Effect of No-reflow During Primary Percutaneous Coronary Intervention for Acute Myocardial Infarction on Six-month Mortality
Overview
Authors
Affiliations
No-reflow is a frequent event during percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI), and it may affect cardiac prognosis. We evaluated the occurrence of no-reflow as a predictor of outcomes in patients who underwent PCI for AMI. We prospectively collected data from 599 consecutive patients who underwent stent-based PCI for ST-elevation AMI by identifying those with no-reflow (Thrombosis In Myocardial Infarction [TIMI] grade <3 flow at completion of the procedure) and analyzing their baseline characteristics and clinical outcomes. Patients with no-reflow (n = 40, 6.7%) were older (67 +/- 13 vs 60 +/- 13 years, p = 0.002) and had longer ischemic times (5.5 +/- 3.7 vs 4.4 +/- 3.0 hours, p = 0.04) with more TIMI grade 0/1 flow at presentation (90% vs 64%, p = 0.001). No-reflow occurred mostly (73%) after stenting and often required intra-aortic balloon pump counterpulsation (30% vs 4.3%, p <0.001). Peak creatine kinase level was higher in patients with no-reflow (2,700 +/- 1,900 vs 2,000 +/- 1,800, p = 0.03) and more often associated with moderate or severe left ventricular dysfunction (68% vs 45%, p = 0.006) and increased 6-month mortality (12.5% vs 4.3%, p = 0.04). By multivariate analysis, no-reflow was an independent predictor of long-term mortality (odds ratio 3.4, p = 0.02). In addition, renal failure (odds ratio 4.39, p = 0.0025) and preprocedure TIMI grade 0/1 flow (odds ratio 2.1, p = 0.003) were independent predictors of no-reflow. In conclusion, the association of no-reflow with longer ischemic time and worse initial TIMI flow may indicate the presence of highly organized thrombus burden with higher propensity for distal embolization. Regardless of its mechanism, no-reflow was an independent predictor of increased mortality.
Ghanta S, Kattamuri L, Odueke A, Mehta J Antioxidants (Basel). 2025; 14(2).
PMID: 40002399 PMC: 11851988. DOI: 10.3390/antiox14020213.
Vascular endothelial cell injury: causes, molecular mechanisms, and treatments.
Xia T, Yu J, Du M, Chen X, Wang C, Li R MedComm (2020). 2025; 6(2):e70057.
PMID: 39931738 PMC: 11809559. DOI: 10.1002/mco2.70057.
Cakmak A, Kocayigit I, Varim P, Saribiyik Cakmak B, Can Y, Vatan M Postepy Kardiol Interwencyjnej. 2024; 20(2):148-156.
PMID: 39022716 PMC: 11249874. DOI: 10.5114/aic.2024.140259.
Sakata T, Mavropoulos S, Mazurek R, Romeo F, Ravichandran A, Marx J J Physiol. 2024; 602(8):1669-1680.
PMID: 38457313 PMC: 11514056. DOI: 10.1113/JP285586.
Ndrepepa G, Cassese S, Xhepa E, Joner M, Sager H, Kufner S Clin Res Cardiol. 2023; 113(7):1006-1016.
PMID: 37962571 PMC: 11219448. DOI: 10.1007/s00392-023-02340-y.