NT-proBNP is a weak indicator of cardiac function and haemodynamic response to exercise in chronic heart failure

2019 
AIMS: N-terminal prohormone of brain natriuretic peptide (NT-proBNP) plays an important role in diagnosis and management of heart failure. The aim of the present study was to assess haemodynamic response to exercise and to evaluate the relationship between NT-proBNP, cardiac function, and exercise tolerance in chronic heart failure. METHODS AND RESULTS: A single-centre, cross-sectional pilot study recruited 17 patients with chronic heart failure with reduced left ventricular ejection fraction (age 67 ± 7 years) and 20 healthy volunteers (age 65 ± 12 years). The NT-proBNP was measured in the heart failure group. All participants completed maximal graded cardiopulmonary exercise stress testing coupled with gas exchange (using metabolic analyser for determination of exercise tolerance, i.e. peak O2 consumption) and continuous haemodynamic measurements (i.e. cardiac output and cardiac power output) using non-invasive bioreactance technology. Heart failure patients demonstrated significantly lower peak exercise cardiac function and exercise tolerance than healthy controls, i.e. cardiac power output (5.0 ± 2.0 vs. 3.2 ± 1.2 W, P < 0.01), cardiac output (18.2 ± 6.3 vs. 13.5 ± 4.0 L/min, P < 0.01), heart rate (148 ± 23.7 vs. 111 ± 20.9 beats/min, P < 0.01), and oxygen consumption (24.3 ± 9.5 vs. 16.8 ± 3.8 mL/kg/min, P < 0.01). There was no significant relationship between NT-proBNP and cardiac function at rest, i.e. cardiac power output (r = -0.28, P = 0.28), cardiac output (r = -0.18, P = 0.50), and oxygen consumption (r = -0.18, P = 0.50), or peak exercise, i.e. cardiac power output (r = 0.18, P = 0.49), cardiac output (r = 0.13, P = 0.63), and oxygen consumption (r = -0.05, P = 0.84). CONCLUSIONS: Lack of a significant and strong relationship between the NT-proBNP and measures of cardiac function and exercise tolerance may suggest that natriuretic peptides should be considered with caution in interpretation of the severity of cardiac dysfunction and functional capacity in chronic heart failure.
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