TEMPORAL CHANGES IN CORONARY NON-CULPRIT HEMODYNAMIC INDICES AFTER ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION: RESULTS FROM THE REDUCE-MVI TRIAL

Abstract

Background: Complete revascularization of ST‐segment elevation myocardial infarction (STEMI) patients with multivessel disease is associated with improved clinical outcome. Fractional flow reserve (FFR), instantaneous wave‐free ratio (iFR) and coronary flow reserve (CFR) are used to guide revascularization. Whether these indices can be used in the acute setting of STEMI remains topic of debate. The aim of the present study was to assess changes in iFR, FFR, CFR and microcirculatory resistance in non‐culprit vessels of STEMI patients from index event to 1 month follow‐up and related these to infarct characteristics. Methods: We included 73 STEMI patients with multivessel disease. Following successful primary PCI, resting and hyperemic non‐culprit intracoronary measurements were performed and repeated at 1‐month follow‐up. iFR, FFR, CFR, resting‐ (BMR) and hyperemic microvascular resistance (IMR) were assessed using a pressure/temperature tipped guidewire. Resistive reserve ratio (RRR = BMR/IMR) was used to determine the hyperemic hemodynamic response. Cardiac magnetic resonance was performed at 2‐7 days and at 1 month follow‐up. Results: iFR did not change significantly from acute moment to follow‐up (0.93±0.06 vs 0.94±0.06, p=0.12). FFR significantly decreased (0.88±0.07 vs 0.86±0.09, p=0.001) whereas CFR significantly increased (2.9±1.4 vs 4.1±2.2, p<0.001). IMR significantly decreased and BMR increased. The drop in distal pressure from rest to hyperemia was smaller at the acute moment vs follow‐up (10.6±11.2 vs 14.1±14.2 mmHg, p=0.01), which was associated with accompanying decrease of FFR values over time. RRR was lower at the acute moment vs follow‐up (3.4±1.7 vs 5.0±2.7, p<0.001). This blunted acute hyperemic response correlated to final infarct size (rho ‐0.25, p=0.04) and was more pronounced in patients with microvascular injury (p=0.04). Conclusion: In the acute setting of STEMI, there is a decreased CFR and increased FFR in non‐culprit vessels. This could be explained by increased microvascular resistance and a blunted hyperemic response at the acute moment which is related to infarct size. Non‐hyperemic iFR did not significantly differ from acute to follow‐up.