Mechanistically, this risk was explained by an increase in central blood pressure by reflected pressure waves.35 In addition, prolonged diastolic filling increases ventricular volumes and pressures, increasing the ventricular load.37,38 These mechanisms combine to increase myocardial wall stress, which may explain why, in historical hypertension trials, BNP and NT-proBNP levels were found to be elevated in patients receiving β-blockers.39 The gene discussed is NPPB; the disease is Hypertension.