This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
HISTORY OF PRESENTATION
A 72-year-old woman presented to the emergencydepartment (ED) with symptoms of rapidly worseningshortness of breath over the past 36 to 48 h. Hersymptoms had progressed rapidly from her usualstate of health to not being able to take a couple ofsteps and to significant dyspnea at even at rest. She
EARNING OBJECTIVES
To make a rapid diagnosis of PE with hemo-dynamic instability by multidisciplinary team(PERT approach), reducing invasive diag-nostic tests, allowing rapid diagnosis, andapplying advanced therapies with likelyreduction in morbidity and mortality.To understand catheter-directed mechanicalthrombectomy use in the setting of massivePE without the risk of critical and fatalhemorrhage associated with thrombolysis.
N 2666-0849
m the Division of Cardiovascular Diseases, Lankenau Medical Center an
od, Pennsylvania. Ashwin Ravichandran, MD, served as Guest Editor for th
ationships relevant to the contents of this paper to disclose.
e authors attest they are in compliance with human studies committees
tutions and Food and Drug Administration guidelines, including patient co
JACC: Case Reports author instructions page.
nuscript received February 24, 2020; revised manuscript received April 2
had no significant chest pain. Physical examinationrevealed the following: blood pressure, 103/56 mm Hg; heart rate, 118 beats/min; respiratory rate,22 breaths/min; and hypoxia with oxygen saturationin the low 80s with respiratory distress. Her lungfields were clear to auscultation, and there was nosignificant evidence of volume overload byexamination.
MEDICAL HISTORY
She had a known history of immunoglobulin G kappamultiple myeloma treated with lenalidomide anddexamethasone, previous history of pulmonary em-bolism (PE), hypertension, hypothyroidism, and dia-betes mellitus. She had completed 1 year ofanticoagulant therapy for a previous episode of PEapproximately 9 years earlier and was not currentlyreceiving anticoagulant therapy. Her other significantmedications included amlodipine, glimepiride, levo-thyroxine, and losartan.
https://doi.org/10.1016/j.jaccas.2020.04.031
d Lankenau Institute for Medical Research, Wynne-
is paper. All authors have reported that they have no
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DIFFERENTIAL DIAGNOSIS
The differential diagnosis included PE, decom-pensated heart failure, pneumonia, and atypical pre-sentation of acute coronary syndrome.
INVESTIGATIONS
On presentation, the electrocardiogram showed si-nus tachycardia, new right bundle branch block, aqR pattern in lead V1, and T-wave inversions inleads V1 and V2 (Figure 1A). Chest radiographyshowed no acute cardiopulmonary disease. Labora-tory study results were significant for the following:mild troponin T elevation, 0.19 ng/ml (referencerange <0.005 ng/ml); elevated lactate, 5.1 mmol/l,with combined metabolic and respiratory acidosison arterial blood gas determination with pH 7.19;partial pressure of carbon dioxide, 42 mm Hg;serum bicarbonate, 14 mEq/l; and creatinine,2.7 mg/dl, compared with baseline creatinine of1.0 mg/dl, indicating acute kidney injury (AKI). Ur-gent bedside transthoracic echocardiography (TTE)showed a small hyperdynamic left ventricular cavitywith hyperdynamic systolic function with an esti-mated ejection fraction >75%, a severely dilatedright ventricle with severely reduced right ventric-ular (RV) systolic function and a hyperdynamic RVapex (the McConnell sign), moderate to severetricuspid regurgitation with elevated estimated RVsystolic pressure of 50 to 55 mm Hg, and a dilatedinferior vena cava (IVC).
MANAGEMENT
The patient was evaluated by a multidisciplinaryheart team comprising ED, pulmonary and criticalcare, and interventional cardiology physicians. Onthe basis of clinical presentation and TTE imaging, adiagnosis of cardiogenic shock secondary to RVfailure resulting from massive PE was made.Because of the patient’s AKI and unstable hemo-dynamics, the multidisciplinary team decided to notpursue confirmatory computed tomography (CT)with angiography. She was treated with intravenousheparin for anticoagulation and underwent emer-gency pulmonary angiography and intervention inthe cardiac catheterization laboratory. She wasevaluated by the multidisciplinary team within60 min, and bedside TTE was performed within90 min. The time from presentation to the EDand the start of mechanical thrombectomy was<120 min.
