Fractional flow reserve computed tomography in the evaluation of coronary artery disease.

Abstract

Amongst patients with suspected obstructive coronary artery disease (CAD), less than a third of patients have obstructive disease on invasive coronary angiography (ICA) and fewer still have flow-limiting obstructive disease as determined by invasive fractional flow reserve (FFR). FFR is a powerful tool in guiding revascularization of flow-limiting lesions which in turn improves clinical outcome in those with haemodynamically significant obstructive disease. However FFR is infrequently performed due to the cost, time and patient discomfort the procedure entails. Further advances in non-invasive imaging has allowed FFR to be derived non-invasively by applying computational fluid dynamic (CFD) modeling to the coronary computed tomography angiography (CCTA) dataset without the need to induce hyperemia or modify the standard CCTA acquisition protocol. FFR derived from CCTA has been shown to have excellent correlation with invasive FFR and remains diagnostically robust in presence of reduced signal-to-noise ratio (SNR), coronary calcification and motion artifact. More recently, new data have emerged evaluating the clinical impact of fractional flow reserve computed tomography (FFRCT) on the assessment and management of patients with stable chest pain. One such study is the Prospective LongitudinAl trial of FFRCT: Outcome and Resource IMpacts (PLATFORM) study which showed an improved patient selection for ICA using CCTA-FFRCT approach by increasing the likelihood of identifying obstructive CAD at ICA amongst those intended for invasive testing. CCTA-FFRCT may therefore serve as efficacious gatekeeper to ICA that enriches the ICA population. The utility of FFRCT has also helped deepened our understanding of CAD. Through CFD modeling, it is now recognized that there are mechanistic forces of wall shear stress (WSS) and axial plaque force acting on coronary plaques. This has created further interest in exploring the possible interplay between these mechanistic forces on the development of coronary plaque and vulnerability of these plaques to rupture.