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Updated: Jul 26, 2025

Evaluation of Coronary Flow Reserve After Myocardial Ischemia Reperfusion in Rats
Published on: June 28, 2019
Coronary angiography-derived index of microcirculatory resistance and evolution of infarct pathology after
Xiao Wang1, Qian Guo1, Ruifeng Guo1
1Center for Coronary Artery Disease, Division of Cardiology, Beijing Anzhen Hospital, Capital Medical University, 2 Anzhen Road, Chaoyang District, Beijing 100029, China.
Aims:
This study sought to evaluate the association of coronary angiography-derived index of microcirculatory resistance (angio-IMR) measured after primary percutaneous coronary intervention (PPCI) with the evolution of infarct pathology during 3-month follow-up after ST-segment-elevation myocardial infarction (STEMI).
Methods And Results:
Patients with STEMI undergoing PPCI were prospectively enrolled between October 2019 and August 2021. Angio-IMR was calculated using computational flow and pressure simulation immediately after PPCI. Cardiac magnetic resonance (CMR) imaging was performed at a median of 3.6 days and 3 months. A total of 286 STEMI patients (mean age 57.8 years, 84.3% men) with both angio-IMR and CMR at baseline were included. High angio-IMR (>40 U) occurred in 84 patients (29.4%) patients. Patients with angio-IMR >40 U had a higher prevalence and extent of MVO. An angio-IMR >40 U was a multivariable predictor of infarct size with a three-fold higher risk of final infarct size >25% (adjusted OR 3.00, 95% CI 1.23-7.32, P = 0.016). Post-procedure angio-IMR >40 U significantly predicted presence (adjusted OR 5.52, 95% CI 1.65-18.51, P = 0.006) and extent (beta coefficient 0.27, 95% CI 0.01-0.53, P = 0.041) of myocardial iron at follow-up. Compared with patients with angio-IMR ≤40 U, those with angio-IMR >40 U had less regression of infarct size and less resolution of myocardial iron at follow-up.
Conclusions:
Angio-IMR immediately post-PPCI showed a significant association with the extent and evolution of infarct pathology. An angio-IMR >40 U indicated extensive microvascular damage with less regression of infarct size and more persistent iron at follow-up.
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