collection of thrombus. The 24 F catheter creates an aspiration flow rate of 143 mLs/second.

      2. Sixteen french curve

         1. Due to the natural curvature of the pulmonary artery to the right, the 24 F catheter takes a turn to the right pulmonary artery typically with little difficulty. The catheter when placed in the left pulmonary artery, typically does not engage the left lower lobe. The 16 french curve catheter is placed within the 24F catheter and is preshaped to point down into the left pulmonary artery for selective thrombus aspiration.

      3. Bloodloss technology

         1. The FlowSaver blood return system is designed to be used with the FlowTriever aspiration catheter to reduced blood loss by filtering aspirated thrombi and blood for reinfusion back to the patient, thus enabling bloodless thrombectomy for pulmonary embolism procedure. The filtration system includes a 40-micro filter. Filtered blood can be reintroduced using a 60-cc collection syringe.

   2. Penumbra, Inc.

      1. The Indigo aspiration system is indicated for use in the peripheral arterial system and the pulmonary arteries, receiving U.S. Food and Drug Administration 510(k) clearance for PE in December 2019.

      2. The Indigo system lightning 12 aspiration catheter that navigates through the right heart and into the selected pulmonary artery. The 12F system, unlike the manual aspiration of the Inari device, is connected to the Penumbra aspiration pump, resulting in a continuous vacuum system at −28.5 mmHg. If thrombus is not aspirated, the system also has a separator wire that can be advanced through the catheter to disrupt thrombus at the distal tip.

6. Intraprocedural complications

   1. Perforation

      1. The most common cause of pulmonary artery perforation is due to a wire complication. Wire perforation causes include treating distal clot, poor wire positioning and overlapping vessel (specifically on the left side)

      2. Avoidance and Management

         1. Limit use of guide wires, and always use Amplatz wire to work over

         2. Use multiple shots to confirm location of wire and catheter

         3. Use multiple angles of monitor to confirm locations

         4. If Perforation does occur, increase supplemental oxygen, stop and reverse anticoagulation and consider placing a occlusion balloon proximal to the perforation.

   2. Right heart trauma

      1. If the tricuspid valve crossed safely with angled pigtail catheter or balloon tip catheter, typically not as concerned. If a end hold catheter was used, through a chordae tendinea of the tricuspid valve.

      2. Always advance with caution as advancing through heart monitoring pain, excessive tension advancing catheter, and any arrhythmias happening

      3. Never advance large bore catheters without dilators

      4. Use buddy wires to assist stability in accessing multiple vessels to avoid kick back

   3. Shock/RV failure

      1. There are several methods of determining right ventricular systolic function. A calculated PAPi in the cardiac cath lab can determine who would benefit from RV mechanical support (ie Abiomed Impella RP). If the PAPi is calculated to be less than 1, and you have achieved enough thrombolytic therapy to allow for distal perfusion, mechanical support should be considered. Extracorporeal membrane oxygenation (ECMO) can also be considered for both hemodynamic support and oxygenation.

7. Closure

   1. Most venous access sites can be closed with manual pressure alone. However, with large bore access we have using the Abbott Medical proglide perclose suture mediated closure. This device has been shown to reduce time to hemostasis, ambulation and discharge compared to manual compression

8. Post Procedure management

   1. ICU avoidance

      1. The use of thrombolysis for the treatment of PE at some institutions requires ICU level care.

      2. Mechanical thrombectomy is a means of direct therapy which can result in immediate clinical response and will commonly not require intensive care management.

      3. Additionally with the avoidance of tissue plasminogen activator (tPA), ICU admission post procedure is commonly unnecessary.

   2. Venous dopplers

      1. The most common source of PE is DVT. Thus, all patients require bilateral venous duplex for confirmation of residual disease.

      2. Based on these results, it is a clinical decision whether therapy is required for DVT.

   3. Hypercoagulable work up

      1. Patients who benefit from this work up include:

         • those with/without a family history of VTE

         • patients age < 45 years

         • recurrent thrombosis or thrombosis in unusual sites

         • arterial thrombosis

         • history of warfarin-induced dermatologic necrosis

      2. These patients will benefit from testing: activated protein C resistance, factor V Leiden, Prothrombin gene mutation, Protein C and S deficiency, Antithrombin deficiency.

   4. DOAC

      1. DOACS such as Factor Xa inhibitors, Apixaban or Rivaroxaban, have become more favorable than Warfarin for anticoagulation due to lower bleeding risk, monitoring for therapeutic INR levels and easier dosing. Apixaban is dosed twice daily while Rivaroxaban is daily dosing. A lower dose is required based on age ≥80, weight ≤60kg and creatinine ≥1.5

   5. Follow up Echo

      1. A follow up echo is used to determine RV dimensions, RV dysfunction and residual pulmonary hypertension.

      2. It is our practice that if there is residual elevation of pulmonary systolic pressure, we refer the patient to a pulmonary hypertension specialist.

