Echocardiographic and Tissue Doppler Imaging of Cardiac Adaptation to High Altitude in Native Highlanders Versus Acclimatized Lowlanders

doi:10.1016/j.amjcard.2009.02.006

The American Journal of Cardiology

Volume 103, Issue 11, 1 June 2009, Pages 1605-1609

https://doi.org/10.1016/j.amjcard.2009.02.006 Get rights and content

High-altitude exposure is a cause of pulmonary hypertension and decreased exercise capacity, but associated changes in cardiac function remain incompletely understood. The aim of this study was to investigate right ventricular (RV) and left ventricular function in acclimatized Caucasian lowlanders compared with native Bolivian highlanders at high altitudes. Standard echocardiography and tissue Doppler imaging studies were performed in 15 healthy lowlanders at sea level; <24 hours after arrival in La Paz, Bolivia, at 3,750 m; and after 10 days of acclimatization and ascent to Huayna Potosi, at 4,850 m, and the results were compared with those obtained in 15 age- and body size–matched inhabitants of Oruro, Bolivia, at 4,000 m. Acute exposure to high altitude in lowlanders caused an increase in mean pulmonary arterial pressure, to 20 to 25 mm Hg, and altered RV and left ventricular diastolic function, with prolonged isovolumic relaxation time, an increased RV Tei index, and maintained RV systolic function as estimated by tricuspid annular plane excursion and the tricuspid annular S wave. This profile was essentially unchanged after acclimatization and ascent to 4,850 m, except for higher pulmonary arterial pressure. The native highlanders presented with relatively lower pulmonary arterial pressures but more pronounced alterations in diastolic function, decreased tricuspid annular plane excursion and tricuspid annular S waves, and increased RV Tei indexes. In conclusion, cardiac adaptation to high altitude was qualitatively similar in acclimatized Caucasian lowlanders and in Bolivian native highlanders. However, lifelong exposure to high altitude may be associated with different cardiac adaptation to milder hypoxic pulmonary hypertension.

Section snippets

Methods

Fifteen Belgian Caucasian lowlanders without histories of high-altitude sickness (7 men and 8 women), as well as 15 Bolivian highlanders (10 men and 5 women), gave informed consent to the study, which was approved by the institutional review board of Erasme University Hospital (Brussels, Belgium) and by the ethics committee of Oruro City Hospital (Oruro, Bolivia). All the Belgian and Bolivian volunteers were healthy nonsmokers with normal clinical examination results. All the lowlanders were

Results

High-altitude exposure was associated with increases in heart rate and cardiac output in the lowlanders and the highlanders. Arterial oxygen saturation was decreased but not differently in highlanders at 4,000 m compared with acclimatized lowlanders at 4,850 m.

In the acutely acclimatized lowlanders, at 3,750 m in the first 24 hours, the systolic RV pressure gradient was increased and the pulmonary flow acceleration time decreased, allowing for an estimated mean Ppa increase from 13 ± 1 to 22 ±

Discussion

The present results confirm the moderate nature of altitude pulmonary hypertension and show that acclimatized lowlanders and native highlanders present with adaptive changes in the diastolic function of both ventricles. However, somewhat paradoxically, indexes of RV systolic function and diastolic function of both ventricles appeared to be better preserved in acclimatized lowlanders, despite milder pulmonary hypertension in native highlanders.

In the present study, the estimated Ppa, cardiac

Acknowledgments

Pascale Jespers helped in the preparation of this report. The assistance of Dr. Alfredo Agata (Oruro, Bolivia) is greatly appreciated. We are grateful to GE Healthcare Ultrasound Belgium for the loan of the Vivid I.

