Circulating BNP and the N-terminal pro-B-type natriuretic peptide (NT-proBNP) increase their levels consequently to increased wall stretching due to volume or load stress in HF caused by systolic and/or diastolic dysfunction, valvular heart disease, left ventricular hypertrophy, ischemia, or a combination of these factors. The gene discussed is NPPB; the disease is ischemia.