Response to the letter entitled “Cardiac reserve in pulmonary stenosis: Role of multimodality imaging”

Abstract

ventricular concentric remodeling, which results in the reductions of SVi and cardiac output together with a compensatory increase in heart rate [2]. It is possible that lower left ventricular outputmay also lead to a “pseudo-normalization” of aortic pressure. Accordingly, in our study based on invasive data obtained during cardiac catheterization, we observed that LFLG patients were characterizedbyaworseprofile bothat theaortic valve andvessel levels compared with normal flow-low gradients. Consequently our study might be considered a confirmatory study obtained with a completely different diagnostic methodology, which does not imply LVOT measurement. Same papers showed that a high value of valvulo-arterial impedance is associated with an increased risk of left ventricular systolic dysfunction development [2]. In our study LFLG patients had preserved EF by definition, but actually the presence of intrinsic myocardial dysfunction cannot be excluded. It should be acknowledge that barely perception of this pathologic entity might have reduced the likelihood of patients referred to cardiac catheterization leading to potential underestimation of the prevalence of this condition. As recently reported in this journal [7], and especially in patients with low MG, an accurate estimation of the severity of aortic stenosis, assessment of comorbidities, particularly the occurrence of CAD, and the risk carried by the individual patient is needed. Authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology.