The hidden risks after Pulmonary Embolism
Clinicians urged to view CTEPH as part of the disease continuum that begins with acute Pulmonary Embolism.
Treat the immediate, life-threatening outcomes of pulmonary embolism (PE) first, but then quickly turn your attention to the long-term complications that may follow. That advice will shape Sunday’s session, “Optimizing Outcomes in Acute Pulmonary Embolism and Right Ventricular Shock Through Multidisciplinary Care.”
During the session, panelist Irene Lang, MD, will delve into one specific complication: chronic thromboembolic pulmonary hypertension (CTEPH).
Lang is a clinical cardiologist and professor of vascular biology at the Medical University of Vienna in Austria. Her presentation, “Beyond the Acute Event: CTEPH as a Sequela of Pulmonary Embolism,” examines this serious form of pulmonary hypertension caused by persistent, organized blood clots in the pulmonary arteries. It is increasingly being recognized as part of a disease continuum that begins with acute PE, she said. The condition is characterized by chronic fibrotic clot material that forms ring-like stenoses, webs and complete or partial arterial blockages despite at least three months of therapeutic anticoagulation.
“In more than 60% of cases, a thromboembolic history can be tracked,” she said. “In parallel, a secondary microvasculopathy is observed that resembles a classical pulmonary arteriopathy.”
In her presentation, Lang emphasizes the importance of multidisciplinary management for intermediate-high and high-risk PE patients, particularly those presenting with right ventricular (RV) dysfunction or hemodynamic instability. She recommends a structured treatment pathway that begins with rapid assessment, identification of shock or RV failure, activation of a Pulmonary Embolism Response Team (PERT), selection of an appropriate reperfusion strategy and ongoing reassessment after stabilization. Treatment options may include systemic thrombolysis, catheter-based thrombectomy, surgical embolectomy and extracorporeal membrane oxygenation (ECMO) support when needed, she said.
“Multidisciplinary assessment is key when considering the optimization of ICU-level care and the escalating role of mechanical circulatory support and catheter-directed aspiration thrombectomy in stabilizing hemodynamically unstable patients,” she said. “Repeated assessments are also important, using clinical metrics, bedside echo, lactate, optimal timing of CDT and circulatory support early and generously.”
According to Lang, clinicians should consider ECMO early for respiratory support rather than positive pressure ventilation in a hemodynamically unstable patient. If intubation is unavoidable, Lang said clinicians should use a tidal volume and respiratory rate without positive end-expiratory pressure to achieve a normal PCO2. Hypercapnia may cause pulmonary vasoconstriction and plateau pressures much lower than 30 cmH2O to limit the risk of adverse hemodynamic effects.
Lang urges clinicians not to view acute high-risk PE and CTEPH as separate diseases, but as interconnected stages along the same clinical spectrum. She said clinicians should maintain a high index of suspicion for CTEPH when evaluating patients with severe PE and consider chronic thromboembolic disease even before pursuing advanced therapies.
“CTEPH more often appears as massive PE than follows it,” she said.
Beyond acute management, Lang underscores the need for structured follow-up care. In particular, she said, high-risk PE survivors should undergo clinical assessment and echocardiographic evaluation within three to six months after the acute event to monitor for the development of CTEPH. Although the condition remains relatively uncommon during long-term follow-up, evidence suggests that CTEPH may occur in approximately 0.8%-3% of patients who experience any acute pulmonary embolism.
