Elevated Pulmonary Artery Pressure and Brain Natriuretic Peptide in High Altitude Pulmonary Edema Susceptible Non-mountaineers

Overview

Journal Sci Rep

Specialty Science

Date 2016 Feb 20

PMID 26892302

Citations 6

Authors

Rajinder K Gupta

G Himashree

Krishan Singh

Poonam Soree

Koundinya Desiraju

Anurag Agrawal

Dishari Ghosh

Deepak Dass

Prassana K Reddy

Usha Panjwani

Shashi Bala Singh

Affiliations

Soon will be listed here.

Abstract

Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo2 = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility.

Citing Articles

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Patchy Vasoconstriction Versus Inflammation: A Debate in the Pathogenesis of High Altitude Pulmonary Edema.

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Subclinical elevated B-type Natriuretic Peptide (BNP) indicates endothelial dysfunction contributing to hypoxia susceptibility in healthy individuals.

Khatri R, Gupta R, Vats P, Bansal V, Yadav A, Reddy P Life Sci. 2020; 260:118408.

PMID: 32926931 PMC: 7486215. DOI: 10.1016/j.lfs.2020.118408.

Subclinical pulmonary dysfunction contributes to high altitude pulmonary edema susceptibility in healthy non-mountaineers.

Gupta R, Soree P, Desiraju K, Agrawal A, Singh S Sci Rep. 2017; 7(1):14892.

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Non-cardiogenic acute pulmonary edema in elderly patient with Dressler syndrome associated pulmonary embolism.

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