Myocardial bridging associates with epicardial spasm

M. El Hirch-Morchid (Mainz)¹, R. Skyes (Clydebank)², D. Ang (Clydebank)², S. Biscaglia (Cona (FE))³, G. Campo (Ferrara)⁴, F. Crea (Rome)⁵, J. Escaned (Madrid)⁶, G. Esposito (Milan)⁷, D. Galante (Rom)⁸, H. Mejia-Renteria (Madrid)⁹, S. Miner (Toronto)¹⁰, J. Oreglia (Milan)¹¹, L. Di Serafino (Napoli)¹², M. Weferling (Bad Nauheim)¹³, A. M. Leone (Rome)⁵, C. Berry (Glasgow)¹⁴, T. Gori (Mainz)^15
1Universitätsmedizin Mainz Zentrum für Kardiologie Mainz, Deutschland; ²School of Cardiovascular and Metabolic Health, University of Glasgow Clydebank, Großbritannien; ³Azienda Ospedaliero-Universitaria S. Anna Cardiovascular Institute Cona (FE), Italien; ⁴Cardiovascular Institute Dipartimento di Medicina Traslazionale U.O. Cardiologia Ferrara, Italien; ⁵Catholic University of the Sacred Heart Agostino Gemelli Hospital Rome, Italien; ⁶Hospital Clinico San Carlos Madrid, Spanien; ⁷Division of Interventional Cardiology, De Gasperis Cardio Center ASST Grande Ospedale Metropolitano Niguarda Milan, Italien; ⁸Center of Excellence in Cardiovascular Rom, Italien; ⁹Department of Cardiology, Hospital Clinico San Carlos IDISSC, Universidad Complutense de Madrid Madrid, Spanien; ¹⁰Southlake Regional Health Centre Cardiology Toronto, Kanada; ¹¹De Gasperis Cardio Center ASST Grande Ospedale Metropolitano Niguarda Division of Interventional Cardiology Milan, Italien; ¹²Department of Advanced Biomedical Sciences, University of Naples Federico II Napoli, Italien; ¹³Kerckhoff Klinik GmbH Abteilung für Kardiologie Bad Nauheim, Deutschland; ¹⁴Golden Jubilee National Hospital, University of Glasgow School of Cardiovascular and Metabolic Health Glasgow, Großbritannien; ¹⁵Universitätsmedizin der Johannes Gutenberg-Universität Mainz Zentrum für Kardiologie Mainz, Deutschland

Background:
A myocardial bridge is an abnormal coronary artery course where a segment of a coronary artery runs within the myocardium, causing compression and mechanical irritation. Previous studies have shown a correlation between myocardial bridges and epicardial coronary artery spasm.

Methods:
In an international multicenter cohort (Micro-SNAPE, NCT06125392) we analyzed 1,118 patients who underwent coronary angiography with physiological assessment. The diagnosis of acetylcholine-induced epicardial coronary artery spasm was based on Micro-SNAPE criteria. MB was adjudicated based on >50% systolic obstruction at angiography. Diagnoses and statistical analysis were performed by a core laboratory. Multivariable logistic regression was adjusted for demographic variables, cardiovascular risk factors, and medical history.

Results:
Among the 1,088 patients analyzed, 124 (11.3%) had a myocardial bridge. Epicardial spasm was observed in 189 patients (17.4%). Patients with myocardial bridges exhibited a higher prevalence of epicardial spasm compared to those without myocardial bridges (31.1% vs. 15.2%; p<0.001). In the adjusted regression model (n = 939 complete cases), an independent association between myocardial bridge and epicardial spasm was demonstrated (OR 2.59, 95% CI 1.62-4.16; p<0.001). Average marginal effects indicated a 12.7% absolute increase in the probability of spasm attributable to MB. In contrast, there was no association with microvascular spasm.

Conclusion:
The presence of myocardial bridges is an independent predictor of epicardial spasm. This supports the hypothesis that myocardial bridges may have a mechanistic role in the development of vasospastic angina.