Pulmonary regurgitation: the still forgotten valvular disease

This editorial refers to ‘Prevalence, aetiology and outcomes of native pulmonary regurgitation in the general adult population’, by J. A. Naser et al., https://doi.org/10.1093/ehjci/jeaf011. The pulmonary valve is characterized by a three-leaflet structure, anatomically analogous to the aortic valve. The pulmonic valve is comparatively thinner, attributable to the diminished pressures prevalent in the right heart compared with those in the left heart.1 The functional dynamics of a severely regurgitant pulmonary valve diverge significantly from those of a severely regurgitant aortic valve. Forward pulmonary blood flow is maintained indirectly through the left heart work, facilitated by systemic venous return and active contraction of the right atrium. Moreover, the pulmonary microvascular bed exhibits lower resistance compared with the systemic microvascular bed. Consequently, the pulmonary microvascular bed contributes a valve-like effect in instances of severe pulmonary regurgitation (PR). PR is usually well tolerated over an extended period; however, it can be exacerbated by conditions that lead to elevated pulmonary artery pressure. The adaptive response of the right ventricle (RV) to the volume overload resulting from PR is contingent upon the severity and duration of the regurgitant flow as well as the inherent properties of the RV and pulmonary arteries.2 Additionally, tricuspid regurgitation may further contribute to dilatation of the RV and right atrium.3