Diagnostic and Prognostic Utility of Brain Natriuretic Peptide in Subjects Admitted to the ICU With Hypoxic Respiratory Failure Due to Noncardiogenic and Cardiogenic Pulmonary Edema

Karmpaliotis, Dimitri; Kirtane, Ajay J.; Ruisi, Christopher P.; Polonsky, Tamar S.; Malhotra, Atul; Talmor, Daniel; Kosmidou, Ioanna; Jarolím, Petr; Lemos, James A. de; Sabatine, Marc S.; Gibson, C. Michael; Morrow, David A.

doi:10.1378/chest.06-1247

Cited by 109 publications

(87 citation statements)

References 42 publications

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“…20 Other studies found that in patients with severe sepsis, the BNP level in nonsurvivors was significantly higher than in survivors; BNP could therefore be used to predict death regardless of the cause of hypoxaemic respiratory failure. 21,22 In the present study, the blood BNP level in patients with ALI/ARDS was significantly higher than in patients without ALI/ARDS. One possible mechanism for this is that under various stresses the release of inflammatory factors and anoxia can cause damage in myocardial cells.…”

Section: Discussionsupporting

confidence: 40%

Assessment of acute lung injury/acute respiratory distress syndrome using B-type brain natriuretic peptide

Sun

Gao

et al. 2015

J Int Med Res

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Objectives: To investigate the clinical value of B-type natriuretic peptide (BNP) in the assessment of severity and prognosis in acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Methods: Plasma BNP level, arterial blood gases, serum C-reactive protein level, alveolar-arterial oxygen tension difference and oxygenation index were measured in patients with and without ALI/ ARDS within 24 h of admission to an intensive care unit. Patients with ALI/ARDS were divided into mild, moderate or severe groups according to the degree of hypoxaemia. Survival >28 days was recorded.Results: A total of 59 patients with ALI/ARDS and 14 patients without ALI/ARDS were included in the study. Of the patients with ALI/ARDS, 18 had mild hypoxaemia, 20 had moderate hypoxaemia and 21 had severe hypoxaemia. The mean AE SD BNP level was significantly higher in all three ALI/ ARDS groups (92.41 AE 28.19 pg/ml, 170.64 AE 57.34 pg/ml and 239.06 AE 59.62 pg/ml, respectively, in the mild, moderate and severe groups) than in the non-ALI/ARDS group (47.27 AE 19.63 pg/ml); the increase in BNP level with increasing severity was also statistically significant. When divided according to outcome, the BNP level in the death group (267.07 AE 45.06 pg/ml) was significantly higher than in the survival group (128.99 AE 45.42 pg/ml). Conclusions: The BNP level may be of value in evaluating severity and prognosis in patients with ALI/ARDS.

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Section: Discussionsupporting

confidence: 40%

Assessment of acute lung injury/acute respiratory distress syndrome using B-type brain natriuretic peptide

Sun

Gao

et al. 2015

J Int Med Res

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“…Elevated plasma NP levels are associated with higher disease severity and mortality rates (18,25,43,50). However, the precise causal relationship between ANP elevation and the severity of ALI remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Atrial natriuretic peptide attenuates LPS-induced lung vascular leak: role of PAK1

