The automatic measurement of transient ischemic dilation in dual-isotope myocardial perfusion SPECT is a clinically useful marker that is sensitive and highly specific for detection of severe and extensive coronary artery disease.

Background We investigated the relationship of quantitative plaque features from coronary CT Angiography (CTA) and coronary vascular dysfunction by impaired myocardial flow reserve (MFR) by 13N-Ammonia Positron Emission Tomography (PET). Methods and Results Fifty-one patients (32 men, 62.4±9.5 years) underwent combined rest-stress 13N-ammonia PET and CTA scans by hybrid PET/CT. Regional MFR was measured from PET. From CTA, 153 arteries were evaluated by semi-automated software, computing arterial non-calcified plaque (NCP), low-density NCP (NCP<30 HU), calcified and total plaque volumes, and corresponding plaque burden (plaque volumex100%/vessel volume), stenosis, remodeling index, contrast density difference (maximum difference in luminal attenuation per unit area in the lesion), and plaque length. Quantitative stenosis, plaque burden and myocardial mass were combined by boosted ensemble machine-learning algorithm into a composite risk score to predict impaired MFR (MFR≤2.0) by PET, in each artery. Nineteen patients (37%) had impaired regional MFR in at least one territory, (41/153 vessels). Patients with impaired regional MFR had higher arterial NCP (32.4 vs.17.2 %), low-density NCP (7 vs 4 %) and total plaque burden (37 vs 19.3 %, p<0.02). In multivariable analysis with 10-fold cross-validation, NCP burden was the most significant predictor of impaired MFR (Odds Ratio 1.35, p=0.021). For prediction of impaired MFR with 10-fold cross-validation, receiver-operating-characteristics-area-under-the-curve for the composite score was 0.83 (95%CI:0.79–0.91), greater than for quantitative stenosis (0.66, 95%CI:0.57–0.76, p = 0.005). Conclusions Compared to stenosis, arterial NCP burden and a composite score combining quantitative stenosis and plaque burden from CTA significantly improves identification of downstream regional vascular dysfunction.

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