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Impact of ultrasound attenuation and plaque rupture as detected by intravascular ultrasound on the incidence of no-reflow phenomenon after percutaneous coronary intervention in ST-segment elevation myocardial infarction.
JACC. Cardiovascular Interventions 2010 May
OBJECTIVES: The aim of this study was to assess whether ultrasound attenuation and plaque rupture as detected by intravascular ultrasound (IVUS) are associated with the incidence of no-reflow phenomenon after percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI).
BACKGROUND: No-reflow phenomenon is associated with worse long-term outcomes after STEMI. Therefore, reliable and feasible intravascular imaging techniques are needed to identify patient subgroups that would be at high risk for no-reflow phenomenon.
METHODS: One hundred seventy consecutive patients with STEMI who underwent PCI within 12 h after symptom onset were enrolled. The IVUS interrogation was performed before PCI.
RESULTS: No-reflow phenomenon occurred in 30 patients (18%), who had a higher incidence of no ST-segment resolution (50% vs. 9%; p < 0.001), a higher peak creatine kinase level (4,090 IU/l vs. 2,823 IU/l; p < 0.001), and a lower left ventricular ejection fraction in the chronic phase (51% vs. 59%; p < 0.01). Multivariate logistic regression analysis revealed that ultrasound attenuation with a longitudinal length of > or =5 mm, plaque rupture, and reperfusion time correlated with no-reflow phenomenon (all p < 0.05). In patients with both ultrasound attenuation > or =5 mm and plaque rupture, the incidence of no-reflow phenomenon was 88%, and the risk of decreased coronary reflow was higher than that predicted by either factor alone (p = 0.004 for interaction).
CONCLUSIONS: In patients with STEMI, a longer ultrasound attenuation and plaque rupture on IVUS are associated with an increased incidence of no-reflow phenomenon, suggesting that this subset of patients might be at high risk for distal embolism.
BACKGROUND: No-reflow phenomenon is associated with worse long-term outcomes after STEMI. Therefore, reliable and feasible intravascular imaging techniques are needed to identify patient subgroups that would be at high risk for no-reflow phenomenon.
METHODS: One hundred seventy consecutive patients with STEMI who underwent PCI within 12 h after symptom onset were enrolled. The IVUS interrogation was performed before PCI.
RESULTS: No-reflow phenomenon occurred in 30 patients (18%), who had a higher incidence of no ST-segment resolution (50% vs. 9%; p < 0.001), a higher peak creatine kinase level (4,090 IU/l vs. 2,823 IU/l; p < 0.001), and a lower left ventricular ejection fraction in the chronic phase (51% vs. 59%; p < 0.01). Multivariate logistic regression analysis revealed that ultrasound attenuation with a longitudinal length of > or =5 mm, plaque rupture, and reperfusion time correlated with no-reflow phenomenon (all p < 0.05). In patients with both ultrasound attenuation > or =5 mm and plaque rupture, the incidence of no-reflow phenomenon was 88%, and the risk of decreased coronary reflow was higher than that predicted by either factor alone (p = 0.004 for interaction).
CONCLUSIONS: In patients with STEMI, a longer ultrasound attenuation and plaque rupture on IVUS are associated with an increased incidence of no-reflow phenomenon, suggesting that this subset of patients might be at high risk for distal embolism.
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