Emootje
Senior Member
- Messages
- 356
- Location
- The Netherlands
Increased atrial and brain natriuretic peptides in adults with cyanotic congenital heart disease: enhanced understanding of the relationship between hypoxia and natriuretic peptide secretion.
http://circ.ahajournals.org/cgi/reprint/109/23/2872
In the present study, both proANP and proBNP were markedly elevated in the cyanotic patients compared with noncyanotic controls. The 4-fold increase in proANP was similar to the finding in our previous report. Even more striking was the 12-fold increase in proBNP levels in cyanotic
patients. We found an 8% relative reduction in percent TBW in the cyanotic patients, although this trend did not reach statistical significance. To the best of our knowledge, the combination of increased natriuretic peptides and reduced body water has not previously been reported. To put the
magnitude of this difference in perspective, an 80-kg person with 42% TBW will have 3.2 L less water than an equivalent person with 46% TBW or 300 mL less plasma volume. Reduced plasma volume may contribute to reduced ventricular filling, stroke volume, and cardiac output and increased blood viscosity. Consistent with reduced preload, transmitral Doppler studies have revealed reduced E-to-A wave ratio and prolonged deceleration time in adult patients with cyanotic congenital heart disease, findings that are very similar to those of the present study. When cardiac output is reduced in adults with cyanotic congenital heart disease, it is because of volume depletion rather than ventricular dysfunction, unlike patients with heart failure. Plasma ANP is also increased in patients with sleep apnea, and levels decrease with continuous positive airway pressure treatment. As in patients with cyanotic congenital heartdisease, plasma volume is decreased, and there is an inverse relationship between plasma ANP and oxygen saturation.
In my case the increased ANP might be caused by inflammation causing plasma volume reduction, reduced preload, reduced ventricular filling, reduced E-A ratio and prolonged deceleration time.
http://circ.ahajournals.org/cgi/reprint/109/23/2872
In the present study, both proANP and proBNP were markedly elevated in the cyanotic patients compared with noncyanotic controls. The 4-fold increase in proANP was similar to the finding in our previous report. Even more striking was the 12-fold increase in proBNP levels in cyanotic
patients. We found an 8% relative reduction in percent TBW in the cyanotic patients, although this trend did not reach statistical significance. To the best of our knowledge, the combination of increased natriuretic peptides and reduced body water has not previously been reported. To put the
magnitude of this difference in perspective, an 80-kg person with 42% TBW will have 3.2 L less water than an equivalent person with 46% TBW or 300 mL less plasma volume. Reduced plasma volume may contribute to reduced ventricular filling, stroke volume, and cardiac output and increased blood viscosity. Consistent with reduced preload, transmitral Doppler studies have revealed reduced E-to-A wave ratio and prolonged deceleration time in adult patients with cyanotic congenital heart disease, findings that are very similar to those of the present study. When cardiac output is reduced in adults with cyanotic congenital heart disease, it is because of volume depletion rather than ventricular dysfunction, unlike patients with heart failure. Plasma ANP is also increased in patients with sleep apnea, and levels decrease with continuous positive airway pressure treatment. As in patients with cyanotic congenital heartdisease, plasma volume is decreased, and there is an inverse relationship between plasma ANP and oxygen saturation.
In my case the increased ANP might be caused by inflammation causing plasma volume reduction, reduced preload, reduced ventricular filling, reduced E-A ratio and prolonged deceleration time.