Autonomic phenotype and antecedent autonomic symptoms in spontaneous coronary artery dissection

Background Spontaneous coronary artery dissection (SCAD) predominantly affects women with limited traditional atherosclerotic risk burden and is frequently accompanied by persistent extra-cardiac symptoms suggestive of autonomic involvement. However, systematic autonomic phenotyping in SCAD is lacking. We quantified autonomic symptom burden and examined its association with antecedent dysautonomic features in SCAD survivors. Methods In this cross-sectional study, 227 adults with angiographically confirmed SCAD completed the Composite Autonomic Symptom Score-31 (COMPASS-31) and EuroQol-5Dimension-5L (EQ-5D-5L). A 10-item Composite Historical Autonomic Predisposition Score (CHAPS) assessed adolescent and early adult autonomic features. Internal consistency (Cronbach’s α=0.76) and known-groups validity were evaluated. Hierarchical linear regression examined independent predictors of autonomic burden with prespecified blocks including demographics (age, body mass index, smoking), SCAD characteristics (recurrence, time since event), and biological phenotype variables (historical predisposition, hypotension, migraine). Results Participants were 97.8% female with median age 53 [47–58] years, assessed a median 3.0 [1.0–5.0] years post-index event; 21.6% reported recurrence. Moderate autonomic burden (COMPASS-31 ≥20) was present in 56.4%, with 16.3% severe (≥40). Cardiovascular (orthostatic intolerance) and gastrointestinal domains contributed most to overall severity. Historical autonomic predisposition correlated with contemporary COMPASS-31 (ρ=0.559; 95%CI 0.459–0.644; p<0.001). In hierarchical modelling, CHAPS was the strongest independent predictor of autonomic burden (β=0.514; p<0.001), with the final model explaining 36.0% of variance; younger age and smoking were also independently associated (both p≤0.01). Migraine was more frequent among those with COMPASS-31 ≥20 (p=0.043). (Table 1.) Participants with COMPASS-31 ≥20 more frequently reported impairment in mobility and pain/discomfort domains of the EQ-5D (all p≤0.03), with lower health utility (0.903 [0.793–0.956] vs 0.924 [0.890–0.968]; p<0.001). Autonomic burden independently predicted reduced health utility in multivariable analysis (β=−0.150; p=0.029). Hypertension (26.0%) and dyslipidaemia (17.6%) were modest, with current smoking uncommon (2.2%), and traditional cardiovascular risk factors were not independently associated with autonomic severity. Autonomic measures were not associated with SCAD recurrence. Conclusion Autonomic symptom burden is common and clinically meaningful in SCAD. The strong and independent association with antecedent dysautonomic features supports a pre-existing autonomic vulnerability rather than a purely reactive consequence of a cardiac event. These findings suggest altered autonomic regulation may represent an under-recognised component of the SCAD phenotype warranting prospective mechanistic investigation.