Abstract

Abstract Background Impaired global coronary flow reserve (G-CFR) is known to predict worse outcomes in patients with coronary artery disease. Phase contrast cine-magnetic resonance imaging (PC-CMR) of the coronary sinus (CS) is a promising approach for quantifying coronary sinus flow (CSF) and G-CFR without the need for ionizing radiation, radioactive tracers, or intravascular catheterization. Although G-CFR impairment is previously reported to be linked with endothelium dysfunction and progression of atherosclerosis, the association of perivascular adipose tissue inflammation with myocardial coronary flow remains to be determined. Purpose We evaluated the association between G-CFR by quantifying CSF using PC-CMR and the extent of coronary inflammation evaluated by perivascular adipose tissue inflammatory status using CT to assess if coronary inflammation is linked with G-CFR in patients with stable angina pectoris (SAP) treated with elective percutaneous coronary intervention (PCI). Methods The study enrolled 74 SAP patients with single denovo lesion who underwent coronary CT angiography and PC-CMR within 90 days before coronary intervention. Proximal 40-mm segments of all three major epicardial coronary vessels were traced and examined. Coronary inflammation was assessed by the CT fat attenuation index of perivascular adipose tissue (FAI-PVAT) defined as the mean attenuation of the perivascular adipose tissue (−190 to −30 Hounsfield units (HU)) in a layer of tissue within a radial distance from the outer coronary artery wall equal to the diameter of the vessel. CMR images were also acquired to assess absolute CSF at rest and during maximum hyperemia before elective PCI. The patients were divided into 4 groups according to the number of inflamed vessels as defined by showing FAI ≥−70.1 HU. Results In the final analysis of 69 patients (mean age 67, Male 45 (65.2%)), 18, 19, 20, 12 patients exhibited none, 1, 2, 3 inflamed vessels with FAI ≥−70.1 HU, respectively. Rest and maximal hyperemic CSF and corrected G-CFR were 1.28 [0.76,1.55] vs 1.47 [1.11, 1.81] vs 1.30 [0.94, 1.64] vs 1.27 [1.11, 2.00] ml/min/g; P=0.49, 3.50 [2.84, 5.25] vs 3.28 [2.62, 4.31] vs 3.11 [2.16, 3.63] vs 2.37 [1.40, 2.98] ml/min/g; P=0.049, 3.57 [2.17, 4.54] vs 2.25 [1.73, 3.49] vs 2.26 [1.64, 3.38] vs 1.89 [0.89, 2.32]; P=0.023, respectively. G-CFR and hyperemic CSF were both significantly lower in the group with larger number of inflamed vessels. Conclusions In SAP patients with significant coronary artery stenosis, G-CFR obtained by PC-CMR significantly associated with the prevalence of inflamed vessels detected by coronary CT. The extent of coronary inflammation may influence global coronary endothelium dysfunction, resulting in decreased G-CFR.

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