Abstract Body (Do not enter title and authors here): Background: The no-reflow has been reported to be associated with larger infarct size and mortality after acute myocardial infarction (AMI). A pathological classification of no-reflow was proposed: structural no-reflow—microvessels within the necrotic myocardium exhibit loss of capillary integrity (it is usually irreversible)—and functional no reflow—patency of microvasculature is compromised due to distal embolization, spasm, ischemic injury, reperfusion injury. It may be reversible. After about 6 hours of AMI, myocardial necrosis occurs, which leads to the coronary microcirculation to injury which contribute to no-reflow. The rate of no-reflow was lower in patients presented with AMI, who had reperfusion in less than 4 hours. In AMI within 4 hours of pain-to-balloon time, the proportion of reversible causes of no-reflow may be higher compared to irreversible causes. The incidence of no-reflow was higher in patients with attenuated plaque ≥5 mm in length as evaluated by intravascular ultrasound (IVUS).

Objective: The aim of this study was to evaluate the effects of no-reflow after PCI and the association between attenuation plaque as detected by IVUS and no-reflow in ACS patients within 4 hours of pain-to-balloon time.

Methods and Results: We retrospectively evaluated 77 ACS patients within 4 hours of pain-to-balloon time between December 2020 and March 2022. Patients were divided into the reflow group (final TIMI 3) (n = 58) and the no-reflow group (final TIMI < 3) (n = 19). The median peak creatine kinase (CK) level was significantly higher in the no-reflow group compared to the reflow group (3754 IU/L [IQR: 4155] vs. 1712 IU/L [IQR: 2849]). Blood pressure decrease during PCI was significantly more pronounced in the no-reflow group (47.4% vs. 8.6%, p < 0.001). The proportion of low attenuation plaque observed by IVUS with a length of ≥5 mm was significantly higher in the no-reflow group compared to the reflow group (52.6% vs. 25.5%, p = 0.032). The proportion of low attenuation plaque with an angle of ≥180 degrees was significantly higher in the no-reflow group compared to the reflow group (68.4% vs. 41.2%, p=0.043).

Conclusion: In ACS patients within 4 hours of pain-to-balloon time, the peak CK and the decrease in blood pressure during PCI were significantly greater and the proportion of low attenuation plaque with a length of ≥5 mm and an angle of ≥180 degrees were significantly higher in the no-reflow group.