Birukova

Xing

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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(ANP) in the models of sepsis, pulmonary edema, and acute respiratory distress syndrome (ARDS) suggest its potential role in the modulation of acute lung injury. We have recently described ANP-protective effects against thrombininduced barrier dysfunction in pulmonary endothelial cells (EC). The current study examined involvement of the Rac effector p21-activated kinase (PAK1) in ANP-protective effects in the model of lung vascular permeability induced by bacterial wall LPS. C57BL/6J mice or ANP knockout mice (Nppa Ϫ/Ϫ ) were treated with LPS (0.63 mg/kg intratracheal) with or without ANP (2 g/kg iv). Lung injury was monitored by measurements of bronchoalveolar lavage protein content, cell count, Evans blue extravasation, and lung histology. Endothelial barrier properties were assessed by morphological analysis and measurements of transendothelial electrical resistance. ANP treatment stimulated Rac-dependent PAK1 phosphorylation, attenuated endothelial permeability caused by LPS, TNF-␣, and IL-6, decreased LPS-induced cell and protein accumulation in bronchoalveolar lavage fluid, and suppressed Evans blue extravasation in the murine model of acute lung injury. More severe LPS-induced lung injury and vascular leak were observed in ANP knockout mice. In rescue experiments, ANP injection significantly reduced lung injury in Nppa Ϫ/Ϫ mice caused by LPS. Molecular inhibition of PAK1 suppressed the protective effects of ANP treatment against LPS-induced lung injury and endothelial barrier dysfunction. This study shows that the protective effects of ANP against LPS-induced vascular leak are mediated at least in part by PAK1-dependent signaling leading to EC barrier enhancement. Our data suggest a direct role for ANP in endothelial barrier regulation via modulation of small GTPase signaling. pulmonary endothelium; permeability; acute lung injury; cytoskeleton; small interfering RNA in vivo ACUTE LUNG INJURY (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), are associated with high morbidity and mortality in patients. During the progression of ALI, the endothelial cell (EC) barrier of the pulmonary vasculature becomes compromised, leading to pulmonary edema, a characteristic feature of ALI. It is well-established that EC barrier dysfunction is initiated by agonist-induced cytoskeletal remodeling, which leads to disruption of cell-cell contacts and formation of paracellular gaps, allowing penetration of protein-rich fluid and inflammatory cells (14, 33). However, far less is known about the processes that determine EC barrier enhancement or protection in the injured lung.Natriuretic peptides (NP) are a family of three peptide hormones: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). Although the major source of ANP is mammalian atrial myocytes, NP are found in other tissues, including aorta, lung, kidney, and brain (2). NP regulate a variety of physiological functions by interacting with receptors at the plasma membrane either to alter le...

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“…In acu te dyspne ic pa ti ents, BNP less than 100 pg/ml and Pro-N-Type BNP less than 300 pg/ml may be suf fi ci ent to exc lu de he art di sea se. 26 Karm pa li o tis et al re por ted that BNP in ALI/ARDS pa ti ents was 325 pg/ml, whe re as it was 1260 pg/ml in pa ti ents with car di o ge nic pul mo nary ede ma, sug ges ting that car di o ge nic pul mo nary edema and ARDS co uld be dif fe ren ti a ted by BNP va lu es. 26 In this ex pe ri ment, both BNP and Pro N-Type BNP le vels in cre a sed with ARDS in duc tion and BNP le vel dec re a sed with tre at ment.…”

Section: Referencesmentioning

confidence: 99%

“…26 Karm pa li o tis et al re por ted that BNP in ALI/ARDS pa ti ents was 325 pg/ml, whe re as it was 1260 pg/ml in pa ti ents with car di o ge nic pul mo nary ede ma, sug ges ting that car di o ge nic pul mo nary edema and ARDS co uld be dif fe ren ti a ted by BNP va lu es. 26 In this ex pe ri ment, both BNP and Pro N-Type BNP le vels in cre a sed with ARDS in duc tion and BNP le vel dec re a sed with tre at ment. The ir in cre a ses we re as so ci a ted with re duc ti on in Pa -O 2 /Fi O 2 ra ti o in ARDS, sug ges ting that BNP re le ase was trig ge red by hypo xi a and sympat he tic ac ti va ti on.…”

Section: Referencesmentioning

confidence: 99%

The Therapeutic Effects of Methylprednisolone and Surfactant in Acute Respiratory Distress Syndrome in a Rat Model

