Journal
EUROPEAN HEART JOURNAL
Volume 27, Issue 7, Pages 832-838Publisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehi772
Keywords
heart failure; brain natriuretic peptide; myocardial stiffness
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Aims Plasma brain natriuretic peptide (BNP) concentration increases in proportion to heart failure (HF) severity. Although plasma BNP decreases to a certain level by optimal treatment, there is significant heterogeneity in the baseline value among individuals. The underlying mechanism of the steady-state plasma BNP levels remains still controversial. We investigated the hypothesis that myocardial stiffness (K-m) is a major determinant of the plasma BNP level. Methods and results In 19 patients with diastolic HF [DHF; left ventricular ejection fraction (LVEF)>= 45%], 18 with systolic HF (SHF; LVEF < 45%), and 12 controls, left ventricular (LV) performance variables and the results of the stress-strain analyses were obtained by the combined simultaneous measurement of echocardiographic and haemodynamic data, and compared with the plasma BNP level. In DHF, a significant correlation was observed between plasma BNP and fractional shortening (P=0.010), pulmonary capillary wedge pressure (P=0.030), end-diastolic pressure (P=0.006), time constant of the LV isovolumic-pressure decline (P=0.049), end-diastolic stress (P=0.012), and K-m (P=0.004), respectively. In SHF, a significant correlation was observed between plasma BNP and end-diastolic stress (P=0.036), chamber stiffness (P=0.048), and K-m (P=0.003), respectively. Conclusion In stable conditions, K-m may be the most important determinant of the plasma BNP production in patients with both DHF and SHF.
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