Plasma Atrial and Brain Natriuretic Peptides in Mitral Stenosis Treated by Valvulotomy

In order to appreciate the effect of changes in left atrial pressure on plasma brain natriuretic peptide, 20 patients with mitral stenosis treated by percutaneous valvulotomy were studied 10 min before and 15 min after the first balloon inflation. They were also studied 24 h before and 48 h after the valvulotomy. At these times the effect of postural changes on brain natriuretic peptide secretion was examined. A group of 10 control subjects was also studied under basal conditions. In each case, plasma atrial natriuretic peptide was measured in parallel with plasma brain natriuretic peptide. 2. Similarly to plasma atrial natriuretic peptide, plasma brain natriuretic peptide was elevated in patients with mitral stenosis (32 ± 2.9 and 32 ± 2.8 pg/ml in the upright and supine position respectively versus 13.5 ± 0.5 and 13.8 ± 1.8 pg/ml in controls; P < 0.01). Changing from standing to lying did not modify plasma brain natriuretic peptide, whereas it produced an increase in plasma atrial natriuretic peptide in controls (13.3 ± 1.6 versus 24.8 ± 5.2 pg/ml; P < 0.01) and in patients 48 h after valvulotomy (52.5 ± 4.6 versus 66.9 ± 6.6 pg/ml; P < 0.01). Plasma brain natriuretic peptide also fell at this time (18.8 ± 1.1 and 19.1 ± 1.1 pg/ml in the upright and supine position respectively; P < 0.01) similarly to plasma atrial natriuretic peptide and cyclic GMP (P < 0.01). The acute left atrial mean pressure variation was significantly correlated with the parallel change in plasma atrial natriuretic peptide (P < 0.001) but not in plasma brain natriuretic peptide. Plasma brain natriuretic peptide measured 24 h before and 48 h after valvulotomy was not correlated with plasma cyclic GMP, contrary to plasma atrial natriuretic peptide (P < 0.001). 3. The results of the present study indicate that plasma brain natriuretic peptide depends on long-term but not on acute changes in left atrial pressure. This difference from atrial natriuretic peptide may result from both its preferential ventricular site of synthesis and its longer biological half-life.