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Current guidelines advise using echocardiography for noninvasive estimation of the likelihood that a patient has pulmonary hypertension (PH). To estimate the echocardiographic probability of PH, the maximal tricuspid regurgitation velocity (TR Vmax) is recommended as the main parameter to use over more complex algorithms that provide an estimation of pulmonary artery pressure. This preference is based on concerns about inaccuracies and amplification of measurement errors that can occur from using derived variables. However, this has not been examined systematically.

The role of erythropoietin (Epo) in myocardial repair after infarction remains inconclusive. We observed high Epo receptor (EPOR) expression in cardiac progenitor cells (CPCs). Therefore, we aimed to characterize these cells and elucidate their contribution to myocardial regeneration on Epo stimulation. High EPOR expression was detected during murine embryonic heart development followed by a marked decrease until adulthood. EPOR‐positive cells in the adult heart were identified in a CPC‐enriched cell population and showed coexpression of stem, mesenchymal, endothelial, and cardiomyogenic cell markers. We focused on the population coexpressing early (TBX5, NKX2.5) and definitive (myosin heavy chain [MHC], cardiac Troponin T [cTNT]) cardiomyocyte markers. Epo increased their proliferation and thus were designated as Epo‐responsive MHC expressing cells (EMCs). In vitro, EMCs proliferated and partially differentiated toward cardiomyocyte‐like cells. Repetitive Epo administration in mice with myocardial infarction (cumulative dose 4 IU/g) resulted in an increase in cardiac EMCs and cTNT‐positive cells in the infarcted area. This was further accompanied by a significant preservation of cardiac function when compared with control mice. Our study characterized an EPO‐responsive MHC‐expressing cell population in the adult heart. Repetitive, moderate‐dose Epo treatment enhanced the proliferation of EMCs resulting in preservation of post‐ischemic cardiac function. StemCells2014;32:2480–2491