“…As a flow-dependent measure, physiological determinants of the cardiac output (systolic and diastolic ventricular function, arterial compliance, vascular resistance, and wave reflections) are expected to have an important impact on the aortic TPG, and thus, they should be taken seriously under consideration when interpreting measurements [ 34 , 37 , 38 , 39 ]. Furthermore, aortic stenosis generally coexists with arterial stiffening, which further increases the left ventricular afterload [ 31 , 38 ], and they are both the consequences of similar pathophysiological progress [ 34 ]. Clinical and experimental data show that, particularly in low flow states (either because of decreased myocardial contractility or increased afterload), the TPG may be low despite the presence of severe aortic stenosis, leading to diagnostic inaccuracies and therapeutic delays [ 40 , 41 , 42 , 43 , 44 , 45 ].…”