Risk Stratification of Hypertension Induced by CGRP Antagonist in Migraine Treatment: A Retrospective Observational Analysis
Suresh Kumar1, Anbu Subramanian2, Maya Salinath3, Sahith Abraham5, Amrith Sankar3, Jenil Patel6, Mahith Ravulapati7, Hanna Sameer4
1Neurology & Headache Center, 2Neurology, Young Scientists of America, 3Neurology, 4Premed, Young Scientist of America, 5Neurology, Young Scientist Of America, 6Assistant Professor Epidemiology, UTHealth Houston School of Public Health, 7Pre Medicine, University Of Austin
Objective:
To compare incidence of hypertension across different CGRP antagonist agents and effect of comorbidities in response to emerging post-market safety signals.
Background:
Advancements in research and understanding of migraine have led to the development of targeted Calcitonin Gene-Related Peptide (CGRP) antagonists as both preventive and abortive therapies. CGRP is a potent vasodilator, and its inhibition may lead to vasoconstriction and increased vascular resistance, thereby contributing to elevated blood pressure. With the growing use of the Gpant class of drugs and other CGRP inhibitors in clinical settings, it is critical to determine which populations are most at risk for developing this side effect.
Design/Methods:
250 patients prescribed any CGRP antagonist, including erenumab, fremanezumab, galcanezumab, eptinezumab, and the gepants (ubrogepant, rimegepant, atogepant, zavegepant).
Variables extracted included: age at start, sex, and body mass index (BMI). Comorbidities: pre-existing hypertension, diabetes, chronic kidney disease, stroke, and obstructive sleep apnea (OSA); OSA treatment status (treated vs untreated) was noted.
Results:
Among 149 adults initiating CGRP antagonist therapy, 93 % developed new-onset hypertension within 6 months, typically within the first month (median = 1 month). Incidence was comparable across erenumab, gepants, and other mAbs. Logistic regression revealed no significant associations with age, sex, BMI, baseline BP, or OSA status. Among patients with OSA, treatment status did not significantly modify risk. Hypertension was persistent in 82 % of cases and transient in 8 %, indicating sustained BP elevation. The Kaplan–Meier curve confirmed an early onset window (1–3 months) without progressive late-onset risk across drug classes.
Conclusions:
Hypertension following CGRP initiation is an early event, occurring within the first few months.Once developed, hypertension tends to persist, with no new cases after 3 months. The pattern is similar across drug classes, indicating that risk is likely related to the CGRP pathway blockade rather than a specific molecule.
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