Key result
Migraine was associated with increased odds of spontaneous coronary artery dissection (aOR 1.96), but this association was no longer significant after adjusting for vascular risk factors.
Why the study?
Although evidence links migraine to SCAD, few studies have examined whether migraine is independently associated with greater odds of SCAD.
Does migraine independently increase the odds of spontaneous coronary artery dissection in adults?
Case-Control (n=2,586)
Does migraine independently increase the odds of spontaneous coronary artery dissection in adults?
Odds Ratio: 1.96 (95% CI 1.48–2.6)
Absolute Event Rate: 11.7% vs 6.5%
p-value: p=<0.001
The previously reported association between migraine and spontaneous coronary artery dissection appears to be mediated by shared vascular comorbidities like hypertension and fibromuscular dysplasia, rather than acting as an independent risk factor.
Migraine may identify higher SCAD risk; leaves open causality and whether screening alters outcomes.
OBJECTIVE: The objective was to determine if migraine is independently associated with a greater odds of spontaneous coronary artery dissection (SCAD) in a case-control study. BACKGROUND: There is growing evidence that migraine is associated with SCAD, a non-atherosclerotic, non-traumatic cause of myocardial infarction. However, few studies have examined the independent association between migraine and SCAD. METHODS: A total of 1295 SCAD cases and 1291 (1:1) age, sex, and race/ethnicity matched controls presenting to the Boston, Massachusetts area, using the International Classification of Diseases ninth revision and 10th revision codes from our Research Patient Data Registry, were identified between the years 1990 and 2022. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated. For mediation, total effects, natural direct, and indirect effects were estimated using causal inference. Receiver operating characteristic (ROC) curves and area under the curve (AUC) was used to determine predictive power. Statistical significance was defined as p < 0.05. RESULTS: Adjusting for age, sex, and race/ethnicity, the data demonstrated an almost two-fold increased odds of SCAD in patients with migraine (aOR 1.96, 95% CI 1.48-2.6; p < 0.001). There was no effect of aura phenotype on this association. Fibromuscular dysplasia (FMD) was found only in patients with SCAD (n = 133). After accounting for vascular risk factors, there was no longer an independent association between migraine and SCAD (aOR 0.90, 95% CI 0.63-1.29; p = 0.568). Using a model that adjusted for only demographic variables produced a ROC curve with the lowest predictive power (AUC 0.55) for SCAD, while the vascular risk factor-adjusted model had a higher predictive power (AUC 0.83). Hypertension appeared to mediate some of the effect of migraine on SCAD (proportion of effect mediated 0.70). FMD was highly associated with an increased risk of SCAD. There remained no independent association between SCAD and migraine when FMD was included in the model. CONCLUSIONS: The migraine-SCAD association can be partially attributed to the connection between migraine and vascular comorbidities including hypertension and FMD.
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Orlova et al. (2025) conducted a case-control in Spontaneous coronary artery dissection (n=2,586). Migraine vs. No migraine was evaluated on Odds of spontaneous coronary artery dissection (aOR 1.96, 95% CI 1.48-2.60, p=<0.001). Migraine was associated with increased odds of spontaneous coronary artery dissection (aOR 1.96), but this association was no longer significant after adjusting for vascular risk factors.
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