Atrial Natriuretic Peptide in Congestive Heart Failure after Acute Myocardial Infarction

Cardiology ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Jens Svanegaard ◽  
Kristian Angelo-Nielsen ◽  
Torben Findborg
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Natriuretic

Plasma Levels of Adrenomedullin in Patients with Acute Myocardial Infarction

1998 ◽  
Vol 94 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Yuji Yoshitomi ◽  
Toshio Nishikimi ◽  
Shunichi Kojima ◽  
Morio Kuramochi ◽  
Shuichi Takishita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Plasma Levels ◽  
The Right

1. Adrenomedullin, a newly identified vasorelaxant peptide, participates in the regulation of the cardiovascular system. To investigate the pathophysiological significance of adrenomedullin in patients with acute myocardial infarction, we measured plasma levels of adrenomedullin. 2. Cardiac catheterization was performed on admission, after 1 day, and after 4 weeks in 36 patients with acute myocardial infarction. We measured plasma levels of adrenomedullin, atrial natriuretic peptide and brain natriuretic peptide in the right atrium, pulmonary artery and aorta. 3. Plasma levels of adrenomedullin in the right atrium (mean ± SEM) were significantly increased on admission (4.2 ± 2.6 h) in patients with acute myocardial infarction (10.6 ± 1.0 pmol/l) compared with controls (5.2 ± 0.3 pmol/l, P < 0.01). In addition, plasma levels of adrenomedullin were further elevated in patients with congestive heart failure (12.3 ± 1.4 pmol/l) compared with patients without congestive heart failure (7.8 ± 0.6 pmol/l, P < 0.01). In patients with congestive heart failure, plasma adrenomedullin on admission significantly correlated with atrial natriuretic peptide and brain natriuretic peptide. 4. These results suggest that plasma adrenomedullin increases in the early phase of acute myocardial infarction and that volume expansion may be one of the additional stimuli for the release of adrenomedullin in patients with acute myocardial infarction complicated by congestive heart failure.

Atrial natriuretic peptide in patients with acute myocardial infarction without functional heart failure

1991 ◽  
Vol 12 (4) ◽  
pp. 503-507 ◽  
Author(s):  
F. M. GUTIEREZ-MARCOS ◽  
A. FERNANDEZ-CRUZ ◽  
J. GUTKOWSKA ◽  
C. HERRERO ◽  
A. BLESA ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Natriuretic

N-terminal pro-atrial natriuretic peptide (N-ANP) and N-terminal pro-B-type natriuretic peptide (N-BNP) in the prediction of death and heart failure in unselected patients following acute myocardial infarction

2004 ◽  
Vol 107 (3) ◽  
pp. 309-316 ◽  
Author(s):  
Iain B. SQUIRE ◽  
Russell J. O'BRIEN ◽  
Bettina DEMME ◽  
Joan E. DAVIES ◽  
Leong L. NG
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Risk Of Death ◽  
Number Of Patients ◽  
Patients At Risk ◽  
Relationship Of ◽  
Atrial Natriuretic

Elevated plasma natriuretic peptide levels after AMI (acute myocardial infarction) are associated with adverse outcome. The aim of the present study was to examine the relationship of plasma N-ANP (N-terminal pro-atrial natriuretic peptide) and N-BNP (N-terminal pro-B-type natriuretic peptide) with mortality and heart failure following AMI. We studied 403 patients with AMI. Blood was sampled for measurement of N-ANP and N-BNP on a single occasion between 72 and 96 h after symptom onset. Natriuretic peptide levels were related to all-cause mortality and heart failure episodes. During follow up (median, 462 days; range 5–764), 43 (10.7%), 25 (6.2%) and 49 (12.2%) patients suffered death, heart failure hospitalization and outpatient heart failure respectively. Only N-BNP (P<0.0005), N-ANP (P=0.005) and previous AMI (P=0.016) were independently predictive of death. N-BNP, but not N-ANP, predicted 30-day mortality. N-ANP, but not N-BNP, predicted mortality after 30 days. N-BNP was the better predictor of heart failure. N-ANP and N-BNP were above the median in 35 and 38 respectively, of 43 patients who later died. N-ANP, N-BNP, or both were above the median in 41 out of 43 patients. Of 25 patients hospitalized with heart failure, N-ANP and N-BNP was above the median in 20 and 24 respectively, and one or other was elevated in all cases. Above-median N-ANP predicted 36 and N-BNP predicted 41 out of 49 episodes of outpatient heart failure. One or other peptide was above the median in 45 out of 49 patients. Our results indicate that N-BNP predicts 30-day and N-ANP >30-day mortality. We conclude that consideration of both N-ANP and N-BNP identifies a greater number of patients at risk of death or heart failure than either peptide alone.

scholarly journals Evaluation of Atrial Natriuretic Peptide and Brain Natriuretic Peptide in Atrial Granules of Rats with Experimental Congestive Heart Failure

2001 ◽  
Vol 49 (10) ◽  
pp. 1293-1300 ◽  
Author(s):  
Gad M. Bialik ◽  
Zaid A. Abassi ◽  
Ilan Hammel ◽  
Joseph Winaver ◽  
Dina Lewinson
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Aortocaval Fistula ◽  
Granule Formation ◽  
Gold Particles ◽  
The Mean ◽  
Atrial Natriuretic

The natriuretic peptides are believed to play an important role in the pathophysiology of congestive heart failure (CHF). We utilized a quantitative cytomorphometric method, using double immunocytochemical labeling, to assess the characteristics of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in atrial granules in an experimental model of rats with CHF induced by aortocaval fistula. Rats with CHF were further divided into decompensated (sodium-retaining) and compensated (sodium-excreting) subgroups and compared with a sham-operated control group. A total of 947 granules in myocytes in the right atrium were analyzed, using electron microscopy and a computerized analysis system. Decompensated CHF was associated with alterations in the modal nature of granule content packing, as depicted by moving bin analysis, and in the granule density of both peptides. In control rats, the mean density of gold particles attached to both peptides was 347.0 ± 103.6 and 306.3 ± 89.9 gold particles/μm2 for ANP and BNP, respectively. Similar mean density was revealed in the compensated rats (390.6 ± 81.0 and 351.3 ± 62.1 gold particles/μm2 for ANP and BNP, respectively). However, in rats with decompensated CHF, a significant decrease in the mean density of gold particles was observed (141.6 ± 67.3 and 158.0 ± 71.2 gold particles/μm2 for ANP and BNP, respectively; p < 0.05 compared with compensated rats, for both ANP and BNP). The ANP:BNP ratio did not differ between groups. These findings indicate that the development of decompensated CHF in rats with aortocaval fistula is associated with a marked decrease in the density of both peptides in atrial granules, as well as in alterations in the quantal nature of granule formation. The data further suggest that both peptides, ANP and BNP, may be regulated in the atrium by a common secretory mechanism in CHF.

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