Abstract
Elevated concentrations of B-type natriuretic peptide (BNP) and N-terminal pro- BNP (NT-proBNP) reflect elevated myocardial wall stress due to volume or pressure overload in cardiac disease. Recently, exercise-induced elevations of (NT-pro)BNP in coronary artery disease (CAD) patients have been reported to result from exercise-induced ischemia associated regional wall abnormalities. Therefore, the study aimed to examine NT-proBNP concentrations in patients with CAD after moderate and brisk walking (MW, BW). We hypothesized that BW induces higher increases than MW.
Methods and results
In randomized order 14 patients with stable CAD (12♂/2♀; 63 ± 9 years; LV ejection fraction: 59±9%) of a out-patient rehabilitation group performed MW with 4.5 ± 0.6 km/h (mean heart rate: 80 ± 11/min) or BWat their allowed upper exercise heart rate of 102±9/min with a speed of 6.2 ± 0.6 km/h for 30 min on a tartan track on two separate days. Blood samples were taken before, immediately, 1 h, 3 h and 1 day after exercise to determine NT-proBNP and cardiac troponin T (cTnT). Echocardiographic LV function was determined before and 1 h after exercise. Median concentrations of NT-proBNP significantly increased from 222 to 295 ng/l (MW) and from 222 to 296 ng/l (BW) without a difference between both modalities. cTnT remained below the detection limit of 0.01 µg/l. LV functions remained unchanged. A cutoff level of 250 ng/l distinguished CAD patients with elevated exercise-induced increases in NT-proBNP and a diminished LV ejection fraction at rest.
Conclusion
BW and MW induce similar increases in NT-proBNP in CAD patients without myocardial damage, which have to be considered when NT-proBNP is determined. Derived from the exercise- induced increase in NTproBNP, the myocardial strain in BW is not elevated in comparison to MW.
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Scharhag, J., Herrmann, M., Weissinger, M. et al. N-terminal B-type natriuretic peptide concentrations are similarly increased by 30 minutes of moderate and brisk walking in patients with coronary artery disease. Clin Res Cardiol 96, 218–226 (2007). https://doi.org/10.1007/s00392-007-0491-2
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DOI: https://doi.org/10.1007/s00392-007-0491-2