Doğan¹,

Aykan²,

Atalay³

et al. 2011

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : To com pa re the ef fi cacy of methy lpred ni so lo ne and sur fac tant in early sta ges of acu te lung in jury in rats and to de ter mi ne whether acu te res pi ra tory dis tress syndro me (ARDS) de ve lop ment and its res ponsi ve ness to me di cal tre at ment co uld be as ses sed by bra in nat ri u re tic pep ti de (BNP) and pro-N type BNP. M Ma a t te e r ri i a al l a an nd d M Me et t h ho od ds s: : Fo urty rats we re ran domly al lo ca ted in to one of fi ve gro ups, with 8 rep li ca tes. Rats in the ba se li ne gro up (gro up B) we re not sub jec ted to e it her trac he o tomy or ARDS in duc ti on, whe re as rats in sham gro up (gro up N) we re sub jec ted only to trac he o tomy. Af ter trac he o tomy and in duc ti on of ARDS by acid as pi ra ti on, re ma i ning rats (n= 24) we re tre a ted with eit her a sing le do se of methy lpred ni so lo ne (20 mg/kg, gro up M) or sur fac tant (100 mg/kg, gro up S) or left un tre a ted (gro up A). Six ho urs la ter, ar te ri al blo od samp les we re col lec ted for blo od ga ses, BNP, and Pro N-Type BNP me a su re ments. R Re e s su ul lt ts s: : Sham trac he o tomy did not af fect Pa O 2 /Fi O 2 ra ti o, BNP and pro-N type BNP le vels, or the acu te lung in jury (ALI) sco re. ARDS in duc ti on dec re a sed Pa O 2 /Fi O 2 ra ti o by 62% and in cre a sed BNP and pro-N type BNP le vels, as well as ALI sco re by 3.5, 2.3, and 2.4-folds, res pec ti vely. Pa -O 2 /Fi O 2 in gro up A was sig ni fi cantly lo wer than the con trols (p< 0.001). We no ted an in cre a se in Pa O 2 /Fi O 2 with methy lpred ni so lo ne and sur fac tant tre at ment (p< 0.001). Both methy lpred ni so lo ne and sur fac tant tre at ments incre a sed Pa O 2 /Fi O 2 ra ti o and dec re a sed BNP and pro-N type BNP le vels. The re was an in cre a se in BNP in the ARDS gro up (p< 0.001). Com pa red to the ARDS gro up, sig ni fi cant reductions we re ob ser ved in the methy lpred ni so lo ne and sur fac tant gro ups (p< 0.001, p< 0.05). BNP va lu e in gro up M was lo wer than the gro up S (p< 0.05). Pro N-Type BNP in cre a sed in rats of the ARDS gro up (p< 0.001). ALI sco re of the ARDS gro up in cre a sed sig ni fi cantly in compa ri son to the nor mal gro up (p< 0.001). Ho we ver, both tre at ment modalities fa i led to re du ce Pro N-Type BNP and ALI sco re. Blo od Pa O 2 /Fi O 2 ra ti o sho wed ne ga ti ve cor re la ti ons with BNP (r= -0.78, p< 0.001) and pro-N type BNP (r= -0.81, p< 0.001) le vels. C Co on nc c l lu u s si i o on n: : Pa O2/Fi O 2 ra ti o in cre a sed whe re as BNP le vel dec re a sed fol lo wing in tra peri to ne al methy lpred ni so lo ne and in trat rac he al sur fac tant ad mi nis tra ti on in ARDS-in du ced rats. Pa O 2 /Fi O 2 ra ti o and BNP may be con si de red as mar kers du ring tre at ment and fol low-up of pa ti ents with ARDS. K Ke ey y W Wo or rd ds s: : Res pi ra tory dis tress syndro me, adult; bra in nat ri u re tic pep ti de-45; methy lpred ni so lo ne; pul mo nary sur fac tant.Ö ÖZ ZE ET T A Am ma aç ç:...

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Diagnostic and Prognostic Utility of Brain Natriuretic Peptide in Subjects Admitted to the ICU With Hypoxic Respiratory Failure Due to Noncardiogenic and Cardiogenic Pulmonary Edema

Abstract: Background-Brain natriuretic peptide (BNP) is useful in diagnosing congestive heart failure (CHF) in patients presenting in the emergency department with acute dyspnea. We prospectively tested the utility of BNP for discriminating ARDS vs cardiogenic pulmonary edema (CPE).

Cited by 109 publications

References 42 publications

Assessment of acute lung injury/acute respiratory distress syndrome using B-type brain natriuretic peptide

Assessment of acute lung injury/acute respiratory distress syndrome using B-type brain natriuretic peptide

Atrial natriuretic peptide attenuates LPS-induced lung vascular leak: role of PAK1

The Therapeutic Effects of Methylprednisolone and Surfactant in Acute Respiratory Distress Syndrome in a Rat Model

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