Prophylactic bosentan does not improve exercise capacity or lower pulmonary artery systolic pressure at high altitude

2009 ◽  
Vol 165 (2-3) ◽  
pp. 123-130 ◽  
Author(s):  
Roger D. Seheult ◽  
Katja Ruh ◽  
Gary P. Foster ◽  
James D. Anholm
Keyword(s):  
Pulmonary Artery ◽  
High Altitude ◽  
Exercise Capacity ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Improve Exercise Capacity

scholarly journals Brain Natriuretic Peptide and NT-proBNP Levels Reflect Pulmonary Artery Systolic Pressure in Trekkers at High Altitude

2013 ◽  
pp. 597-603 ◽  
Author(s):  
D. R. WOODS ◽  
A. MELLOR ◽  
J. BEGLEY ◽  
M. STACEY ◽  
J. O’HARA ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Brain Natriuretic Peptide ◽  
High Altitude ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Central Feature ◽  
Post Exercise ◽  
Echocardiographic Assessment

Our objective was to evaluate the utility of the natriuretic peptides BNP (brain natriuretic peptide) and NT-proBNP as markers of pulmonary artery systolic pressure (PASP) in trekkers ascending to high altitude (HA). 20 participants had BNP and NT-proBNP assayed and simultaneous echocardiographic assessment of PASP performed during a trek to 5150 m. PASP increased significantly (p=0.006) with ascent from 24±4 to 39±11 mm Hg at 5150 m. At 5150 m those with a PASP≥40 mm Hg (n=8) (versus those with PASP<40 mm Hg) had higher post-exercise BNP (pg/ml): 54.5±36 vs. 13.4±17 (p=0.012). Their resting BNP at 5150 m was also higher: 57.3±43.4 vs. 12.6±13 (p=0.017). In those with a pathological (≥400 pg/ml) rise in NT-proBNP at 5150 m (n=4) PASP was significantly higher: 45.9±7.5 vs. 32.2±6.2 mm Hg (p=0.015). BNP and NT-proBNP may reflect elevated PASP, a central feature of high altitude pulmonary oedema, at HA.

Nitric oxide and cardiopulmonary hemodynamics in Tibetan highlanders

2005 ◽  
Vol 99 (5) ◽  
pp. 1796-1801 ◽  
Author(s):  
Brian D. Hoit ◽  
Nancy D. Dalton ◽  
Serpil C. Erzurum ◽  
Daniel Laskowski ◽  
Kingman P. Strohl ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
High Altitude ◽  
Sea Level ◽  
Pulmonary Blood Flow ◽  
Geometric Mean ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Exhaled No

When O2 availability is reduced unavoidably, as it is at high altitude, a potential mechanism to improve O2 delivery to tissues is an increase in blood flow. Nitric oxide (NO) regulates blood vessel diameter and can influence blood flow. This field study of intrapopulation variation at high altitude tested the hypothesis that the level of exhaled NO (a summary measure of pulmonary synthesis, consumption, and transfer from cells in the airway) is directly proportional to pulmonary, and thus systemic, blood flow. Twenty Tibetan male and 37 female healthy, nonsmoking, native residents at 4,200 m (13,900 ft), with an average O2 saturation of hemoglobin of 85%, participated in the study. The geometric mean partial pressure of NO exhaled at a flow of 17 ml/s was 23.4 nmHg, significantly lower than that of a sea-level reference group. However, the rate of NO transfer out of the airway wall was seven times higher than at sea level, which implied the potential for vasodilation of the pulmonary blood vessels. Mean pulmonary blood flow (measured by cardiac index) was 2.7 ± 0.1 (SE) l/min, and mean pulmonary artery systolic pressure was 31.4 ± 0.9 (SE) mmHg. Higher exhaled NO was associated with higher pulmonary blood flow; yet there was no associated increase in pulmonary artery systolic pressure. The results suggest that NO in the lung may play a key beneficial role in allowing Tibetans at 4,200 m to compensate for ambient hypoxia with higher pulmonary blood flow and O2 delivery without the consequences of higher pulmonary arterial pressure.

Effect of acute lower respiratory tract infection on pulmonary artery pressure in children with post-tricuspid left-to-right shunt

2021 ◽  
pp. 1-5
Author(s):  
Sakshi Sachdeva ◽  
Shyam S. Kothari ◽  
Saurabh K. Gupta ◽  
Sivasubramanian Ramakrishnan ◽  
Anita Saxena
Keyword(s):  
Tract Infection ◽  
Pulmonary Artery ◽  
Respiratory Tract ◽  
Respiratory Tract Infection ◽  
Lower Respiratory Tract Infection ◽  
Pulmonary Artery Pressure ◽  
Lower Respiratory Tract ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Artery Pressure

