The responsible mechanisms still remain to be fully elucidated, but both experimental and clinical myocardial infarction is associated with gradual and sustained elevation of circulating BNP levels [29] and cardiac BNP expression as verified by cardiac biopsies of hypoxic ventricular areas is of the same magnitude in patients with CAD and with normal left ventricular function as in patients with congestive heart failure but no myocardial ischemia [29]. This evidence concerns the gene NPPB and myocardial infarction.