It has been shown that in experimental acute myocardial infarction, NT-pro BNP synthesis is augmented not only in infarcted tissue but also in non-infarcted tissue.21 In addition, NT-pro BNP levels have been shown to increase transiently after uncomplicated percutaneous transluminal coronary angioplasty, even when intracardiac filling pressures remain unchanged.22 Therefore, we may suggest that transient ischemia increases wall stress and induces BNP synthesis and the release in proportion to the degree of ischemic insult. This evidence concerns the gene NPPB and myocardial infarction.