Background Recent studies have reported the association between pericoronary inflammation assessed by pericoronary adipose tissue attenuation (PCATA) on computed tomography angiography and worse outcomes in patients with coronary artery disease. We investigated the determinants predicting increased PCATA in patients with known or suspected coronary artery disease. Methods and Results A total of 540 patients who underwent computed tomography angiography and invasive coronary angiography were studied. Mean computed tomography attenuation values of PCAT (−190 to −30 Hounsfield units) (PCATA) were assessed at the proximal 40‐mm segments of all 3 major coronary arteries by crude analysis. Univariable and multivariable analyses were performed to determine the predictors of increased PCATA surrounding the proximal right coronary artery. Mean right coronary artery‐PCATA was −72.22±8.47 Hounsfield units and the average of 3‐vessel PCATA was −70.24±6.60 Hounsfield units. Multivariable linear regression analysis revealed that the independent determinants of right coronary artery‐PCATA were male (β coefficient=4.965, P <0.001), left ventricular mass index (β coefficient=0.040, P =0.025), and angiographically significant stenosis (diameter stenosis >50%) (β coefficient=2.418, P =0.008). Sex‐related determinants were NT‐proBNP level (N‐terminal pro‐B‐type natriuretic peptide; β coefficient <0.001, P =0.026), Agatston score (β coefficient=−0.002, P =0.010), left ventricular mass index (β coefficient=0.041, P =0.028), and significant stenosis (β coefficient=4.006, P <0.001) in male patients and left ventricular ejection fraction (β coefficient=−0.217, P =0.010) and significant stenosis (β coefficient=3.835, P =0.023) in female patients. Conclusions Right coronary artery‐PCATA was associated with multiple clinical characteristics, established risk factors, and the presence of significant stenosis. Our results suggest that clinically significant factors such as sex, left ventricular hypertrophy, ejection fraction, calcification, and epicardial stenosis should be taken into account in the assessment of pericoronary inflammation using computed tomography angiography.

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BackgroundMeasurement of the contrast-flow quantitative flow ratio (cQFR) is a novel method for rapid computational estimation of fractional flow reserve (FFR). Discordance between FFR and cQFR has not been completely characterised.MethodsWe performed a post-hoc analysis of 504 vessels with angiographically intermediate stenosis in 504 patients who underwent measurement of FFR, coronary flow reserve (CFR), the index of microcirculatory resistance (IMR) and Duke jeopardy score.ResultsIn total, 396 (78.6%) and 108 (21.4%) lesions showed concordant and discordant FFR and cQFR functional classifications, respectively. Among lesions with a reduced FFR (FFR+), those with a preserved cQFR (cQFR−) showed significantly lower IMR, shorter mean transit time (Tmn), shorter lesion length (all, p<0.01) and similar CFR and Duke jeopardy scores compared with lesions showing a reduced cQFR (cQFR+). Furthermore, lesions with FFR+ and cQFR− had significantly lower IMR and shorter Tmn compared with lesions showing a preserved FFR (FFR−) and cQFR+. Of note, in cQFR+ lesions, higher IMR lesions were associated with decreased diagnostic accuracy (high-IMR; 63.0% and low-IMR; 75.8%, p<0.01). In contrast, in cQFR− lesions, lower IMR lesions was associated with decreased diagnostic accuracy (high-IMR group; 96.8% and low-IMR group; 80.0%, p<0.01). Notably, in total, 31 territories (6.2%; ‘jump out’ group) had an FFR above the upper limit of the grey zone (>0.80) and a cQFR below the lower limit (≤0.75). In contrast, five territories (1.0%; ‘jump in’ group) exhibited opposite results (FFR of ≤0.75 and cQFR of >0.80). The ‘jump out’ territories showed significantly higher IMR values than ‘jump in’ territories (p<0.01).ConclusionsFFR− with cQFR+ is associated with increased microvascular resistance, and FFR+ with cQFR− showed preservation of microvascular function with high coronary flow. Microvascular function affected diagnostic performance of cQFR in relation to functional stenosis significance.

Background Impaired global coronary flow reserve (g‐CFR) is related to worse outcomes. Inflammation has been postulated to play a role in atherosclerosis. This study aimed to evaluate the relationship between pre‐procedural pericoronary adipose tissue inflammation and g‐CFR after the urgent percutaneous coronary intervention in patients with first non–ST‐segment–elevation acute coronary syndrome. Methods and Results Phase‐contrast cine‐magnetic resonance imaging was performed to obtain g‐CFR by quantifying coronary sinus flow at 1 month after percutaneous coronary intervention in a total of 116 first non–ST‐segment–elevation acute coronary syndrome patients who underwent pre‐percutaneous coronary intervention computed tomography angiography. On proximal 40‐mm segments of 3 major coronary vessels on computed tomography angiography, pericoronary adipose tissue attenuation was assessed by the crude analysis of mean computed tomography attenuation value. The patients were divided into 2 groups with and without impaired g‐CFR divided by the g‐CFR value of 1.8. There were significant differences in age, culprit lesion location, N‐terminal pro‐B‐type natriuretic peptide levels, high‐sensitivity C‐reactive protein (hs‐CRP) levels, mean pericoronary adipose tissue attenuation between patients with impaired g‐CFR and those without (g‐CFR, 1.47 [1.16, 1.68] versus 2.66 [2.22, 3.28]; P <0.001). Multivariable logistic regression analysis revealed that age (odds ratio [OR], 1.060; 95% CI, 1.012–1.111, P =0.015) and mean pericoronary adipose tissue attenuation (OR, 1.108; 95% CI, 1.026–1.197, P =0.009) were independent predictors of impaired g‐CFR (g‐CFR <1.8). Conclusions Mean pericoronary adipose tissue attenuation, a marker of perivascular inflammation, obtained by computed tomography angiography performed before urgent percutaneous coronary intervention, but not hs‐CRP, a marker of systemic inflammation was significantly associated with g‐CFR at 1‐month after revascularization. Our results may suggest the pathophysiological mechanisms linking perivascular inflammation and g‐CFR in patients with non–ST‐segment–elevation acute coronary syndrome.

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