Dynamic left ventricular dyssynchrony contributes to B-type natriuretic peptide release during exercise in patients with systolic heart failure.

AIMS Plasma B-type natriuretic peptide (BNP) is an emerging biomarker in heart failure. In this setting, the extent of left ventricular (LV) dyssynchrony contributes to exercise symptoms. Whether exercise-induced changes in LV dyssynchrony might be a trigger of BNP release has never been investigated. METHODS AND RESULTS Fifty-seven patients with systolic LV dysfunction underwent quantitative analysis of BNP, mitral regurgitation (MR), and dyssynchrony at rest and during exercise. None had inducible ischaemia on perfusion imaging. By multiple regression analysis, end-systolic volume index (P < 0.0001), effective regurgitant orifice (ERO) (P < 0.001), and E/Ea (P = 0.002) emerged as independent determinants of BNP at baseline (R(2) = 0.67). Exercise induced a significant rise in BNP levels (P < 0.0001). In multivariate analysis, a smaller change in systolic blood pressure (P = 0.04), a larger increase in ERO (P = 0.017), and in systolic dyssynchrony index (P = 0.006) during exercise emerged as independent determinants of exercise-induced increases in BNP (R(2) = 0.45). CONCLUSION MR severity, volume overload, and LV filling pressure are surrogates of BNP at rest. During exercise, changes in BNP reflect the presence of dynamic changes in both LV dyssynchrony and MR severity in the absence of inducible ischaemia.