Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers.
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ABSTRACT:
SUBMITTER: Gupta RK
PROVIDER: S-EPMC4759542 | biostudies-other | 2016 Feb
REPOSITORIES: biostudies-other
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Project description:High altitude pulmonary edema (HAPE) susceptibility is associated with EGLN1 polymorphisms, we hypothesized that HAPE-susceptible (HAPE-S, had HAPE episode in past) subjects may exhibit abnormal HIF1α levels in normoxic conditions. We measured HIF1α levels in HAPE-S and HAPE resistant (HAPE-R, no HAPE episode) individuals with similar pulmonary functions. Hemodynamic responses were also measured before and after normobaric hypoxia (Fi02 = 0.12 for 30 min duration at sea level) in both groups. . HIF1α was higher in HAPE-S (320.3 ± 267.5 vs 58.75 ± 33.88 pg/ml, P < 0.05) than HAPE-R, at baseline, despite no significant difference in baseline oxygen saturations (97.7 ± 1.7% and 98.8 ± 0.7). As expected, HAPE-S showed an exaggerated increase in pulmonary artery pressure (27.9 ± 6 vs 19.3 ± 3.7 mm Hg, P < 0.05) and a fall in peripheral oxygen saturation (66.9 ± 11.7 vs 78.7 ± 3.8%, P < 0.05), when exposed to hypoxia. HIF1α levels at baseline could accurately classify members of the two groups (AUC = 0.87). In a subset of the groups where hemoglobin fractions were additionally measured to understand the cause of elevated hypoxic response at baseline, two of four HAPE-S subjects showed reduced HbA. In conclusion, HIF 1 α levels during normoxia may represent an important marker for determination of HAPE susceptibility.
| S-EPMC4876441 | biostudies-other
Project description:BackgroundNatriuretic peptides have been proposed as biomarkers of cardiovascular disease, especially heart failure. Brain natriuretic peptide (BNP) has also been shown to be upregulated at the transcriptional and translational levels by pro-inflammatory cytokines in cardiac myocytes. Although we often measure plasma BNP levels in cancer patients, it remains unknown whether cancer-related inflammation affects the plasma BNP levels. We investigated the relationship between the BNP and human cancers.MethodsWe retrospectively studied 2,923 patients in whom the plasma BNP levels and serum C-reactive protein (CRP) were measured and echocardiography was performed. Patients with clinically evident heart failure (NYHA II or higher), heart disease requiring medical treatment or surgery, renal dysfunction, and inflammatory disease were excluded. There were 234 patients in the final analysis. Blood sampling was performed before surgery and chemotherapy. In addition, we evaluated the relationship between the inflammation and plasma BNP levels in mouse models of colon cancer.ResultsOf the 234 patients, 80 were diagnosed with cancer. Both the plasma BNP and serum CRP levels were significantly higher in cancer patients than those without. There were no significant differences in the echocardiographic parameters. There was a significant positive correlation between the plasma BNP and serum CRP levels in cancer patients (r = 0.360, P<0.01) but not in those without. In cancer patients, only the CRP correlated with the BNP independent of the age, creatinine level, hypertension, and body mass index. In addition, in nude mice with subcutaneous colon cancer, the plasma BNP level was elevated compared with that in non-cancer mice, and there was a significant relationship between the plasma BNP and serum levels of the inflammatory markers.ConclusionsIn cancer patients, as well as colon cancer model mice, the plasma BNP levels were elevated, possibly due to cancer-related inflammation. The effect of cancer on the BNP levels should be considered when using BNP as an indicator of heart failure in cancer patients.
| S-EPMC5453551 | biostudies-literature
Project description:High Altitude Pulmonary Edema (HAPE) is a type of idiopathic non-cardiogenic pulmonary oedema at high altitude with a severe clinical course and high mortality rate. Therefore, this study aims to investigate transcriptomic signatures in HAPE based on whole-transcriptome sequencing. We identified the differential expression of mRNAs, miRNAs, circRNAs, lncRNAs, alternative splicing (AS) events, gene fusions and novel transcripts, constructed ceRNA networks and immune cell infiltration landscapes, and annotated the biological functions of target genes based on bioinformatics analysis. This study will clarify the differential expression of coding and non-coding RNAs (ncRNAs) in HAPE, identify novel transcripts and genes, increase our understanding of the transcriptional characteristics of HAPE, elucidate disease-associated pathways and biological processes, and provide underlying mechanisms for HAPE diagnosis and treatment.
