Longitudinal myocardial blood flow gradient and CAD detection.

Conventional myocardial perfusion scintigraphy with SPECT/CT or with PET/CT has been established as pivotal clinical imaging modality for the identification of hemodynamically obstructive coronary artery disease (CAD) and risk stratification of patients with suspected or known CAD. While the assessment of the relative distribution of radiotracer uptake in the left-ventricular (LV) myocardium during vasomotor stress identifies the "culprit" or most severe CAD lesion in multivessel disease, flow-limiting effects of remaining but less severe epicardial lesions may be missed. This limitation principally may be overcome by the possibility of PET/CT with radiotracer-kinetic modeling to concurrently assess left-ventricular (LV) myocardial blood flow (MBF) in ml/g/min at rest and during vasomotor stress and the resulting myocardial flow reserve (MFR). While a stress-induced regional reduction in radiotracer uptake or perfusion identifies the most advanced epicardial lesion, flow-limiting effects of the other epicardial lesions may principally be identified by regional reductions in MFR. Conversely, reductions in MFR in CAD may be appreciated as suboptimal as they reflect not only the consequences of flow-limiting effects of epicardial stenosis but also of microvascular dysfunction. The relatively low specificity of a reduced therefore MFR may hamper a clear identification of the downstream hemodynamic effects of an epicardial lesion on hyperemic coronary flow increases. In this scenario, there is increasing evidence that the PET assessment of an abnormal decrease in MBF from the base to the apex of the LV during hyperemic flows, a so-called longitudinal flow gradient, is primarily related to fluid dynamic consequences of CAD-induced diffuse luminal and/or focal narrowing of the epicardial artery. The combined evaluation of the MFR and corresponding longitudinal MBF gradient could emerge as new a novel analytic concept to further optimize the identification and characterization of hemodynamic CAD burden in multivessel disease, which, however, warrants further clinical validation.