Mechanisms involved in increased plasma brain natriuretic peptide after heart transplantation

Increased brain natriuretic peptide (BNP), reflecting increased ventricular wall stress and pressure, is a well-known diagnostic and prognostic marker in patients with chronic heart failure. Heart transplantation (HT), the process of replacing the failing heart and restoring haemodynamics, should normalize cardiac endocrine function. Nevertheless, BNP levels remain raised after HT, likely because of increased secretion and/or decreased clearance of the cardiac hormone. Thus, BNP increases in proportion to the extent of left and right ventricular dysfunction after HT. Clinically complicated cardiac transplantation (cardiac systolic dysfunction, renal failure) is associated with the higher level of circulating BNP, and clinically successful cardiac transplantation (mild cardiac diastolic dysfunction) is associated with moderately increased BNP values. Surprisingly, however, increased BNP has also been found after HT in the absence of haemodynamic perturbations or allograft rejection, raising the hypothesis that even subtle modification in the immune system might influence BNP expression. In view of the potential interest in the cardiac hormone for subjects' risk stratification and therapy, a better knowledge of the mechanisms involved in the BNP increase after HT might be helpful for HT recipients' follow-up.