Evaluation of the relationship between primary coronary slow-flow phenomenon and coronary microvascular dysfunction

https://doi.org/10.1007/s00392-025-02625-4

Stefan Lan Cheong Wah (Bad Nauheim)1, T. Keller (Bad Nauheim)2, A. Rolf (Bad Nauheim)1, C. Liebetrau (Frankfurt)3, J. S. Wolter (Bad Nauheim)1, M. Haas (Bad Nauheim)1, S. T. Sossalla (Bad Nauheim)1, M. Weferling (Bad Nauheim)1

1Kerckhoff Klinik GmbH Abteilung für Kardiologie Bad Nauheim, Deutschland; 2Justus-Liebig-Universität Giessen Medizinische Klinik I, Kardiologie Bad Nauheim, Deutschland; 3Cardioangiologisches Zentrum Bethanien (CCB) Kardiologie Frankfurt, Deutschland

 

Background:

Primary coronary microvascular dysfunction (CMD) comprises structural and/or functional alterations of the coronary microvasculature in the absence of relevant epicardial or myocardial disease. CMD can be a cause of angina and/or ischemia in non-obstructive coronary arteries (ANOCA/INOCA). Historically, CMD has been linked to the coronary slow-flow phenomenon (CSFP), although current studies have questioned this association. This study investigated the relationship between primary CSFP and CMD. 

 

Methods:

Between January 2022 and August 2024, patients with suspected coronary artery disease undergoing coronary angiography but without relevant epicardial disease were included in a prospective registry. CMD was assessed by measuring coronary flow reserve (CFR) and the index of microcirculatory resistance (IMR). TIMI frame count (TFC), as a measure of CSFP, was assessed in each epicardial vessel via coronary angiography. CMD was defined as CFR<2 and/or IMR>/=25. Patients with and without CMD were compared according to the TFC of the main coronary arteries (LAD, RCX and RCA) and in terms of clinical parameters. Finally, independent predictors of CMD were assessed by using logistic regression analysis and receiver operating curve (ROC) analysis.

 

Results:

Seventy-nine patients (48% female, mean age 63.3±9.3 y) were included: 41 were diagnosed with CMD. The TFC of the LAD was significantly higher in the CMD group than in the group without CMD (40±12 vs. 33±8; p=0.008), and the TFC of the RCX and the RCA were not different between the groups. When adjusted for age, sex, and cardiovascular risk factors, the TFC of the LAD remained the sole independent predictor of CMD (OR 1.09; 95%CI (1.01-1.16); p=0.018). ROC analysis with assessment of Youden Index identified a TFC of the LAD of 34 as the best cut-off value to distinguish between CMD and no CMD (AUC 0.675, p=0.013).

 

Conclusion:

Primary coronary slow flow present in the LAD can serve as an indicator for CMD. When diagnosed, this parameter might encourage interventional cardiologists to perform further invasive testing on patients with suspected CMD and consequently identify more patients with ANOCA/INOCA who may then be managed therapeutically. Further studies with larger sample sizes are needed to validate these findings. 

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