High-Intensity Plaques on Noncontrast T1-Weighted Imaging as a Predictor of Periprocedural Myocardial Injury.

Although percutaneous coronary intervention (PCI) routinely achieves good angiographic success, 5% to 30% of patients experience periprocedural myocardial injury (pMI), which is associated with long-term adverse outcomes and immediate adverse events (1). Because coronary high-intensity plaques (HIPs) detected by noncontrast T1-weighted imaging (T1WI) represent plaque instability (2,3), we examined the relationship between cardiac magnetic resonance (CMR) characteristics of HIPs and pMI following elective PCI in patients with coronary artery disease (CAD). Between October 2012 and March 2014, 57 patients with CAD (mean age 68 11 years) underwent CMR within 3 months (median 2 days; interquartile range [IQR]: 1 to 24 days) of PCI. The plaque-to-myocardial signal intensity ratio (PMR) was calculated (2,3). pMI during PCI was defined as an increase in serum cardiac troponin T (cTnT) levels to more than 5 times the upper limit of normal (0.07 ng/ml) at 24 h after PCI. Intravascular ultrasound (IVUS) images were also obtained. All patients were scannedwith a 3-TMR imager (MAGNETOMVerio, Siemens AGHealthcare, Erlangen, Germany) equipped with a 32-channel cardiac coil. Plaque imaging (Figure 1A) was performed using an inversion recovery prepared 3-dimensional T1W turbo FLASH (fast low angle shot) sequence with electrocardiogram-triggered, navigator-gated free breathing and fat suppression in transaxial sections covering the entire heart (inversion time 650 ms; field of view 280 228 mm; acquisition matrix 256 187; reconstruction matrix 512 374; acquisition slice thickness 1.0 mm; acquisition slice number 104 to 120; reconstruction spatial resolution 0.6 0.5 0.6 mm; fat suppression; effective repetition time/echo time 4.7 ms/2.13 ms; flip angle 12 ; GRAPPA factor 2; navigator gating window 1.5 to 2.5 mm; and data acquisition window duration time 84 to 120 ms). The trigger delay and acquisition window were set according to the phase with minimal motion of the right coronary artery as determined using cine MR imaging. Clinical characteristics, cTnT levels at baseline, target vessels, or type B2/C lesions were comparable between the non-pMI (n 1⁄4 42) and pMI groups (n 1⁄4 15). All lesions were treated with stent implantation. Transient slow or no reflow was observed significantly more frequently in patients with pMI than those without (27% vs. 5%; p 1⁄4 0.036). Importantly, the median (IQR) of the PMR of PCI lesions was higher in patients with pMI than those without (1.3 [1.1 to 2.0] vs. 1.0 [0.8 to 1.2]; p 1⁄4 0.014) (Figure 1B). Receiveroperating characteristic (ROC) analysis revealed that the optimal PMR cutoff value for predicting pMIwas 1.3 and the area under the ROC curve was 0.71 (Figure 1C). At this value, the sensitivity and specificity for predicting pMI were 67% and 86%, respectively. The present cutoff value of PMR $1.3 for pMI is consistent with our previous finding that PMR $1.4 predicts future cardiac events (3). In the univariate logistic regression analysis, PMR $1.3 (odds ratio [OR]: 12.0; 95% confidence interval [CI]: 3.2 to 52.2; p < 0.001), ultrasound attenuation (attenuation arc $180 : OR: 6.1; 95% CI: 1.64 to 24.6; p 1⁄4 0.007), remodeling index based on IVUS >1.05 (OR: 5.97; 95% CI: 1.54 to 29.2; p 1⁄4 0.008), and total plaque area (OR: 0.88; 95% CI: 0.77 to 0.98; p1⁄40.021) were significantly associatedwith pMI. Although the etiology of pMI associated with PCI is multifactorial, the predominant mechanism involves distal embolization of plaque debris, intraluminal thrombus at the time of balloon inflation or stent deployment, or both (1). As described herein, noncontrast T1WI provided clinically and procedurally important information on high-risk features of coronary plaques without exposure to ionizing radiation and contrast media. This less invasive, quantitative technique may have an impact by identifying individuals who are more likely to have periprocedural complications a priori and thereby change therapeutic strategies.