Although NT-proBNP is released by the ventricular myocardium as a counterregulatory response to increased stress on the wall, vasoconstriction, and sympathetic tone, it may also be associated with the regulation of numerous physiologic functions that control energy metabolism [12], myocardial ischemia due to CAD or other cardiac pathological conditions [42, 43], and the development of end-organ damage including left ventricular hypertrophy, peripheral arterial disease, and glomerulosclerosis [44]. Here, NPPB is linked to left ventricular hypertrophy.