Drug-induced pulmonary hypertension in cancer patients

SESSION TITLE: Pulmonary Vascular Disease Posters 6 SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/10/2023 12:00 pm - 12:45 pm PURPOSE: Drug-induced pulmonary hypertension is a recognized etiology for World Health Organization (WHO) Group I Pulmonary Arterial Hypertension (PAH) and is associated with significant morbidity and mortality. With the advent of new molecular and targeted therapies, our aim was to identify those agents associated with drug-induced PAH and to evaluate characteristics of the patients, treatments, and outcomes. METHODS: A retrospective review of all cancer patients undergoing right heart catheterization (RHC) at The University of Texas MD Anderson Cancer Center from 1/2011 to 2/2020 was performed. Those diagnosed with PAH secondary to medications were identified. Demographic data, cancer history, clinical characteristics, and diagnostic studies were analyzed. Diagnostic criteria from 6th World Symposium on Pulmonary Hypertension from 2019 were used. RESULTS: A total of 20 patients with drug-induced PAH were identified. 75% were women, and the median age at the time of the RHC was 60.15 (± 15.61). 60% of the patients had a New York Heart Association functional class II. Cancer diagnoses included solid organ tumors (breast, ovarian, and melanoma) in 20% and hematologic malignancies (acute myeloid and lymphoid leukemias, chronic myeloid leukemia ,multiple myeloma) in 80% of the patients, with 87% accounting for acute and chronic leukemias. 35% had undergone stem cell transplantation. Drugs identified included tyrosine kinase inhibitors (TKI) in 70% of cases, including dasatinib, bosutinib and ponatinib. Other drugs included proteasome inhibitor (carfilzomib) and monoclonal antibody (demcizumab). Echocardiogram showed normal systolic function in all patients, diastolic dysfunction in 25% (5), and elevated RVSP (>40mmHg) in 80%(16) of the patients. RHC revealed a mean (mmHg) right atrial pressure of 14 (± 5.5), mean pulmonary artery pressure 43.35 (± 10.87), pulmonary capillary wedge pressure 11.1 (± 5.39), cardiac output by Ficks 4.36 (± 2.1), and pulmonary vascular resistance 7.25WU (± 3.26). PAH targeted therapy was initiated in 80%(16) cases, including PDE-5 inhibitor (88%), endothelin receptor antagonists (44%), and combination therapy (25%) . The implicated medication was discontinued in all patients, and favorable response to therapy was noted in 70% of the patients based on clinical and echocardiographic findings. Pulmonary vasodilator therapy was titrated off in 56% of the patients. CONCLUSIONS: In our cohort, drug-induced PAH was mostly related to TKIs. Drug cessation and treatment with pulmonary vasodilator therapy resulted in improved pulmonary pressures and clinical status. Pulmonary hypertension was often reversible and more than half the patients were weaned off vasodilator therapy. CLINICAL IMPLICATIONS: Drug-induced PAH should be considered in cancer patients (especially in those receiving TKI) and treatment includes drug cessation and pulmonary vasodilator therapies. DISCLOSURES: No relevant relationships by Saadia Faiz No relevant relationships by Maryam Kaous No relevant relationships by Nauman Khan No relevant relationships by Oriana Salamo