Atrial Natriuretic Peptide is Secreted Directly into the Left Atrial Cavity

1988 ◽  
Vol 74 (s18) ◽  
pp. 61P-62P
Author(s):  
K P Walsh ◽  
T D M Williams ◽  
S R Morris ◽  
A J Drake-Holland ◽  
M I M Noble ◽  
...  
1990 ◽  
Vol 11 (12) ◽  
pp. 1065-1073 ◽  
Author(s):  
J. P. WOLF ◽  
J. C. DUSSAULE ◽  
A. VAHANIAN ◽  
P. L. MICHEL ◽  
J. ACAR ◽  
...  

2019 ◽  
Vol 29 (2) ◽  
pp. 187-192 ◽  
Author(s):  
Kunal Bhakhri ◽  
Sara Volpi ◽  
Davide Gori ◽  
Martin Goddard ◽  
Jason M Ali ◽  
...  

AbstractOBJECTIVESDiffuse cardiac amyloidosis is a significant diagnosis with a poor prognosis. Isolated atrial amyloidosis (IAA) is the most common form of cardiac amyloidosis caused by accumulation of alpha-atrial natriuretic peptide. IAA has been associated with dysrhythmia, but otherwise remains a poorly characterized condition. The impact of incidental IAA on postoperative outcome following cardiac surgery has not previously been reported. The purpose of this study was to examine the impact of isolated atrial amyloid on patient outcomes following cardiac surgery.methodsA retrospective analysis was performed of all patients having excision of the left atrial appendage during cardiac surgery at our centre over a 5-year period. Patients with histological evidence of IAA were compared to patients without this diagnosis. IAA was diagnosed by immunohistochemistry for atrial natriuretic peptide.RESULTSA total of 167 patients underwent left atrial appendage excision and of these 26 (15.6%) were found to have IAA. Preoperative characteristics were similar between the 2 groups. A significantly greater proportion of patients with IAA experienced dysrhythmia requiring implantation of a permanent pacemaker (23.1% vs 7.8%, P = 0.03). There was also a significantly elevated incidence of perioperative death in the IAA group (11.5% vs 1.4%, P = 0.03) and inferior 1-year survival (84.6% vs 96.5%, P = 0.02).CONCLUSIONSThe presence of IAA may be associated with inferior outcomes following cardiac surgery, with increased morbidity in the early postoperative period and inferior long-term survival. Knowledge of the diagnosis preoperatively may facilitate management of patients.


1985 ◽  
Vol 63 (6) ◽  
pp. 739-742 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
C. A. Courneya ◽  
A. J. Rankin

A heterologous radioimmunoassay was used to measure the concentration of immunoreactive atrial natriuretic peptide (iANP) in plasma from the femoral artery of eight chloralose anaesthetized dogs. Mitral obstruction which increased left atrial pressure by 11 cmH2O increased plasma iANP from 97 ± 10.3 (mean ± SE) to 135 ± 14.3 pg/mL. Pulmonary vein distension increased heart rate but did not increase plasma iANP. Bilateral cervical vagotomy and administration of atenolol (2 mg/kg) did not prevent the increase in iANP with mitral obstruction. Samples of blood from the coronary sinus had plasma iANP significantly higher than simultaneous samples from the femoral artery confirming the cardiac origin of the iANP. Release of iANP depends on direct stretch of the atrium rather than on a reflex involving left atrial receptors.


1994 ◽  
Vol 87 (6) ◽  
pp. 671-677 ◽  
Author(s):  
Pierre-Louis Tharaux ◽  
Jean-Claude Dussaule ◽  
Jérôme Hubert-Brierre ◽  
Alec Vahanian ◽  
Jean Acar ◽  
...  

1. 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.


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