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Background Computed tomography coronary angiography (CTCA) image analysis enables plaque characterization and non-invasive fractional flow reserve (FFR) calculation. We analyzed various parameters derived from CTCA images and evaluated their associations with ischemia. Methods 49 (61 lesions) patients underwent CTCA and invasive FFR. Lesions with diameter stenosis (DS) ≥ 50% were considered obstructive. CTCA image processing incorporating analytical and numerical methods were used to quantify anatomical parameters of lesion length (LL) and minimum lumen area (MLA); plaque characteristic parameters of plaque volume, low attenuation plaque (LAP) volume, dense calcium volume (DCV), normalized plaque volume (NP Vol), plaque burden, eccentricity index and napkin-ring (NR) sign; and hemodynamic parameters of resistance index, stenosis flow reserve (SFR) and FFR B . Ischemia was defined as FFR ≤ 0.8. Results Plaque burden and plaque volume were inversely related to FFR. Multivariable logistic regression analysis identified the best anatomical, plaque and hemodynamic predictors, respectively, as DS (≥50% vs B (≤0.8 vs >0.8; OR: 44.4; 95% CI: 8.8–224.8). AUC increased from 0.70 with DS as the sole predictor to 0.81 after adding NP Vol and NR Sign; further addition of FFR B increased AUC to 0.93. Conclusion Normalized plaque volume, napkin-ring derived from plaque analysis, and FFR B from numerical simulations on CTCA images substantially improved discrimination of ischemic lesions, compared to assessment by DS alone.

To the Editor:Patients with systemic lupus erythematosus (SLE) are at in-creased risk of premature atherosclerosis, mediated by endothelialdysfunction and increased arterial stiffness[1]. The latter, mostcommonly assessed using carotid-femoralpulse wave velocity, isincreased in patients with SLE and is associated with cardiovascu-lar risk factors[1]. Recently, a more sensitive measure of arterialstiffness (effective arterial elastance; Ea), and ventricular-arterialcoupling (ratio of arterial and end-systolic ventricular elastance;Ea/Ees) demonstrated incremental prognostic value in patientswith chronic heart failure[2]. We aimed to assess the potential ofEa and Ea/Ees as novel biomarkers of cardiovascular risk in SLEwomen without ischemic heart disease.Women whosatisfiedtherevised American College of Rheumatolo-gy classification criteria for SLE were prospectively recruited from therheumatology clinics, as described previously [3]. Patients with recentactive flares, ischemic heart disease (all patients underwent nuclearstress perfusion imaging as part of the study), cardiomyopathies(including myocarditis) and valvular heart disease of≥ moderateseverity were excluded. Cardiovascular risk was defined as historyof hypertension, hyperlipidemia, diabetes mellitus, current tobacco use,cerebrovascularevents,familyhistoryofcoronaryarterydiseaseandsec-ondary anti-phospholipid syndrome. Age-matched control women wererecruited from the community. Left ventricular mass, diastolic functionand systolic ejection fraction were assessed with echocardiography;Ea was estimated as 0.9 x (arm-cuff systolic pressure/Doppler strokevolume) and Ees was calculated by the well-validated approach ofusing arm-cuff pressures, Doppler stroke volumes, ejection fraction,pre-ejection and systolic periods [4,5]. The study was conducted inaccordance with the Declaration of Helsinki and approved by the localresearch ethics committee. Written informed consent was obtainedfrom all participants.Continuousvariableswerepresentedinmean±SDormedian[inter-quartile range] and compared using either the Student t test or Mann-Whitney U test, as appropriate. The mean differences in Ea and Ea/Eeswere adjusted for age,systolic ejection fraction and systolicblood pres-sure. We assessed associations using the Pearson (r) or Spearman (ρ)correlation, as appropriate. All statistical analyses were performedwiththeSPSSversion19(SPSSInc,Chicago,USA).Atwo-sidedP b0.05 was considered statistically significant.Forty-eight patients with SLE (43±9 years old; disease durationof 14±6 years; 1 [0,2] risk factors) and 20 control women (42±9years old) were recruited. There were no differences in left ventricu-lar mass, diastolic function and Ees between SLE and control women(PN0.50 for all;Table 1). Compared to control individuals, patientswithSLEhadlowersystolicejectionfraction,albeitasmalldifference(71±8 versus 75±7%; P=0.04). Despite similar systolic blood pres-sure compared with control women (116±12 versus 119±16mmHg; P=0.52), patients with SLE had increased Ea (1.77±0.56versus 1.37±0.27 mmHg/mL; adjusted mean difference 0.30mmHg/mL, 95% confidence interval [CI] 0.08 to 0.53 mmHg/mL,Pb0.001) and Ea/Ees (0.61±0.18versus 0.50±0.07; adjusted meandifference 0.06, 95% CI 0.01 to 0.12, P=0.04). Furthermore, Ea wasassociated with increasing cardiovascular risk (ρ=0.35; P=0.02),systolic blood pressure (r=0.55, Pb0.001) and duration of predniso-lone use (ρ=0.33, P=0.03).Over 3 years of follow-up (median 31 [17,37] months), 8% ofpatients with SLE developed cardiovascular events (event rate 3.2 per100 person-years; non-fatal myocardial infarction, n=2; stroke, n=1