2024-10-10 | GSE260910 | GEO
Project description:AimElevated pulmonary artery pressure (ePAP) in response to high-altitude hypoxia is a critical physiopathological factor in the hypoxic adaptation that may lead to high-altitude pulmonary edema in the acute phase or high-altitude pulmonary hypertension in the long term. However, the sea-level predictors of risk factors for altitude-induced ePAP have not been examined. Thus, we aimed to identify the baseline systemic blood predictors of ePAP after acute high-altitude exposure.Materials and methodsA total of 154 participants were transported to a high altitude 3,700 m from sea level within 2 h. Echocardiography examinations were performed to assess the mean pulmonary artery pressure (mPAP) and hemodynamics at both altitudes. All the individuals underwent blood tests to determine the concentrations of vascular regulatory factors. Univariate and adjusted logistic regression analyses were performed to identify the independent predictors of ePAP and factors related to ePAP.ResultsThe mPAP increased significantly from sea level to high altitude (19.79 ± 6.53-27.16 ± 7.16 mmHg, p < 0.05). Increased levels of endothelin (ET-1), Ang (1-7), Ang II, and bradykinin were found after high-altitude exposure, while the levels of nitric oxide (NO), prostaglandin E2 (PEG2), and serotonin decreased sharply (all p-values < 0.05). At high altitude, 52.6% of the subjects exhibited ePAP, and the mPAP was closely correlated with the baseline Ang II level (r = 0.170, p = 0.036) and follow-up levels of NO (r = -0.209, p = 0.009), Ang II (r = 0.246, p = 0.002), and Ang (1-7) (r = -0.222, p = 0.006) and the left atrial inner diameter (LAD, r = 0.270, p < 0.001). Both the baseline and follow-up NO and Ang II levels were significantly different between the ePAP and non-ePAP groups. Finally, we identified the baseline Ang II and NO concentrations as two independent predictors of ePAP (p < 0.05). We also found that two vascular regulatory factors with inverse roles, namely, Ang (1-7) and Ang II, at high altitudes were independently associated with ePAP. Additionally, ET-1, NO, PEG2, and LAD were associated with ePAP.ConclusionThe baseline concentrations of Ang II and NO at sea level are two independent predictors of ePAP after acute high-altitude exposure. Furthermore, Ang (1-7) and Ang II combined with ET-1, NO, PEG2, and LAD at high altitudes may contribute to the development of ePAP.
| S-EPMC9226344 | biostudies-literature
Project description:High-altitude pulmonary edema (HAPE) is a potentially fatal condition, occurring at altitudes greater than 3,000 m and affecting rapidly ascending, non-acclimatized healthy individuals. However, the lack of biomarkers for this disease still constitutes a bottleneck in the clinical diagnosis. Here, ultra-high performance liquid chromatography coupled with Q-TOF mass spectrometry was applied to study plasma metabolite profiling from 57 HAPE and 57 control subjects. 14 differential plasma metabolites responsible for the discrimination between the two groups from discovery set (35 HAPE subjects and 35 healthy controls) were identified. Furthermore, 3 of the 14 metabolites (C8-ceramide, sphingosine and glutamine) were selected as candidate diagnostic biomarkers for HAPE using metabolic pathway impact analysis. The feasibility of using the combination of these three biomarkers for HAPE was evaluated, where the area under the receiver operating characteristic curve (AUC) was 0.981 and 0.942 in the discovery set and the validation set (22 HAPE subjects and 22 healthy controls), respectively. Taken together, these results suggested that this composite plasma metabolite signature may be used in HAPE diagnosis, especially after further investigation and verification with larger samples.
