Key result
Exercise induced a significant rise in BNP levels (P<0.0001), which was independently determined by dynamic changes in left ventricular dyssynchrony (P=0.006) and mitral regurgitation (P=0.017).
Why the study?
Does exercise-induced left ventricular dyssynchrony contribute to B-type natriuretic peptide release in patients with systolic heart failure?
Observational (n=57)
Does exercise-induced left ventricular dyssynchrony contribute to B-type natriuretic peptide release in patients with systolic heart failure?
p-value: p=<0.0001
Dynamic changes in left ventricular dyssynchrony and mitral regurgitation severity during exercise independently contribute to BNP release in patients with systolic heart failure.
Dynamic LV dyssynchrony may drive exercise BNP release in systolic HF; hypothesis-generating and requires prospective validation.
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.
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Lancellotti et al. (2008) conducted an observational in Systolic heart failure (n=57). Exercise vs. Rest was evaluated on Exercise-induced increases in BNP (p=<0.0001). Exercise induced a significant rise in BNP levels (P<0.0001), which was independently determined by dynamic changes in left ventricular dyssynchrony (P=0.006) and mitral regurgitation (P=0.017).
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