Caught in Transit: Mobile Right Atrial Thrombus in Intermediate-High-Risk Pulmonary Embolism Treated With Half-Dose Alteplase

Introduction

Acute pulmonary embolism outcome ranges from incidental, low-risk events to sudden cardiovascular collapse. Outcomes are largely driven by the right ventricular response to an abrupt rise in afterload rather than by clot location alone. Current European guidance therefore recommends early risk stratification using clinical scores, such as the simplified pulmonary embolism severity index (sPESI), imaging evidence of right ventricle (RV) dysfunction, and biomarkers of myocardial injury to identify patients who need intensive monitoring and those who may benefit from advanced therapies [1–3].

Management becomes especially nuanced in intermediate-high-risk pulmonary embolism, where patients may be normotensive yet physiologically fragile [1]. A right-heart thrombus, particularly a mobile clot-in-transit, further increases concern and has been associated with worse outcomes compared with pulmonary embolism without intracardiac thrombus [4]. This case is noteworthy because clot-in-transit is uncommon in intermediate-high-risk pulmonary embolism and it can transform a watch-and-wait strategy into a time-critical decision about reperfusion.

Case Report

A 45-year-old woman with bronchial asthma and a prior history of pulmonary embolism presented with sudden onset of progressive shortness of breath. She reported having stopped apixaban 2 days earlier. From the available admission history, no procedural or physician-directed reason for interruption was identified. On arrival, she was tachypneic and visibly distressed. Oxygen saturation was 88% on room air, respiratory rate 30 breaths/min, and heart rate 115 beats/min. Blood pressure was preserved, but her labored breathing and tachycardia suggested a narrow physiological reserve.

A focused review for provoking factors did not identify recent surgery or immobilization, malignancy, hormonal therapy, pregnancy/postpartum state, long-haul travel, or infection, and family history was negative for pulmonary embolism. Because this represented recurrent pulmonary embolism without a clear provoking factor, thrombophilia testing was sent on admission as part of the etiologic work-up; the result was pending at discharge.

Bedside transthoracic echocardiography was performed early. This showed marked RV dilation and pressure overload. A mobile echogenic mass was seen within the right atrium, consistent with a clot-in-transit (Figure 1). The thrombus measured approximately 2.22×0.99 cm (Figure 2). Continuous-wave Doppler across the tricuspid valve showed a markedly elevated tricuspid regurgitation (TR) velocity (TR Vmax 4.84 m/s; peak gradient 96.7 mmHg), supporting severe RV pressure overload (Figure 3). Left Ventricular Outflow Tract Doppler suggested reduced forward flow parameters, consistent with RV-left ventricle interdependence in acute pulmonary embolism physiology (Figure 4).

Computed tomography (CT) pulmonary angiography confirmed multiple bilateral segmental and subsegmental pulmonary arterial filling defects. Laboratory testing supported the echocardiographic impression of RV strain, with elevated cardiac biomarkers and a raised lactate level, suggesting early hypoperfusion despite maintained blood pressure [3]. Duplex ultrasound of the lower limbs did not show deep vein thrombosis. Initial laboratory values were: D-dimer 1.07 mg/mL, troponin 0.39 ng/mL, BNP/NT-proBNP 1609 pg/mL, and lactate 2.5 mmol/L.

By European Society of Cardiology criteria, this was intermediate-high-risk pulmonary embolism: the patient was normotensive but had clear RV dysfunction and biomarker evidence of myocardial injury [1]. The Pulmonary Embolism Response Team (PERT) was activated, the patient was admitted to the intensive care unit (ICU) for continuous monitoring, and unfractionated heparin was started (weight-based bolus followed by infusion). The classification as intermediate-high-risk pulmonary embolism was supported by her pulmonary embolism severity index (PESI) score: sPESI=3 (Table 1), positive cardiac biomarkers (troponin 0.39 ng/mL, BNP/NT-proBNP 1609 pg/mL), raised lactate 2.5 mmol/L, and imaging evidence of RV dysfunction (RV dilation with TR Vmax 4.84 m/s) plus a mobile right atrial thrombus (2.22×0.99 cm). The patient’s criteria are summarized in Table 2.

The central management question was whether to wait or to reperfuse. Waiting was attractive because she was not hypotensive; however, the combination of severe RV pressure overload, biomarker positivity, lactate rise, and a mobile clot-in-transit felt unsafe. A multidisciplinary discussion involving several departments, Critical Care, Cardiology, Pulmonology, Hematology, and Pharmacy, weighed the options.

Catheter-directed therapy, including catheter-directed thrombolysis or mechanical thrombectomy, was considered. In our setting, the team was concerned that intracardiac and pulmonary arterial instrumentation in the presence of a mobile right atrial thrombus could precipitate thrombus detachment and further embolization. We also aimed to minimize bleeding risk and therefore avoided full-dose systemic thrombolysis, choosing a reduced-dose regimen instead, consistent with published data supporting lower-dose strategies in selected pulmonary embolism patients [5–7].

