scholarly journals Pulmonary arterial pressure at rest and during exercise in chronic mountain sickness: a meta-analysis

2019 ◽  
Vol 53 (6) ◽  
pp. 1802040 ◽  
Author(s):  
Rodrigo Soria ◽  
Matthias Egger ◽  
Urs Scherrer ◽  
Nicole Bender ◽  
Stefano F. Rimoldi
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Pulmonary Arterial Pressure ◽  
Meta Analysis ◽  
Right Heart Failure ◽  
Exercise Intolerance ◽  
Point Estimate ◽  
Chronic Mountain Sickness ◽  
Pulmonary Arterial ◽  
Mountain Sickness

Up to 10% of the more than 140 million high-altitude dwellers worldwide suffer from chronic mountain sickness (CMS). Patients suffering from this debilitating problem often display increased pulmonary arterial pressure (PAP), which may contribute to exercise intolerance and right heart failure. However, there is little information on the usual PAP in these patients.We systematically reviewed and meta-analysed all data published in English or Spanish until June 2018 on echocardiographic estimations of PAP at rest and during mild exercise in CMS patients.Nine studies comprising 287 participants fulfilled the inclusion criteria. At rest, the point estimate from meta-analysis of the mean systolic PAP was 27.9 mmHg (95% CI 26.3–29.6 mmHg). These values are 11% (+2.7 mmHg) higher than those previously meta-analysed in apparently healthy high-altitude dwellers. During mild exercise (50 W) the difference in mean systolic PAP between patients and high-altitude dwellers was markedly more accentuated (48.3 versus 36.3 mmHg) than at rest.These findings indicate that in patients with CMS PAP is moderately increased at rest, but markedly increased during mild exercise, which will be common with activities of daily living.

scholarly journals Functional impact of exercise pulmonary hypertension in patients with borderline resting pulmonary arterial pressure

2017 ◽  
Vol 7 (3) ◽  
pp. 654-665 ◽  
Author(s):  
Rudolf K. F. Oliveira ◽  
Mariana Faria-Urbina ◽  
Bradley A. Maron ◽  
Mario Santos ◽  
Aaron B. Waxman ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Oxygen Uptake ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Exercise Capacity ◽  
Pulmonary Arterial Pressure ◽  
Peak Oxygen Uptake ◽  
Exercise Intolerance ◽  
Functional Impact ◽  
Pulmonary Arterial

Borderline resting mean pulmonary arterial pressure (mPAP) is associated with adverse outcomes and affects the exercise pulmonary vascular response. However, the pathophysiological mechanisms underlying exertional intolerance in borderline mPAP remain incompletely characterized. In the current study, we sought to evaluate the prevalence and functional impact of exercise pulmonary hypertension (ePH) across a spectrum of resting mPAP’s in consecutive patients with contemporary resting right heart catheterization (RHC) and invasive cardiopulmonary exercise testing. Patients with resting mPAP <25 mmHg and pulmonary arterial wedge pressure ≤15 mmHg (n = 312) were stratified by mPAP < 13, 13–16, 17–20, and 21–24 mmHg. Those with ePH (n = 35) were compared with resting precapillary pulmonary hypertension (rPH; n = 16) and to those with normal hemodynamics (non-PH; n = 224). ePH prevalence was 6%, 8%, and 27% for resting mPAP 13–16, 17–20, and 21–24 mmHg, respectively. Within each of these resting mPAP epochs, ePH negatively impacted exercise capacity compared with non-PH (peak oxygen uptake 70 ± 16% versus 92 ± 19% predicted, P < 0.01; 72 ± 13% versus 86 ± 17% predicted, P < 0.05; and 64 ± 15% versus 82 ± 19% predicted, P < 0.001, respectively). Overall, ePH and rPH had similar functional limitation (peak oxygen uptake 67 ± 15% versus 68 ± 17% predicted, P > 0.05) and similar underlying mechanisms of exercise intolerance compared with non-PH (peak oxygen delivery 1868 ± 599 mL/min versus 1756 ± 720 mL/min versus 2482 ± 875 mL/min, respectively; P < 0.05), associated with chronotropic incompetence, increased right ventricular afterload and signs of right ventricular/pulmonary vascular uncoupling. In conclusion, ePH is most frequently found in borderline mPAP, reducing exercise capacity in a manner similar to rPH. When borderline mPAP is identified at RHC, evaluation of the pulmonary circulation under the stress of exercise is warranted.

scholarly journals Evaluation of the sensitivity of pulmonary arterial pressure to elevation using a reaction norm model in Angus Cattle

2020 ◽  
Vol 98 (5) ◽  
Author(s):  
Scott E Speidel ◽  
Milton G Thomas ◽  
Timothy N Holt ◽  
R Mark Enns
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Genetic Relationship ◽  
Pulmonary Arterial Pressure ◽  
Genetic Correlations ◽  
Reaction Norm ◽  
High Elevation ◽  
Random Regression ◽  
Angus Cattle ◽  
Pulmonary Arterial

