Intracoronary and Noninvasive Imaging for Prediction of Distal Embolization and Periprocedural Myocardial Infarction During Native Coronary Artery Percutaneous Intervention

The incidence of periprocedural myocardial infarction (MI) after percutaneous coronary intervention (PCI) ranges from 2% to 50%, depending on the clinical presentation, type of procedure, choice of biomarker (creatine kinase [CK]-MB or troponin), and the threshold used to qualify the diagnosis.1 Because of this heterogeneity of definition, the prognostic implications of periprocedural MI are controversial.2 However, several studies have demonstrated that periprocedural MI is associated with worse in-hospital, short-term, and long-term clinical outcomes, including death, recurrent MI, and need for revascularization.3–5Various mechanisms can lead to periprocedural MI, such as side branch occlusion or vessel spasm; however, distal embolization of atheroma or thrombus seems to be a dominant cause.6 In a cardiac MRI (cMRI) study of patients undergoing complex native coronary PCI, elevated troponin levels post-PCI correlated with new myocardial enhancement because of side branch occlusion in 43% of cases and in the apical myocardium distal to the stent in 57% of cases, as would be expected with distal embolization.7Numerous studies have documented the occurrence of distal embolization during both elective and urgent PCI and have characterized its histopathologic substrate. In an analysis of catheter-retrieved materials from human studies of patients undergoing PCI for acute coronary syndrome (ACS),8 those with no-reflow had significantly higher amounts of visible atheroma and microscopic components such as platelet–fibrin complexes, cholesterol crystals, and macrophages.8 In another study of 37 lesions in 35 patients undergoing elective PCI, microscopic particles were captured by embolic protection devices (EPDs) in 28 (75.6%) lesions.9 Thrombotic components (fibrin strand–entrapped platelets, leukocytes, and red cells) accounted for the majority (≈75%) of captured debris, whereas plaque components (fibrous tissue, calcium spots, acellular amorphous material, macrophages, foam cells, and cholesterol clefts) accounted for the minority (≈25%).9 Similar findings were demonstrated among 33 …