| S-EPMC4602305 | biostudies-literature
Project description:IntroductionPulse-pressure variation (PPV) due to increased right ventricular afterload and dysfunction may misleadingly suggest volume responsiveness. We aimed to assess prediction of volume responsiveness with PPV in patients with increased pulmonary artery pressure.MethodsFifteen cardiac surgery patients with a history of increased pulmonary artery pressure (mean pressure, 27 +/- 5 mm Hg (mean +/- SD) before fluid challenges) and seven septic shock patients (mean pulmonary artery pressure, 33 +/- 10 mm Hg) were challenged with 200 ml hydroxyethyl starch boli ordered on clinical indication. PPV, right ventricular ejection fraction (EF) and end-diastolic volume (EDV), stroke volume (SV), and intravascular pressures were measured before and after volume challenges.ResultsOf 69 fluid challenges, 19 (28%) increased SV > 10%. PPV did not predict volume responsiveness (area under the receiver operating characteristic curve, 0.555; P = 0.485). PPV was >or=13% before 46 (67%) fluid challenges, and SV increased in 13 (28%). Right ventricular EF decreased in none of the fluid challenges, resulting in increased SV, and in 44% of those in which SV did not increase (P = 0.0003). EDV increased in 28% of fluid challenges, resulting in increased SV, and in 44% of those in which SV did not increase (P = 0.272).ConclusionsBoth early after cardiac surgery and in septic shock, patients with increased pulmonary artery pressure respond poorly to fluid administration. Under these conditions, PPV cannot be used to predict fluid responsiveness. The frequent reduction in right ventricular EF when SV did not increase suggests that right ventricular dysfunction contributed to the poor response to fluids.
| S-EPMC2911757 | biostudies-literature
Project description:AimTo investigate the prognostic value of early post-transplant hemodynamic measurements on 5-year mortality in cardiac recipients (HTx).MethodsA right heart catheterization was performed in 290 heart transplantation (HTx) recipients at a one-year post-HTx evaluation. To study the effect of post-HTx hemodynamic variables on 5-year outcome, the cohort was stratified into several subgroups. For right atrial pressure (RAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and pulmonary vascular resistance (PVR), patients with values from the upper 10th percentile (high), were compared with those with values from the remaining lower 90th percentile (normal). For cardiac index (CI), patients with values from the lower 10th percentile (low) were compared with those with values from the remaining upper 90th percentile (normal).ResultsDeath or re-transplantation within 5 years after the one-year control occurred in 44 patients (13%). Of those, death or re-HTx was related to graft failure in 20 of cases (45%) and non-cardiac causes in 24 of cases (55%). The risk of death or re-HTx was higher in the subgroup with MPAP above 23 mmHg than those equal to or below this value [hazard ratio 3.22, 95% confidence interval (CI) 1.49-6.97; P = 0.003]. The association remained significant despite adjustment for several comorbidities. There were no differences in outcome between subgroups stratified with respect to high versus low RAP, PAWP, CI or PVR.ConclusionElevated pulmonary artery pressure at a first annual evaluation after HTx was the only hemodynamic variable that predicted impaired outcome in cardiac recipients.
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Project description:Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) exert their physiological actions by binding to natriuretic peptide receptor A (NPRA), a receptor guanylate cyclase (rGC) that synthesizes cGMP in response to both ligands. The family of rGCs is rapidly expanding, and it is plausible that there might be additional, as yet undiscovered, rGCs whose function is to provide alternative signalling pathways for one or both of these peptides, particularly given the low affinity of NPRA for BNP. We have investigated this hypothesis, using a genetically modified (knockout) mouse in which the gene encoding NPRA has been disrupted. Enzyme assays and NPRA-specific Western blots performed on tissues from wild-type mice demonstrate that ANP-activated cGMP synthesis provides a good index of NPRA protein expression, which ranges from maximal in adrenal gland, lung, kidney, and testis to minimal in heart and colon. In contrast, immunoreactive NPRA is not detectable in tissues isolated from NPRA knockout animals and ANP- and BNP-stimulatable GC activities are markedly reduced in all mutant tissues. However, testis and adrenal gland retain statistically significant, high-affinity responses to BNP. This residual response to BNP cannot be accounted for by natriuretic peptide receptor B, or any other known mammalian rGC, suggesting the presence of a novel receptor in these tissues that prefers BNP over ANP.
