Home / Cardiology / SEATTLE II

Stephanie Haimowitz, PGY3


AS is a 43 yo F, on OCPs for menorrhagia, h/o recent left ACL tear and as a result decreased ambulation x3 weeks, p/w SOB, worse on exertion x2 weeks but acutely worsening on the day of presentation. On the day of presentation, the patient complained of an episode of acutely worsening dyspnea, now occurring at rest and associated with lightheadedness, chest pressure, and diaphoresis.

On Exam, the patient was mildly tachycardic with an O2 sat of 98% on RA at rest. She appeared to be breathing comfortably, although at times noted to take shallow breaths, and the remainder of her exam was unremarkable.

Labs were notable for an elevated troponin of 0.302. EKG showed sinus tach with a ventricular rate of 106 and an incomplete RBBB. CT w/PE protocol showed large bilateral pulmonary emboli in both the right and left main pulmonary arteries with extension into segmental and subsegmental branches, as well as flattening of the interventricular septum with dilatation of the right ventricle.


The patient was started on a heparin drip and admitted to the CCU for hemodynamic monitoring and catheter directed thrombolysis via EKOS, which uses ultrasound to enhance the effects of catheter directed thrombolysis. The patient underwent the endovascular intervention with improvement in her symptoms and repeat echo showed improved RV function. She was switched to Lovenox and discharged home on xarelto.

There are many factors to consider when choosing the appropriate treatment modality for a patient with a PE. In a well-appearing hemodynamically stable patient with evidence of a peripheral or subsegmental PE, anticoagulation with either heparin, a low molecular weight heparin such as lovenox, or one of the newer factor Xa inhibitor oral agents is the most common treatment modality. Factors to consider when deciding whether to escalate treatment include hemodynamic instability, evidence of right heart strain, a large central thrombus on CT, and overall clinical appearance.

While this patient was hemodynamically stable, she had clear evidence of right heart strain (e.g. troponemia, dilated right ventricle, flattening of interventricular septum, and McConnell’s sign- diminished RV systolic function with sparing of the apical wall seen here), and large bilateral pulmonary emboli on CT scan. The RV dysfunction seen on echo is often considered to be predictive of a poor short-term prognosis, thus warranting more aggressive therapeutic measures.[1]

The decision was made to use ultrasound enhanced catheter directed fibrinolysis.

The SEATTLE II Study, published in August of this year, investigated the efficacy of this technique. The use of full dose systemic thrombolysis has fallen out of favor over the past few years due to the risks of severe bleeding and intracranial hemorrhage. By using the ultrasound guided catheter directed approach, a lower dose of thrombolytic can be used because it is injected adjacent to the PE. The study was a single-arm, multicenter design with the inclusion criteria of a proximal PE, age >18, PE symptom duration <14 days, and RV/LV diameter ratio >0.9 on CT. A total of 150 patients were enrolled at 22 sites across the US, at urban, non-urban, teaching, and non-teaching hospitals. The primary outcome was a change in RV/LV diameter ratio pre and post procedure. The primary safety outcome was major bleeding within 72 hours of initiation of therapy. Major bleeding was defined as either intracranial hemorrhage or bleeding causing hemodynamic compromise and requiring intervention such as blood transfusion. Patients enrolled in the study had a mean difference RV/LV diameter of 0.42. There were 16 major bleeding events, however none of these were intracranial hemorrhage.[2]

The most glaring limitation of the study was the lack of a comparator group, such as full dose systemic fibrinolysis, half dose systemic fibrinolysis, or a/c alone. Thus, while the results of the study appear promising, additional comparative clinical studies are necessary to help define the role of ultrasound facilitated catheter directed fibrinolysis in the treatment of acute PE.




[1] 14.Grifoni S, Olivotto I, Cecchini P, et al. Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction. Circulation 2000; 101:2817.

[2] Piazza, Gregory, Benjamin Hohlfelder, Michael R. Jaff, Kenneth Ouriel, Tod C. Engelhardt, Keith M. Sterling, Noah J. Jones, John C. Gurley, Rohit Bhatheja, Robert J. Kennedy, Nilesh Goswami, Kannan Natarajan, John Rundback, Immad R. Sadiq, Stephen K. Liu, Narinder Bhalla, M. Laiq Raja, Barry S. Weinstock, Jacob Cynamon, Fakhir F. Elmasri, Mark J. Garcia, Mark Kumar, Juan Ayerdi, Peter Soukas, William Kuo, Ping-Yu Liu, and Samuel Z. Goldhaber. “A Prospective, Single-Arm, Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism.”JACC: Cardiovascular Interventions 8.10 (2015): 1382-392. Web.


  • Can you tell us more about the context in which the ED treatment was made? Specifically, did the ED clinicians know the patient was ultimately going for catheter-directed thrombolysis?

    What we have is a young patient with a provoked VTE with multiple signs of RVD. Assuming she was normotensive, her troponin is actually the most substantial positive predictor of mortality even despite the CT-evidence of RVD and central location of the emboli. Given that she’s young, what was the thought process about potentially systemically thrombolysing her in the ED?

    I think a young person with PE and evidence of RVD has the best to benefit:harm ratio from thrombolysis. (
    It seems empiric that PE patients with an indication for thrombolysis and a bleeding risk are the ideal candidates for a catheter-directed approach. Did they consider her history of menorrhagia to be a contraindication? Based on that history alone, I don’t think I would have withheld VI tPA. We have a lot of information about systemic thrombolysis and relatively little about catheter-directed; so to me, the ED-to-CCU discussion about ED treatment of this patient is potentially going to give us the most learning we can get from this case (given that we don’t have comparators for the study you’re referencing; We don’t have a trial of full or half-dose IV vs. catheter-directed thrombolysis for submassive PE patients…yet).

    Thanks for sharing this treatment option.


  • siuf

    Should we tpa / tnk her when we see the ct, despite good vitals in the ED? Does she need the icu? Does icu / ccu reduce mortality in patients with massive PEs?

    I signed out the pt to a pretending. Her reaction the next day was pretty funny (started with “holy”).

    • What do you think, Siuf? There’s a decent amount of literature on sub-massive PE, but I don’t think there’s a lot on whether admitting to an ICU will actually help reduce mortality. It’s the same issue as syncope. No one has shown that the admissions we do for syncope actually reduces the risk of mortality. We can only identify people at short term risk of mortality. The standard of care (admitting massive PE to ICU, admitting “higher risk” syncope patients) works against that line of thinking.

      What are your thoughts on tenecteplase in the ED for this patient, if they presented to an institution where catheter-directed isn’t an option?


Leave a Reply