Coronary microvascular dysfunction is a hallmark of all subtypes of MINOCA

Andrea Milzi; Rosalia Dettori; Richard Karl Lubberich; Sebastian Reith; Michael Frick; Kathrin Burgmaier; Nikolaus Marx; Mathias Burgmaier

doi:10.1007/s00392-023-02294-1

Coronary microvascular dysfunction is a hallmark of all subtypes of MINOCA

Clin Res Cardiol. 2023 Sep 2. doi: 10.1007/s00392-023-02294-1. Online ahead of print.

Authors

Andrea Milzi¹, Rosalia Dettori², Richard Karl Lubberich², Sebastian Reith³, Michael Frick², Kathrin Burgmaier⁴, Nikolaus Marx², Mathias Burgmaier^{2

4}

Affiliations

¹ Department of Internal Medicine I, University Hospital of the RWTH, Aachen, Germany. amilzi@ukaachen.de.
² Department of Internal Medicine I, University Hospital of the RWTH, Aachen, Germany.
³ Department of Cardiology, Angiology and Electrophysiology, St. Franziskus Hospital, Münster, Germany.
⁴ Faculty of Applied Healthcare Science, Deggendorf Institute of Technology, Deggendorf, Germany.

PMID: 37658913
DOI: 10.1007/s00392-023-02294-1

Abstract

Introduction: Myocardial infarction without obstructive coronary artery disease (MINOCA) is a heterogeneous clinical condition presenting with myocardial necrosis not due to an obstruction of a major coronary artery. Recently, a relevant role of coronary microvascular dysfunction (CMD) in the pathogenesis of MINOCA has been suggested; however, data on this are scarce. Particularly, it is unclear if CMD is equally present in all subtypes of MINOCA or differentially identifies one or more of these conditions. Therefore, the aim of this study was to assess CMD in all three coronary vessels of MINOCA patients, relating it with the clinical subtype.

Methods: We retrospectively assessed coronary microvascular function in all three coronary territories by means of angiography-based index of microvascular resistance (aIMR) in 92 patients (64 with working diagnosis of MINOCA, 28 control patients). To further assess the association of CMD with MINOCA subtypes, MINOCA patients were subdivided according to clinical data in coronary cause (n = 13), takotsubo (n = 13), infiltrative or inflammatory cardiomyopathy (n = 9) or unclear (n = 29).

Results: Patients with working diagnosis of MINOCA showed a significantly elevated average aIMR compared to control patients (30.5 ± 7.6 vs. 22.1 ± 5.9, p < 0.001) as a marker of a relevant CMD; these data were consistent in all vessels. Among MINOCA subtypes, no significant difference in average aIMR could be detected between patients with coronary cause (33.2 ± 6.6), takotsubo cardiomyopathy (29.2 ± 6.9), infiltrative or inflammatory cardiomyopathy (28.1 ± 6.8) or unclear cause (30.6 ± 8.5; p = 0.412). Interestingly, aIMR was significantly elevated in the coronary vessel supplying the diseased myocardium compared with other vessels (31.9 ± 11.4 vs. 27.8 ± 8.2, p = 0.049).

Conclusion: Coronary microvascular dysfunction is a hallmark of all MINOCA subtypes. This study adds to the pathophysiological understanding of MINOCA and sheds light into the role of CMD in MINOCA.

Keywords: Coronary artery; Coronary microvascular dysfunction; Coronary physiology; Disease; MINOCA.