CTEPH: When the Clots Are Gone, the RV Strain Remains

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Chest

Abstract

INTRODUCTION: Percutaneous mechanical thrombectomy is a mainstay therapy in the management of high-risk acute pulmonary embolism (PE). However, its role in the management of acute-on-chronic PE or chronic thromboembolic pulmonary hypertension (CTEPH) remains undefined. We present a case that reveals how established interventions for acute PE may have unexpected consequences in the setting of acute-on-chronic thromboembolic disease. CASE PRESENTATION: A 46-year-old man presented to the emergency department with four days of worsening dyspnea and pleuritic chest pain. Past medical history is significant for class II obesity and multiple pulmonary emboli over 10 years. Although he had never been formally evaluated with ventilation-perfusion scan or right heart catheterization, there was high suspicion for CTEPH in his case because prior computed tomography scans had demonstrated classic findings (large chronic PE, right ventricular dilatation and remodeling, dilated main pulmonary artery, and bronchial artery hypertrophy). He reported intermittent compliance with apixaban and missed every dose for 10 days prior to presentation. On arrival, he was mildly tachycardic and hypoxic, requiring 4L/min oxygen. Computed tomography pulmonary angiography revealed multiple bilateral pulmonary emboli with an RV:LV ratio of 1.5. A point-of-care ultrasound also demonstrated signs of right ventricular strain. Following pulmonary embolism response team (PERT) recommendations, catheter-directed thrombectomy was performed. Preintervention invasive pulmonary artery pressure was 91/23mmHg (mean 51mmHg) with cardiac index 1.8L/min/m2 . Despite documented removal of both acute and chronic thrombi from the right pulmonary artery, post-intervention pressures remained elevated at 98/28mmHg (mean 57mmHg) with unchanged cardiac index. He was also noted to become tachypneic and hypoxic immediately following aspiration of thrombi. Following the thrombectomy, he was persistently hypoxic, requiring up to 8L/min oxygen. Over the next several days, dyspnea and oxygen requirements improved with intravenous diuresis and continued anticoagulation. Transthoracic echocardiogram prior to discharge revealed normal left ventricular function, severely enlarged right ventricle with normal systolic function, and severe right atrial enlargement. He was referred for further outpatient evaluation for CTEPH. DISCUSSION: This case presents several novel insights into the management of acute-on-chronic PE or suspected CTEPH. First, it demonstrates that mechanical thrombectomy in these cases may lead to non-improvement or even transient worsening of pulmonary function, possibly due to pulmonary edema similar to a reperfusion lung injury. Second, this case challenges the conventional paradigm that PE with right ventricular strain requires extraction. This may paradoxically worsen pulmonary hemodynamics in the setting of chronic PE or CTEPH. The persistence of elevated pulmonary pressures post-thrombectomy despite successful thrombus extraction reflects the underlying irreversible vascular remodeling that is characteristic of CTEPH. CONCLUSIONS: Our experience suggests several practical recommendations. First, clinicians should maintain a high index of suspicion for CTEPH in patients with recurrent PE and evidence of right heart dysfunction either clinically or on imaging studies. Second, mechanical thrombectomy should be approached cautiously in cases of chronic PE or suspected CTEPH. If thrombectomy is deemed necessary, pre-emptive measures such as caution with IV fluids and early diuresis should be considered. This case emphasizes that effective PE management requires careful consideration of the underlying pathophysiology, moving beyond a one-size-fits-all approach.

Volume

168

Issue

4S

First Page

6783A

Comments

American College of Chest Physicians CHEST Annual Meeting, October 19-22, 2025, Chicago, IL

Last Page

6784A

DOI

10.1016/j.chest.2025.07.3804

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