Right-sided heart catheterization was per-formed through a right femoral veinapproach. The pulmonary angiogram showeda large clot burden in the right pulmonaryartery (PA). The right femoral venous sheathwas up-sized to a 22-F DrySeal sheath (W.L.Gore & Associates, Newark, Delaware). AnAmplatz Super Stiff wire (Boston Scientific,Natick, Massachusetts) was placed underfluoroscopic guidance in the right PA, and aFlowTriever catheter (Inari Medical, Irvine,California) was advanced, followed by suc-cessful mechanical aspiration of large clotfragments and excellent flow noted on the
angiogram. Subsequently, a pulmonary angiogram ofthe left PA showed complete obstruction of flow(Figure 2A). Several clot aspirations were similarlyperformed. A large clot was noticed on the tip of theFlowTriever cannula; this clot was unable to bemoved despite disk deployment. With negative suc-tion maintained, the clot was pulled down to the iliacvein, and an infrarenal IVC filter was placed through aleft jugular vein approach. A repeat angiogram of theleft PA showed the establishment of significant flow(Figure 2B).
The procedure was complicated by hemoptysisrequiring reversal of anticoagulation with protamine.Emergency intubation, mechanical ventilation, andflexible bronchoscopy were performed, with no activebleeding. Small to moderate-sized blood clots wereseen in the airways, without obstruction. These clotswere removed with saline wash and suctioning.
The patient continued to have persistent hypo-tension, tachycardia with narrow pulse pressure, andRV dysfunction noted on TTE. RV failure was treatedwith a ProtekDuo (Tandem [Liva Nova], London,United Kingdom) heart percutaneous RV assist de-vice. The device was placed through a right internaljugular access, with inotropic support and an epo-prostenol infusion. She had an episode of atrialfibrillation with rapid ventricular response requiringDC cardioversion, and sinus rhythm was maintainedwith an amiodarone infusion.
FOLLOW-UP
Follow-up TTE within 24 h showed significantimprovement, with only mild RV dilation and mod-erate systolic dysfunction (Figure 3B). Her hemody-namics improved over 48 h, and she was successfullyweaned from the RV assist device and epoprostenol.Repeat bronchoscopy showed no evidence of
FIGURE 1 Initial and Post-Procedure ECGs
(A) Electrocardiogram (ECG) on presentation showing sinus tachycardia, right bundle branch block, and a qR pattern in lead V1. (B) Elec-
trocardiogram 24 h post-procedure showing resolution of sinus tachycardia, right bundle branch block, and the qR pattern in lead V1.
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bleeding, and she was extubated in 72 h, followed bysignificant improvement in clinical status. She wasdischarged within 1 week of admission on an antico-agulant regimen with rivaroxaban. Follow-up TTE5 weeks post-discharge showed normal RV size andfunction with mild tricuspid regurgitation and RVsystolic pressure of 26 mm Hg (Figures 3A to 3F, whichalso show the patient’s initial findings for compari-son). An IVC filter was removed in 3 months.
DISCUSSION
The PE response team (PERT) approach to patientswho present with intermediate- to high-risk PE hasbeen described to provide rapid access to advancedtherapies (1,2). Our patient presented with clinicalmanifestations consistent with massive PE withseveral features suggestive of adverse prognosis,including sinus tachycardia, new right bundle
FIGURE 2 Initial and Post-Procedure Angiograms
(A) Pulmonary angiogram showing complete obstruction of the left pulmonary artery. (B) Pulmonary angiogram showing re-establishment of
flow in the left pulmonary artery following mechanical thrombectomy.
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branch block, a qR pattern in lead V1, an elevatedtroponin T level, RV dilatation, hypokinesis, theMcConnell sign, severe tricuspid regurgitation, andevidence of pulmonary hypertension on TTE. TheMcConnell sign has a 94% specificity for the diag-nosis of acute PE, and with the clinical presentationsuggesting a high pre-test probability of PE, confir-matory testing with CT angiography was not per-formed (3). Acute massive or submassive PE has anexceedingly high mortality rate, and an elevatedlactate level is a strong independent predictor ofmortality (4,5). The magnitude of lactate elevationcorrelates with the risk of death and is >35% forlactate levels higher than 5 mmol/l (5). Systemicthrombolysis has been the recommended treatmentof choice in this setting; however, it is associatedwith major systemic bleeding, including a risk ofintracranial hemorrhage (6,7).
