Predictors of no-reflow after percutaneous coronary intervention for culprit lesion with plaque rupture in infarct-related artery in patients with acute myocardial infarction

Summary Background We investigated the predictors of the no-reflow phenomenon after percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) patients with plaque rupture (PR). Methods The study group comprised 112 AMI patients who underwent pre- and post-PCI intravascular ultrasound (IVUS) and stent implantation. Angiographic no-reflow was defined as TIMI flow grade 0, 1, and 2 after PCI. IVUS findings included multiple ruptured plaques (PRs separated by a >5-mm length of artery containing smooth lumen contours), thrombus (had a layered lobulated appearance, evidence of blood flow within the mass, and speckling or scintillation), and plaque prolapse (tissue extrusion through the stent struts). Results Of 112 patients, no-reflow was observed in 17 patients (15.2%). High-sensitivity C-reactive protein (hs-CRP) was significantly higher (6.2 ± 6.0 mg/dl vs. 2.2 ± 2.9 mg/dl, p = 0.002) and baseline TIMI flow grade was significantly lower in no-reflow group (TIMI flow grade < 3: 59% vs. 18%, p < 0.001). Lesion site plaque plus media area was significantly greater (12.9 ± 2.6 mm2 vs. 10.8 ± 4.2 mm2 , p = 0.009), remodeling index was significantly higher (1.14 ± 0.17 vs. 1.03 ± 0.20, p = 0.031), and the presence of IVUS-detected thrombus (88% vs. 56%, p = 0.012), culprit lesion multiple PRs (71% vs. 37%, p = 0.009), and plaque prolapse (65% vs. 34%, p = 0.015) were significantly more common in no-reflow group. In the multivariate analysis, plaque prolapse (OR = 33.02; 95% CI 3.38–322.75, p = 0.003), hs-CRP (OR = 1.03; 95% CI 1.01–1.05, p = 0.013), and culprit lesion multiple PRs (OR = 15.73; 95% CI 1.61–153.46, p = 0.018) were independent predictors of post-PCI no-reflow in AMI patients with PR. Conclusions Elevated hs-CRP and IVUS-detected multiple PRs and plaque prolapse are associated with no-reflow after PCI for PR-containing culprit lesion in infarct-related arteries in AMI patients.