Pulmonary Arterial Hypertension Associated With Calcitonin Gene-Related Peptide Antagonist Therapy for Migraine: A Case Series.
K, L., LM, B., N, M., J, B., PJ, L., & SG, R. (2026). Pulmonary Arterial Hypertension Associated With Calcitonin Gene-Related Peptide Antagonist Therapy for Migraine: A Case Series.. Chest. https://doi.org/10.1016/j.chest.2025.12.032
K L, LM B, N M, J B, PJ L, SG R. Pulmonary Arterial Hypertension Associated With Calcitonin Gene-Related Peptide Antagonist Therapy for Migraine: A Case Series.. Chest. 2026; doi: 10.1016/j.chest.2025.12.032
K L, LM B, N M, et al. Pulmonary Arterial Hypertension Associated With Calcitonin Gene-Related Peptide Antagonist Therapy for Migraine: A Case Series.[J]. Chest. 2026. DOI: 10.1016/j.chest.2025.12.032.
@article{k2026,
author = {Lu K and Barros LM and Murinova N and Buber J and Leary PJ and Rayner SG},
title = {Pulmonary Arterial Hypertension Associated With Calcitonin Gene-Related Peptide Antagonist Therapy for Migraine: A Case Series.},
journal = {Chest},
year = {2026},
doi = {10.1016/j.chest.2025.12.032},
note = {PMID: 42264575},
}
TY - JOUR AU - Lu K AU - Barros LM AU - Murinova N AU - Buber J AU - Leary PJ AU - Rayner SG TI - Pulmonary Arterial Hypertension Associated With Calcitonin Gene-Related Peptide Antagonist Therapy for Migraine: A Case Series. T2 - Chest PY - 2026 DO - 10.1016/j.chest.2025.12.032 AN - PMID:42264575 ER -
Calcitonin gene-related peptide (CGRP)-targeted therapies are a recent addition to the migraine field. Monoclonal antibodies became available in 2018 and gepants in 2020, both now widely used for migraine prevention and acute treatment. CGRP is also a potent endogenous pulmonary vasodilator, and its blockade worsens pulmonary hypertension in experimental models. Yet the cardiopulmonary risks of CGRP pathway inhibition in humans have not been studied systematically. We report 3 patients with hemodynamically confirmed pulmonary arterial hypertension (PAH) diagnosed while they were receiving CGRP-targeted therapy. Two patients lacked traditional PAH risk factors; the third patient had suspected portal hypertension. All patients presented with markedly elevated pulmonary vascular resistance, and 2 patients improved after CGRP-targeted therapy was discontinued and PAH treatment was initiated. Although causality cannot be inferred from these cases, the temporal association and biologic plausibility suggest a potential safety signal deserving of further study. Clinicians should remain vigilant for cardiopulmonary symptoms in patients receiving CGRP-targeted therapies.