Catheter-directed mechanical thrombectomy withthe FlowTriever Retrieval/Aspiration System hasbeen found to be beneficial in intermediate-risk PE(8). This case demonstrates the use of this system
in a patient with PE with cardiogenic shock.Thrombectomy was performed by engaging thethrombus, disrupting it with self-expanding nitinoldisks, and extracting it by simultaneously aspiratingand withdrawing it through a 20-F guide catheter,with appropriate mechanical circulatory supportused for shock. Hemoptysis is a known complicationof PE as a result of ischemic pulmonary paren-chymal necrosis. Although an obvious site ofbleeding could not be identified on bronchoscopy,wire perforation as a cause of hemoptysis could notbe ruled out and should be recognized as a poten-tial complication of the procedure. In this case, thePERT approach with multidisciplinary expertsallowed treatment without confirmatory CT angi-ography and immediate treatment with advancedtherapies, thus reducing the time to treatment. Atotal of 70 ml of iodine contrast material was usedfor the procedure. The CT angiogram PE protocolrequires approximately 60 to 150 ml of iodinecontrast material (9). Hence possible harm fromadditional iodine contrast medium exposure–
FIGURE 3 Transthoracic Echocardiograms
(A to F) Transthoracic echocardiograms on presentation and at follow-up. (A, C, E) Initial images: Severe right ventricular dilatation, severe
tricuspid regurgitation with elevated pulmonary artery pressure, and dilated inferior vena cava. (B, D, F) Follow-up images: Normal right
ventricular size, mild tricuspid regurgitation with normal pulmonary artery pressure, and normal-size inferior vena cava. Grad ¼ gradient;
Max ¼ maximum; PG ¼ peak gradient; TR ¼ tricuspid regurgitation; Vmax ¼ maximum velocity.
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induced renal dysfunction in the setting of AKI wasavoided.
CONCLUSIONS
This case highlights a multidisciplinary approach(PERT) to the use of catheter-directed thrombectomyin massive PE with cardiogenic shock, with anexcellent long-term outcome. This approach avoids
the risk of critical and fatal hemorrhage associatedwith thrombolysis.
ADDRESS FOR CORRESPONDENCE: Dr. Manju Ben-galuru Jayanna, Lankenau Medical Center and Lan-kenau Institute for Medical Research, 100 EastLancaster Avenue, 356 MOB East, Wynnewood,Pennsylvania 19096. E-mail: [email protected].
RE F E RENCE S
1. Rosovsky R, Zhao K, Sista A, Rivera-Lebron B,Kabrhel C. Pulmonary embolism response teams:purpose, evidence for efficacy, and future researchdirections. Res Pract Thromb Haemost 2019;3:315–30.
2. Mahar JH, Haddadin I, Sadana D, et al.A pulmonary embolism response team (PERT)approach: initial experience from the ClevelandClinic. J Thromb Thrombolysis 2018;46:186–92.
3. McConnell MV, Solomon SD, Rayan ME,Come PC, Goldhaber SZ, Lee RT. Regional rightventricular dysfunction detected by echocardiog-raphy in acute pulmonary embolism. Am J Cardiol1996;78:469–73.
4. Kucher N, Rossi E, De Rosa M, Goldhaber SZ.Massive pulmonary embolism. Circulation 2006;113:577–82.
5. Vanni S, Viviani G, Baioni M, et al. Prognostic valueof plasma lactate levels among patients with acutepulmonary embolism: the thrombo-embolism lactateoutcome study. Ann Emerg Med 2013;61:330–8.
6. Jaff MR, McMurtry MS, Archer SL, et al. Man-agement of massive and submassive pulmonaryembolism, iliofemoral deep vein thrombosis, andchronic thromboembolic pulmonary hypertension:a scientific statement from the American HeartAssociation. Circulation 2011;123:1788–830.
7. Marti C, John G, Konstantinides S, et al. Sys-temic thrombolytic therapy for acute pulmonary
embolism: a systematic review and meta-analysis.Eur Heart J 2015;36:605–14.
8. Tu T, Toma C, Tapson VF, et al. A prospective,single-arm, multicenter trial of catheter-directedmechanical thrombectomy for intermediate-riskacute pulmonary embolism: the FLARE study.J Am Coll Cardiol Intv 2019;12:859–69.
9. Moore AJE, Wachsmann J, Chamarthy MR,Panjikaran L, Tanabe Y, Rajiah P. Imaging of acutepulmonary embolism: an update. Cardiovasc DiagnTher 2018;8:225–223.
KEY WORDS pulmonary hypertensionright-sided catheterization, thrombosis
