THE VALIDITY OF B-TYPE NATRIURETIC PEPTIDE BLOOD LEVELS TO DETECT HEART FAILURE IN HEART TRANSPLANT PATIENTS.

Abstract

Purpose The usefulness of B-type natriuretic peptide (BNP) to detect symptomatic heart failure in the nontransplanted patient has been well established. However, the clinical utility of measuring BNP levels following heart transplantation is unclear. The purpose of our study was to determine whether BNP levels correlate with symptomatic heart failure, confirmed hemodynamically, in cardiac transplant recipients. Methods We evaluated 130 consecutive patients transplanted between July 2001 and November 2003 whose BNP levels were assessed at time of right heart catheterization and clinical examination. BNP values drawn within 8 weeks prior to an initial episode of treated rejection were also identified (n = 10). Heart failure was defined as both the presence of symptoms (dyspnea, edema, or documented increase in diuretic dose) and a PCWP 15 mm Hg. BNP samples taken during the first 3 months post-transplant (when levels are known to be elevated), as well as patients with renal failure (Cr > 1.9) were excluded. Patients had an average follow-up of 28 months. Results Of the 130 patients, 67 patients had 124 BNP measurements with a PCWP 15. The BNP was 150 pg/mL in only 42 of 124 (33.8%) measurements. In 29 patients with symptomatic heart failure and PCWP 15, the BNP was 150 on only 19 of 42 (45.2%) occasions. Therefore, a BNP level of 150 was found to have a sensitivity of only 45.2%, a specificity of 64.9%, a positive predictive value of 3.7%, and a negative predictive value of 2.4% for the detection of heart failure in heart transplant recipients. In addition, a BNP value 150 within 8 weeks of a clinically significant episode of rejection was noted in only 5 of 10 (50%) cases. Conclusions BNP levels are not effective in determining clinically relevant heart failure following heart transplantation. In addition, it does not appear to predict rejection. The discrepancy between the utility of BNP in detecting heart failure in the transplant and nontransplant population may be due to denervated cardiac physiology but requires further investigation.