We hypothesize that two biomarkers, CRP, and NT-proBNP, by acting as surrogates for different pathophysiologic mechanisms, inflammation and myocardial strain, respectively, will independently predict the degree of CRF impairment in patients with HF across the spectrum of LVEF including both HFrEF and HFpEF. The gene discussed is NPPB; the disease is hydrops fetalis.