Deep echo attenuation without calcification increases the risk of periprocedural myonecrosis after elective percutaneous coronary intervention in patients with coronary artery disease

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Abstract

Objective To investigate the clinical factors, including intravascular ultrasound (IVUS) findings, associated with percutaneous coronary intervention (PCI)-related periprocedural myonecrosis (PM) in patients with stable coronary artery disease (CAD). Methods The study included 46 patients (mean age 65±2 y, 37 men) with stable CAD who underwent elective PCI using IVUS and a Doppler flow guidewire. In addition to routine IVUS measurements, the presence of deep echo attenuation (DEA) without calcification was assessed. The sum of all high-intensity transient signals (HITS) after a balloon deflation procedure was calculated using a Doppler flow guidewire. PM was defined as an elevation in troponin T to >0.03 ng/mL 24-hour after PCI. Patients were divided into 2 groups on the basis of the presence or absence of PM. Results PM was identified in 17 patients (37%). Estimated glomerular filtration ratio was lower in the PM group (p=0.021). Target vessel distribution was different between the groups (p=0.004). Positive remodeling and DEA, as observed on IVUS, were more common in the PM group (p=0.03 and p<0.0001, respectively). The total number of HITS was higher in the PM group (p=0.003). Logistic regression analysis demonstrated that the presence of DEA (p=0.003) was the sole factor associated with the occurrence of PM. Conclusion These results demonstrated that DEA is an important factor associated with PM in patients who underwent an elective PCI. Therefore, IVUS to determine the presence of DEA should be performed before PCI. © 2012 The Japanese Society of Internal Medicine.

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Mitsuba, N., Teragawa, H., Hata, T., Nishioka, K., Fujii, Y., Mikami, S., … Kihara, Y. (2012). Deep echo attenuation without calcification increases the risk of periprocedural myonecrosis after elective percutaneous coronary intervention in patients with coronary artery disease. Internal Medicine, 51(7), 691–698. https://doi.org/10.2169/internalmedicine.51.6732

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