1993
DOI: 10.1016/0140-6736(93)93125-k
|View full text |Cite
|
Sign up to set email alerts
|

Circulating N-terminal atrial natriuretic peptide as a marker for symptomless left-ventricular dysfunction

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

11
129
0
10

Year Published

1997
1997
2020
2020

Publication Types

Select...
8
2

Relationship

0
10

Authors

Journals

citations
Cited by 297 publications
(150 citation statements)
references
References 23 publications
11
129
0
10
Order By: Relevance
“…ANP , by contrast, has found to be a much more stable peptide with a longer halflife and higher plasma concentrations [11,12]. Therefore, ANP (1-98) measurements may be more suitable for assessment of cardiac patients [13][14][15][16].…”
Section: Introductionmentioning
confidence: 99%
“…ANP , by contrast, has found to be a much more stable peptide with a longer halflife and higher plasma concentrations [11,12]. Therefore, ANP (1-98) measurements may be more suitable for assessment of cardiac patients [13][14][15][16].…”
Section: Introductionmentioning
confidence: 99%
“…In patients with the suspicion of heart failure several other studies showed natriuretic peptides to be useful indicators for the detection of heart failure (Lerman et al, 1993;Davidson et al, 1996;Cowie et al, 1997;Hammerer-Lercher et al, 2001;Maisel et al, 2002Maisel et al, , 2003. In the follow-up of patients with an acute cardiac event levels of natriuretic peptides were proved to be of prognostic value for outcome (Hall et al, 1994;Omland et al, 1996;de Lemos et al, 2001;Koglin et al, 2001;Richards et al, 2003).…”
mentioning
confidence: 99%
“…ANP is secreted into the blood by myocardial cells in response to atrial stretch [29], whereas the primary regulators of BNP release are left ventricular stretch or wall tension [30]. Because ANP is mainly secreted by the atria in response to the stretch that occurs as a result of the increased left atrial pressure associated with heart failure [31,32], the increased levels of ANP and BNP seen in this study after CPB might suggest a deterioration of haemodynamic status after CABG. Removal of ANP and BNP from the circulation, and therefore the regulation of their plasma concentrations, is achieved mainly via ligand-receptor internalisation and enzymatic degradation by neural endopeptidase [30], which is found in particularly high concentrations in the lung and kidney.…”
Section: Discussionmentioning
confidence: 86%