Key result
Prior coronary stenting shows no difference in microvascular dysfunction or spasm after propensity matching.
Why the study?
The independent impact of prior PCI on coronary spasm and microvascular dysfunction phenotypes remained poorly defined in the ANOCA population.
Does prior coronary stenting increase the prevalence of epicardial coronary spasm, microvascular spasm, or coronary microvascular dysfunction in patients with angina and nonobstructive coronary arteries?
Cohort (n=674)
Yes
Does prior coronary stenting increase the prevalence of epicardial coronary spasm, microvascular spasm, or coronary microvascular dysfunction in patients with angina and nonobstructive coronary arteries?
Prior coronary stenting is not independently associated with subsequent epicardial spasm, microvascular spasm, or coronary microvascular dysfunction in patients with ANOCA after adjusting for baseline clinical comorbidities.
Prior stenting is not independently associated with CMD or spasm in ANOCA; supports comorbidity adjustment in future vasomotor analyses.
BACKGROUND/INTRODUCTION Interventional diagnostic procedures (IDPs) are essential for characterizing coronary vasomotor and microvascular physiology in patients with angina and nonobstructive coronary arteries (ANOCA). Although IDPs effectively identify coronary spasm and microvascular dysfunction (CMD), the independent impact of prior percutaneous coronary intervention (PCI) on these functional phenotypes remains poorly defined in the ANOCA population. Purpose We aimed to clarify the impact of prior PCI history on epicardial coronary spasm, microvascular spasm (MVS) and CMD phenotypes. Methods This sub-analysis of the prospective, multicenter J-CMD Registry included 674 ANOCA patients undergoing comprehensive IDPs, comprising acetylcholine provocation and bolus thermodilution-based physiological assessment. We compared the prevalence of epicardial spasm, microvascular spasm (MVS), and CMD between patients with and without prior stenting. MVS was defined as induced ischemic symptom and electrocardiographic change without angiographic during SPT. CMD was defined as coronary flow reserve <2.5. Propensity score matching was employed to adjust for baseline clinical disparities. Results Prior stenting was present in 10.1% (n=68) of the cohort. In the unadjusted analysis, rates of positive spasm provocation (48.5% vs. 48.5%, P=0.10) and MVS (17.6% vs. 20.5%, P=0.70) were comparable, whereas CMD was significantly more prevalent in stented patients (38.2% vs. 26.1%, P=0.04). However, after propensity score matching (n=56 pairs), this association was eliminated; no significant differences were observed in the prevalence of positive epicardial spasm provocation, MVS, or CMD between the groups. Conclusions In this prospective nationwide multicenter registry, prior coronary stenting was not independently associated with functional coronary abnormalities. The higher crude prevalence of CMD among stented patients likely reflects a burden of clinical comorbidities rather than a direct sequela of stenting. These findings suggest that stenting per se does not predispose patients to subsequent coronary vasomotor or microvascular dysfunction.
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Usui et al. (2026) conducted a cohort in Angina and nonobstructive coronary arteries (ANOCA) (n=674). Prior coronary stenting (percutaneous coronary intervention) vs. No prior stenting was evaluated on Prevalence of coronary microvascular dysfunction (CMD, defined as coronary flow reserve <2.5), epicardial spasm, and microvascular spasm (p=0.04). Prior coronary stenting showed higher unadjusted CMD prevalence vs no stenting (38.2% vs 26.1%, P=0.04), but no difference in spasm or CMD after propensity matching (56 pairs).
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