Structurally, pressure overload in the heart initially increases left ventricular mass and cell size to elevate force of contraction, which can progress to left ventricular hypertrophy [2], high serum levels of natriuretic peptides get released, brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) [3], cardiomyocyte contractility declines and the formation of reactive oxygen species increases (ROS) [4], all of which resulting in heart failure (HF) [5,6,7]. This evidence concerns the gene NPPB and left ventricular hypertrophy.