5.5 Mechanical thrombectomy case reports

• Case 1

  • A 33-year-old woman with no significant past medical history presented to our emergency department after multiple syncopal episodes. An ambulance service was called by family and the patient arrived hypotensive and poorly responsive. She required 6 L of supplemental oxygen and vasopressor support to keep a mean arterial pressure greater than 60 mmHg and oxygen saturation greater than 92%. A bedside anterior-posterior chest X-ray showed a normal cardiac silhouette and clear lung fields. A 12-lead electrocardiogram was consistent with a sinus tachycardia and right bundle branch block. Initial laboratory data was positive for an elevated d-dimer (> 5000 ng/mL), positive troponin (0.4 ng/mL), and pro-brain natriuretic peptide (> 10,000 pg/mL). A stat CT angiogram of the chest demonstrated a massive PE with complete occlusion of the left lower lobe and a RV/LV ratio of 1.5.

  • The patient was moved emergently to the cardiac catheterization laboratory for immediate therapeutic aspiration thrombectomy. Access was obtained in the right femoral vein using ultrasound guidance. Initial systolic PA pressure was 60 mmHg and the mean PA pressure was 35 mmHg. A pulmonary angiogram confirmed complete occlusion of the left lower lobe (Figure 2). The 24-F Triever aspiration catheter (Triever24) was positioned in the left pulmonary artery. A 20-F Triever Curve catheter, capable of curving up to 260° to aid in navigating in difficult anatomies, (Figure 3) was used coaxially with the Triever24 catheter to angle to the lower lobe where two aspirations were performed. A large amount of thrombus was removed (Figure 4) and repeat pulmonary angiography showed almost complete pulmonary artery opacification and large reduction in thrombus burden (Figure 5). Within minutes there was hemodynamic improvement and oxygen requirements returned to room air alone. Post-thrombectomy pulmonary artery systolic pressure was 33 mmHg. The patient was transferred to the general medical ward and started on oral Factor Xa inhibitor and discharged home the following day.

• Case 2

  • A 75-year-old man with a past medical history of metastatic prostate cancer with known spinal involvement, presented to our emergency room with acute onset of shortness of breath and chest tightness. Initial oxygen saturation was 82% requiring high flow oxygen with a non-rebreather mask. Initial blood pressure was 110/80 mmHg and heart rate of 110 bpm. The pretest probability of PE was high thus the first diagnostic test was a CT pulmonary angiogram, which confirmed a saddle pulmonary embolism and large thrombus burden in the left and right lobes. The RV/LV ratio was 1.4.

  • Pulmonary angiography was consistent with CT findings (Figure 6). With a known history of spinal metastasis, thrombolytic therapy was contraindicated. The femoral vein access site was dilated to accommodate a 24-F sheath, the Flowtriever System was positioned into the mainstem pulmonary artery and a single aspiration was performed. The catheter was then positioned into the left pulmonary artery performing a single aspiration, followed by the right pulmonary artery, again requiring a single aspiration. Repeat angiography confirmed thrombus resolution and large clot removal (Figure 7). The patient was transferred to the general medical floor on room air. An echocardiogram performed the next day demonstrated normal right ventricular size and function with normal pulmonary pressures. The patient was discharged home the following day.

• Case 3

  • A 44-year-old woman with a recent history of COVID-19 pneumonia presented from home with acute worsening of dyspnea and new pleuritic chest pain. Prior to this admission she required no supplemental oxygen, however, now was on 10 L of oxygen to maintain a saturation > 96%. A CT angiogram of the chest was consistent with a massive right middle lobe pulmonary embolism. The patient was taken to the cardiac catheterization laboratory for emergent intervention. Due to rapid decline in respiratory status and acute hypoxic respiratory failure, the patient was placed on mechanical ventilation. In order to provide rapid therapy, aspiration thrombectomy was performed in the right pulmonary artery. Initial pulmonary angiogram clearly demonstrated large thrombus burden of the right pulmonary artery (Figure 8, left). After a single aspiration was performed, repeat angiogram confirmed almost complete resolution (Figure 8, right), and large thrombus debulking (Figure 9). At the conclusion of the procedure, the patient required <40% fraction of inspired oxygen (Fio2) and positive end-expiratory pressure (PEEP) of 5, maintaining an oxygen saturation > 99%. That evening while in the intensive care unit she was successfully extubated and required 2 L of oxygen by nasal cannula. Seventy-two hours after her initial presentation, she was discharged home on room air.

Figure 2.

Pre-treatment pulmonary angiogram showing complete occlusion of the left lower lobe in a patient with massive pulmonary embolism.

Figure 3.

Intra-procedure pulmonary angiogram showing the Triever20 curve catheter coaxial within the larger Triever24 catheter in the left lower lobe of the lung in a PE patient.

Figure 4.

A large amount of thrombus extracted with the FlowTriever® system from a PE patient.

Figure 5.

Post-thrombectomy pulmonary angiogram showing almost complete pulmonary artery opacification and large reduction in thrombus burden.

Figure 6.

Pre-thrombectomy pulmonary angiography of the right and left lungs demonstrating a saddle pulmonary embolism with large thrombus burden.

Figure 7.

Thrombus extracted using the FlowTriever® system.

Figure 8.

Pre- (left) and post-thrombectomy (right) pulmonary angiograms demonstrating large thrombus burden prior to thrombectomy with the FlowTriever® system and subsequent resolution post-thrombectomy.

Figure 9.

Large amount of thrombus extracted with the FlowTriever® system in a patient with history of COVID-19.