Abstract Pulmonary arterial pressure (PAP) is a diagnostic measure used to determine an individual’s susceptibility to developing high-altitude disease. The importance of PAP measures collected at elevations lower than the intended breeding elevation of the bulls (i.e., ≥1,520 m) is unknown. Therefore, the objective of this study was to determine the genetic relationship between PAP measures collected in a range of elevations using reaction norm models. A total of 9,177 PAP and elevation observations on purebred Angus cattle, which averaged 43.49 ± 11.32 mmHg and 1,878.6 ± 296.8 m, respectively, were used in the evaluation. The average age of the individuals in the evaluation was 434.04 ± 115.9 d. A random regression model containing the effects of sex, a linear covariate of age, a quadratic fixed covariate of elevation, and random effects consisting of a contemporary group and a linear regression of PAP on elevation was used for the evaluation of PAP. Two forms of PAP were evaluated with this model. First, to address the non-normality of the data, PAP was raised to the power of −2.6 (ptPAP) based on the results of a Box–Cox analysis. Second, raw PAP (rPAP) phenotypes were evaluated to compare the results to those obtained from the transformed data. For ptPAP, heritability ranged from 0.25 to 0.37 corresponding to elevations of 1,900 and 1,215 m, respectively. For rPAP, heritability ranged from 0.22 to 0.41 corresponding to elevations of 1,700 and 2,495 m, respectively. Generally, lower elevations corresponded to decreased heritabilities while higher elevations corresponded to increased heritability estimates. For ptPAP, genetic correlations ranged from 0.18 (elevation: 1,215 and 2,495 m) to 1.00. For rPAP, genetic correlations ranged from 0.08 (elevation: 1,215 and 2,495 m) to 1.00. In general, the closer the elevations in which PAP was measured, the greater the genetic relationship. The greater the difference in elevation between PAP measures resulted in lower genetic correlations. The rank correlation between expected progeny differences (EPD) for 1,215 and 2,495 m was 0.65 and 0.49 for the ptPAP and rPAP, respectively. These results suggested that PAP measures collected in lower elevations may be used as an indicator of high-altitude adaptability. In the estimation of EPD to rank sires for their suitability for use in high-elevation production systems, it is important to account for the relationships among varied altitudes.

scholarly journals Assessment of right atrial dyssynchrony by 2D speckle-tracking in healthy young men following high altitude exposure at 4100 m

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247107
Author(s):  
Chunyan He ◽  
Hedong Xiang ◽  
Chuan Liu ◽  
Shiyong Yu ◽  
Jie Yang ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Speckle Tracking ◽  
Pulmonary Arterial Pressure ◽  
Young Men ◽  
Right Atrial ◽  
Peak Strain ◽  
Altitude Exposure ◽  
2D Speckle Tracking ◽  
Pulmonary Arterial

Background High altitude exposure induces overload of right-sided heart and may further predispose to supraventricular arrhythmia. It has been reported that atrial mechanical dyssynchrony is associated with atrial arrhythmia. Whether high altitude exposure causes higher right atrial (RA) dyssynchrony is still unknown. The aim of study was to investigate the effect of high altitude exposure on right atrial mechanical synchrony. Methods In this study, 98 healthy young men underwent clinical examination and echocardiography at sea level (400 m) and high altitude (4100 m) after an ascent within 7 days. RA dyssynchrony was defined as inhomogeneous timing to peak strain and strain rate using 2D speckle-tracking echocardiography. Results Following high altitude exposure, standard deviation of the time to peak strain (SD-TPS) [36.2 (24.5, 48.6) ms vs. 21.7 (12.9, 32.1) ms, p<0.001] and SD-TPS as percentage of R–R’ interval (4.6 ± 2.1% vs. 2.5 ± 1.8%, p<0.001) significantly increased. Additionally, subjects with higher SD-TPS (%) at high altitude presented decreased right ventricular global longitudinal strain and RA active emptying fraction, but increased RA minimal volume index, which were not observed in lower group. Multivariable analysis showed that mean pulmonary arterial pressure and tricuspid E/A were independently associated with SD-TPS (%) at high altitude. Conclusion Our data for the first time demonstrated that high altitude exposure causes RA dyssynchrony in healthy young men, which may be secondary to increased pulmonary arterial pressure. In addition, subjects with higher RA dyssynchrony presented worse RA contractile function and right ventricular performance.

scholarly journals Relationship of pulmonary arterial pressure and terrain use of Angus cows grazing high-altitude foothill rangelands

2016 ◽  
Vol 190 ◽  
pp. 76-80 ◽  
Author(s):  
Derek W. Bailey ◽  
Milton G. Thomas ◽  
Tim N. Holt ◽  
Mitch B. Stephenson ◽  
R. Mark Enns ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Relationship Of

Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen

1987 ◽  
Vol 63 (2) ◽  
pp. 521-530 ◽  
Author(s):  
B. M. Groves ◽  
J. T. Reeves ◽  
J. R. Sutton ◽  
P. D. Wagner ◽  
A. Cymerman ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Right Heart Failure ◽  
Barometric Pressure ◽  
Systemic Arterial Pressure ◽  
Right Atrial ◽  
Pulmonary Resistance ◽  
Systemic Control ◽  
Pulmonary Arterial

High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347 (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 +/- 0.9 to 34 +/- 3.0 mmHg and from 1.2 +/- 0.1 to 4.3 +/- 0.3 mmHg.l–1 X min, respectively. During near maximal exercise PAP increased from 33 +/- 1 mmHg at sea level to 54 +/- 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.

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