Alteplase 50 mg was administered intravenously over 2 hours, with careful bleeding surveillance. The clinical response was prompt: oxygen requirements fell, tachycardia improved, and lactate normalized. There were no major bleeding events, including no intracranial hemorrhage. She was transitioned to lifelong apixaban before discharge. A day-1 post-thrombolysis echocardiogram showed modest improvement in RV size and function compared with the results obtained 1 day earlier (Figure 5). At her 2-month follow-up, she remained in excellent clinical condition.

Discussion

This case is familiar to many clinicians: a patient whose blood pressure looks reassuring while every other signal says the RV is under threat. In acute pulmonary embolism, obstruction and vasoconstriction abruptly raise pulmonary vascular resistance. The RV is not built for this. As afterload rises, RV dilation and ischemia can follow, and the circulation may fail quickly through reduced left ventricle filling and falling cardiac output [8].

The clot-in-transit was the turning point. Registry data show that right-heart thrombi in pulmonary embolism identify patients with a worse prognosis, particularly when RV dysfunction is present [4]. Unlike an already-embedded pulmonary clot, a mobile intracardiac thrombus feels dynamic: it can disappear in seconds, and when it does, it may have embolized. That uncertainty is what often pushes teams toward earlier escalation. In the Right-Heart Thrombi European Registry (RiHTER), 30-day pulmonary embolism-related mortality among normotensive patients with right-heart thrombi was 12%, and this mortality increased to 16% when RV dysfunction was present [4]. Notably, thrombus characteristics, including mobility, did not independently predict mortality, reinforcing that escalation should be guided by the full risk profile rather than clot appearance alone [4].

Guidelines advise against routine systemic thrombolysis in intermediate-risk pulmonary embolism because the bleeding penalty is real [1,5]. At the same time, they support escalation when clinical deterioration is likely or unfolding, and they acknowledge that an individualized approach is sometimes necessary [1]. In our patient, the question was not whether she met the universal definition of shock, but rather how long she would stay compensated.

The PERT chose reduced-dose alteplase to balance speed of reperfusion against hemorrhagic risk. In a large retrospective cohort, half-dose alteplase showed similar mortality and major bleeding compared with full-dose therapy, although treatment escalation was more frequent [6]. In a randomized, multicenter trial, a 50 mg/2 h alteplase regimen demonstrated similar improvements in right ventricular dysfunction and clot burden, with fewer bleeding events compared with 100 mg/2 h, supporting dose reduction in selected patients [7]. The Moderate Pulmonary Embolism Treated with Thrombolysis (MOPETT) trial also supported the feasibility of safe-dose thrombolysis in moderate pulmonary embolism, although its population differs from intermediate-high-risk pulmonary embolism complicated by clot-in-transit [9]. However, randomized evidence for reduced-dose systemic alteplase specifically in intermediate-high-risk pulmonary embolism complicated by clot-in-transit remains limited. In this case, the dose choice reflected a patient-specific risk-benefit discussion rather than a guideline-standard strategy [1,5–7].

Catheter-directed strategies are increasingly used and can be attractive when bleeding risk is high [1]. In our case, the immediate concern was the mobile right atrial thrombus: any intracardiac or pulmonary arterial manipulation raised the worry of precipitating embolization. While this risk is not precisely quantifiable, it was persuasive in real time. Reduced-dose systemic thrombolysis offered a rapidly deployable option without instrumentation, and ICU monitoring allowed close observation for both response and bleeding. We recognize that catheter-directed thrombolysis or thrombectomy may be appropriate alternatives in other settings, particularly when expertise and immediate access are available, or when systemic lysis is contraindicated [1]. In our patient, the decision was influenced by thrombus mobility, concern about thrombus detachment during instrumentation, and the need for treatment that could be delivered without delay in a monitored ICU environment.

Emerging evidence continues to refine the status of catheter-based reperfusion. The Thrombectomy in High-Risk Pulmonary Embolism - Device Versus Thrombolysis Netherlands (TORPEDO-NL) randomized trial was designed to evaluate catheter-directed thrombectomy vs systemic thrombolysis in high-risk pulmonary embolism [11]. For ultrasound-assisted catheter-directed thrombolysis, the Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement (PRESERVE) study reported preserved RV recovery and quality of life at 90 days in submassive pulmonary embolism, with no deaths or major hemorrhage in that cohort [12].

The broader, generalizable message is that we have to treat the physiology we see, not the single vital sign we want to see. A structured approach combining PESI, cardiac biomarkers, and RV imaging can help to identify a patient who is normotensive but not safe [1–3,10,13].

Conclusions

Intermediate-high-risk pulmonary embolism can leave very little room for error, especially when a clot-in-transit is present. In this patient, bedside echocardiography exposed severe RV pressure overload and a mobile right atrial thrombus, shifting the team away from watchful waiting. Reduced-dose systemic alteplase was followed by rapid clinical recovery without bleeding. While evidence is still evolving, a multidisciplinary, risk-based approach remains the safest way to decide when to escalate.