Cardiovascular comorbidities are risk factors for increased oxidative stress and DNA damage in migraine patients: a prospective cohort study.

Background: Migraine is a prevalent neurovascular disorder frequently linked with oxidative stress and an elevated risk of cardiovascular diseases (CVDs), particularly in patient with comorbidities. This study aimed to investigate the relationships between oxidative stress and DNA damage biomarkers, cardiovascular comorbidities, and the effects of six months of migraine prophylaxis.

Methods: A prospective cohort study was conducted between January and September 2024 at a tertiary neurology clinic, enrolling 75 women who were divided into three groups: migraine with cardiovascular comorbidities (MC, n = 25), migraine without comorbidities (M, n = 25), and age-matched healthy controls (C, n = 25). Migraine diagnosis was confirmed according to the International Classification of Headache Disorders, 3rd edition (ICHD-3), and patients with renal/hepatic dysfunction, active infections, migraine with aura, pregnancy, or other neurological/psychiatric disorders were excluded. Venous blood samples were obtained during the interictal period (≥ 72 h migraine-free) at baseline and after 6 months of standard acute migraine treatment. Biochemical analyses included total oxidant status (TOS), total antioxidant status (TAS), and calculation of oxidative stress index (OSI) using automated colorimetric assays. DNA damage was quantified by comet assay (single-cell gel electrophoresis), whereas ischemia-modified albumin (IMA) and hypoxia-inducible factor-1α (HIF-1α) were measured via ELISA. Statistical analyses were performed using ANOVA, paired and independent t tests, and Pearson correlation, with p < 0.05 considered significant.

Results: Migraine patients exhibited significantly higher oxidative stress and DNA damage levels compared to controls, with the highest levels in those with cardiovascular comorbidities. After six months of treatment, biomarker levels decreased but remained elevated relative to controls. Ischemic markers (IMA and HIF-1α) were consistently higher in migraine patients, especially in the MC group, and although reduced post-treatment, did not normalise to control values.

Conclusions: Cardiovascular comorbidities substantially increase oxidative stress and DNA damage in migraine patients, potentially heightening long-term cardiovascular risks. Monitoring these biomarkers may facilitate personalised risk stratification and management in clinical practice.