| S-EPMC1222070 | biostudies-other
Project description:Patients with heart failure (HF) are reportedly at high risk for 'all-cause' re-hospitalization. A biomarker for HF, N-terminal pro-brain natriuretic peptide (NT-proBNP), enables to simply detect patients with possible HF (pHF). We examined the hospitalization and medical cost of Japanese patients detected by an elevated serum NT-proBNP, and also evaluated the effects of institutional team approaches for HF on their all-cause hospitalizations.We retrospectively extracted all adult patients with serum NT-proBNP ≥400 pg/ml measured between January and March 2012 in Hiroshima University Hospital as pHF-positive patients. We studied their all-cause hospitalization records during the past 3-year period. We also extracted all pHF-negative patients with NT-proBNP <400 pg/ml and studied as well. In the pHF-positive patients followed for 3 years after starting interprofessional team approaches to prevent the onset and exacerbation of HF in the hospital, we compared the hospitalization and medical cost between the 3-year periods before and after the start of the team approaches.We enrolled 432 pHF-positive and 485 pHF-negative patients with one or more hospitalization records. Compared to the pHF-negative patients, the pHF-positive patients had longer total hospitalization days (median [interquartile range], 30 [13-58] versus. 18 [8-39], p <0.0001) and higher total medical cost for hospitalizations (2.42 [1.07-5.08] versus. 1.80 [0.79-3.65] million yen, p <0.0001). A subset of 303 pHF-positive patients was followed for 3 years after starting the team approaches, and we found that both total hospitalization days (30 [13-57] to 8 [0-31]) and medical cost for hospitalizations (2.59 [1.37-5.05] to 0.76 [0-2.38] million yen) showed marked reduction in them.Patients with an elevated serum NT-proBNP have longer hospitalizations and higher costs for all-cause hospitalizations than those without. Institutional team approaches for HF may reduce them.
| S-EPMC5755927 | biostudies-literature
Project description:ObjectivesThis study aims to examine the utility of von Willebrand factor (vWF) as a biomarker in lcSSc, in particular the ability of vWF to predict the future development of disease manifestations in this disease.MethodsvWFAg concentrations were measured in the serum of patients with lcSSc at baseline and at 3 years, during the QUINs trial [Prevention of Vascular Damage in Scleroderma with Angiotensin-Converting Enzyme (ACE) Inhibition]. %DL(CO), %KCO, %FVC, pulmonary artery pressure (PAP) estimation by echocardiography, Raynaud's attack frequency, Raynaud's severity, digital ulcer frequency, urinary protein excretion, estimated glomerular filtration rate (eGFR), modified Rodnan skin score and Medsger disease activity score were also measured at baseline and 3 years.ResultsBaseline serum vWF concentrations were related to concurrent Medsger disease activity score, %DL(CO), %FVC, urinary protein excretion, eGFR and PAP >30?mmHg. In logistic regression models, baseline serum vWF concentrations were able to predict the future development of elevated PAP by echocardiography (PAP >40?mmHg, P?=?0.001).ConclusionsPulmonary artery hypertension is a life-threatening complication of lcSSc. vWF is a marker of endothelial cell activation. Raised serum concentrations of vWF in lcSSc increase the risk of developing subsequent elevation in PAP. Therefore screening patients with lcSSc for vWF may identify a group at risk of developing PAH. These patients could potentially be targeted with agents that stabilize the endothelium, e.g. statins.
| S-EPMC3418644 | biostudies-literature