Impact of reproductive status on clinical presentation and outcomes of spontaneous coronary artery dissection: a tertiary-centre experience

Abstract Background Spontaneous coronary artery dissection (SCAD) predominantly affects women and is increasingly recognised as a cause of acute coronary syndromes in younger females. Beyond its female predominance, hormonal status may modulate vascular integrity and mechanisms of arterial wall fragility. Oestrogen deficiency after menopause may promote a more atherosclerotic phenotype, whereas hormonal exposure during reproductive age favours a trigger-related, non-atherosclerotic form. Comparative data between reproductive and postmenopausal women remain limited. Purpose To compare clinical presentation, angiographic features and outcomes of SCAD according to hormonal status, contrasting reproductive-age and postmenopausal women and exploring early versus typical-age menopause. Methods A single-centre observational study included 64 patients diagnosed with SCAD between November 2009 and August 2025. Analyses were limited to 60 women with complete hormonal data, classified as reproductive age or postmenopausal. Clinical, angiographic, and follow-up data were extracted from a prospectively maintained registry. The primary endpoint was major adverse cardiac events (MACE). Statistical tests included χ²/Fisher, t-test or Mann–Whitney, and linear-by-linear association for trend analyses. Significance was set at p0.05. Results Of 60 women, 30 were reproductive-age and 30 postmenopausal (27 typical, 3 premature). Mean age was 45.5 ± 9.3 vs 61.0 ± 8.0 years. Reproductive women had fewer cardiovascular risk factors and more precipitating triggers (63% vs 23%; p=0.002; RR 2.7 1.3–5.5). Two cases occurred during pregnancy or puerperium, both type 2 and fully recovered with conservative management. Angiographically, type 2 predominated (70% vs 53%), with type 2a almost exclusive to reproductive women (33% vs 6%; p≈0.04). Multivessel disease was infrequent and management predominantly conservative (90% vs 93%). Within postmenopause, premature cases resembled the reproductive phenotype, while typical-age menopause showed more hypertension, dyslipidaemia, and occasional type 1 lesions. Over a median 70-month follow-up, MACE occurred in 9 patients (14.5% overall): 3 reproductive and 6 postmenopausal (9.7% vs 19.4%; RR 2.0 0.5–7.6; p=0.47). No MACE occurred in premature menopause, compared with 21% in typical-age menopause (p=0.24). Two pregnancies after SCAD were uneventful under close follow-up. Conclusions Hormonal status influences the clinical phenotype but not prognosis in SCAD. Reproductive-age women show a trigger-driven, non-atherosclerotic pattern, whereas postmenopausal women display greater cardiometabolic burden. Despite phenotypic contrasts, outcomes were similar under conservative management. These results suggest that hormonal milieu, more than age, shapes disease expression and recovery. Table MACE