Abstract We sought to examine the influence of clinically severe lower respiratory tract infection on pulmonary artery pressure in children having CHD with post-tricuspid left-to-right shunt, as it may have physiological and clinical implications. In a prospective single-centre observational study, 45 children with post-tricuspid left-to-right shunt and clinically severe lower respiratory tract infection were evaluated during the illness and 2 weeks after its resolution. Pulmonary artery systolic pressure was estimated non-invasively using shunt gradient by echocardiography and systolic blood pressure measured non-invasively. Median pulmonary artery systolic pressure during lower respiratory tract infection was only mildly (although statistically significantly) elevated during lower respiratory tract infection [60 (42–74) versus 53 (40–73) mmHg, (p < 0.0001)]. However, clinically significant change in pulmonary artery systolic pressure defined as the increase of >10 mmHg was present in only 9 (20%) patients. In the absence of hypoxia or acidosis, only a small minority (9%, n = 4) showed significant pulmonary artery systolic pressure rise >10 mmHg. In the absence of hypoxia or acidosis, severe lower respiratory tract infection in patients with acyanotic CHD results in only mild elevation of pulmonary artery systolic pressure in most of the patients.

scholarly journals Serum-Free Thyroxine Levels Were Associated with Pulmonary Hypertension and Pulmonary Artery Systolic Pressure in Euthyroid Patients with Coronary Artery Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-8
Author(s):  
Bingjie Wu ◽  
Jingjing Jiang ◽  
Minghui Gui ◽  
Lin Liu ◽  
Qiqige Aleteng ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Pulmonary Hypertension ◽  
Regression Analysis ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Free Thyroxine ◽  
Pulmonary Artery Systolic Pressure ◽  
Serum Free ◽  
Artery Disease

The aim of this study was to evaluate the association between thyroid hormone levels, pulmonary hypertension (PH), and pulmonary artery systolic pressure (PASP) in euthyroid patients with coronary artery disease (CAD). A cross-sectional study was conducted in individuals who underwent coronary angiography and were diagnosed as CAD from March 2013 to November 2013. 811 subjects (185 women and 626 men) were included in this study. PASP was measured by transthoracic Doppler echocardiography. 86 patients were diagnosed as PH and had significantly higher free thyroxine (FT4) levels than those without PH. Multiple logistic regression analysis demonstrated an independent association of FT4 levels with PH after adjustment of gender, age, body mass index, systolic blood pressure, left ventricular ejection fraction, hypertension, and medication use of calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and nitrates. Serum-free triiodothyronine (FT3) and thyroid-stimulating hormone (TSH) were not associated with PH. Furthermore, multivariate linear regression analysis showed that FT4 levels emerged as an independent predictor for PASP, while FT3 and TSH levels were not associated with PASP. Our study demonstrated that, in euthyroid patients with CAD, FT4 was an independent risk factor for PH, and FT4 levels were independently associated with PASP.

Abstract 15388: Persistent Pulmonary Hypertension After Transcatheter Aortic Valve Implantation: Impact on Mortality

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Maria Drakopoulou ◽  
Konstantinos Stathogiannis ◽  
Konstantinos Toutouzas ◽  
George Latsios ◽  
Andreas Synetos ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Aortic Stenosis ◽  
Pulmonary Artery ◽  
Severe Aortic Stenosis ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Pulmonary Artery Systolic Pressure ◽  
End Point ◽  
The Right ◽  
The Impact

Objective: Severe aortic stenosis leads to increased pulmonary arterial systolic pressure. A controversy still remains regarding the impact of persistent pulmonary hypertension (PHT) on prognosis of patients undergoing transcatheter aortic valve implantation (TAVI). We sought to investigate the impact of persistent PHT on 2-year all-cause mortality of patients with severe aortic stenosis following TAVI. Methods: Patients with severe and symptomatic aortic stenosis (effective orifice area [EOA]≤1 cm 2 ) who were scheduled for TAVI with a self-expanding valve at our institution were prospectively enrolled. Prospectively collected echocardiographic data before and after TAVI were retrospectively analyzed in all patients. Pulmonary artery systolic pressure was estimated as the sum of the right ventricular to the right atrial gradient during systole and the right atrial pressure. PHT following TAVI was classified as absent if <35 mmHg and persistent if ≥35 mmHg. Primary clinical end-point was 2-year all-cause mortality defined according to the criteria proposed by the Valve Academic Research Consortium-2. Results: Hundred and forty patients (mean age: 82±9 years) were included in the study. The primary clinical end point occurred in 17 patients (12%) during a median follow-up period of 2 years. Mean pulmonary artery systolic pressure was reduced in all patients following TAVI (45±9 versus 41±6 mmHg, p<0.01). Mortality rate was higher in patients with persistent PHT compared to patients with normal pulmonary artery systolic pressure following TAVI (26% versus 14 %, p<0.01). Patients that reached the primary clinical end point had a higher post procedural mean systolic pulmonary pressure (43±9 versus 39±6 mmHg, p=0.02). In multivariate regression analysis, persistence of PHT (OR: 2.51, 95% CI: 1.109-7.224, p=0.01) was an independent predictor of long-term mortality. Conclusions: The persistence of pulmonary hypertension after TAVI is associated with long term mortality. Identifying the population that will clearly benefit from TAVI is still need to be validated by larger trials.

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