The battle of new biomarkers for right heart failure in pulmonary hypertension: is the queen of hearts NT-proBNP defeated at last?

Abstract

Pulmonary hypertension (PH) induces right ventricular (RV) pressure overload. Initially, the right ventricle is able to adapt to the augmented afterload by increasing contractility to maintain cardiac output [1]. Consequently, RV function is preserved through adaptive RV hypertrophy, with minimal dilation and fibrosis. Nevertheless, due to maintained pressure overload, RV adaptation eventually fails, and patients die from right heart failure. RV adaptation is heterogeneous among PH patients and the transition from the adaptive to the maladaptive RV phenotype is not fully understood. Several pathological processes have been associated with the RV maladaptive phenotype in PH, including: a metabolic shift to glycolysis, mitochondrial dysfunction, inflammation, capillary rarefaction, sympathetic overstimulation, increased RV diastolic stiffness, and RV fibrosis [2–8]. These insights have been obtained using human tissue of end-stage disease or animal models. However, to fully recapitulate the transition from RV adaptation to maladaptation, longitudinal assessment of the pathological processes in patients is necessary. One way to obtain longitudinal pathophysiological insights is to identify a disease-related circulating biomarker. The search for new biomarkers for right ventricular maladaptation in pulmonary hypertension is exciting. At this moment we are missing some key information that hampers full-scale clinical implementation. https://bit.ly/37xbgwx