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High-altitude pulmonary edema is associated with elevated systolic pulmonary artery pressure (sPAP) and increased extravascular lung water (EVLW). We investigated sPAP and EVLW during repeated exposures to high altitude (HA).
Healthy lowlanders underwent two identical 7-day HA-cycles, where subjects slept at 2900 m and spent 4–8 h daily at 5050 m, separated by a weeklong break at low altitude (LA). Echocardiography and EVLW by B-lines were measured at 520 m (baseline, LA₁), on day one, two and six at 5050 m (HA₁_–₃) and after descent (LA₂).
We included 21 subjects (median 25 years, body mass index 22 kg/m², SpO₂ 98%). SPAP rose from 21 mmHg at LA₁ to 38 mmHg at HA₁, decreased to 30 mmHg at HA₃ (both p < 0.05 vs LA₁) and normalized at 20 mmHg at LA₂ (p = ns vs LA₁). B-lines increased from 0 at LA₁ to 6 at HA₂ and 7 at HA₃ (both p < 0.05 vs LA₁) and receded to 1 at LA₂ (p = ns vs LA₁). Overall, in cycle two, sPAP did not differ (mean difference (95% confidence interval) −0.2(−2.3 to 1.9) mmHg, p = 0.864) but B-lines were more prevalent (+2.3 (1.4–3.1), p < 0.001) compared to cycle 1. Right ventricular systolic function decreased significantly but minimally at 5050 m.
Exposure to 5050 m induced a rapid increase in sPAP. B-lines rose during prolonged exposures to 5050 m, despite gradual decrease in sPAP, indicating excessive hydrostatic pressure might not be solely responsible for EVLW-development. Repeated HA-exposure had no acclimatization effect on EVLW. This may affect workers needing repetitive ascents to altitude and could indicate greater B-line development upon repeated exposure.
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Pulmonary vasculopathy, right heart structural and functional abnormalities occur even in normoxemic chronic obstructive pulmonary disease (COPD) patients. Despite being associated with functional limitation, exacerbations, and disease progression, their detection and proper management is still delayed.
Our aim was to establish the frequency of stress-induced right ventricular diastolic dysfunction (RVDD) in non-severe COPD patients, free of overt cardiovascular disease, who complain of exertional dyspnea and to look for echocardiographic predictors of it.
We applied cardio-pulmonary exercise testing (CPET) in 104 non-severe, COPD patients. A ramp protocol was performed. Echocardiography was done before and 1−2 min after peak exercise. Cut-off values for stress induced RVDD were E/e’ >6. Receiver operating curves were constructed for echo parameters at rest to determine if any of them may discriminate stress induced RV E/e’>6 or <6. Uni- and multivariable linear regression analysis was also performed to assess the predictive power of each of them. A p-value < 0.05 was considered significant.
A total of 78% of the patients had stress-induced RVDD. Right atrium volume index (RAVI) (cut-off >20.55 ml/m²; sensitivity - 86%; specificity - 86%), RV wall thickness (RVWT) (cut-off >5.25 mm; sensitivity - 100%; specificity - 63%), and RV E/A ratio at rest (cut-off >1.05; sensitivity - 79.7%; specificity - 90.5%) were the best predictors of stress RV E/e. In univariate regression analysis E/A showed the highest OR 19.73 (95% CI – 18.52–21.01); followed by RAVI - OR 3.82; (95% CI – 2.04–7.14).
There is a high prevalence of stress-induced RVDD in non-severe COPD patients with exertional dyspnea, free of overt cardiovascular disease. RAVI, RVWT, E/A, and E/e’ ratio at rest may be used as predictors for stress RVDD and may facilitate patients’ risk stratification and proper management.
Cardiac performance with chronic hypoxia: mechanisms regulating stroke volume
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When humans are exposed to high altitude hypoxia for a sustained period, the cardiac stroke volume is reduced. The changes in cardiac performance seen at high altitude are a result of complex and concomitant changes in preload, afterload and contractility, although the precise mechanisms underpinning the decrease in stroke volume are not known despite being of scientific interest for over fifty years. In this review, we briefly revisit the seminal work performed in the area before focusing on recent developments that have applied mechanistic experimental models and novel imaging technologies to further understand why stroke volume is decreased in chronic hypoxia. First, the review focuses on systolic contractile function before considering the role of diastolic function and ventricular filling.
Altitude and the right heart
2018, Revue des Maladies Respiratoires
La pression partielle inspiratoire en oxygène diminue avec l’altitude. L’hypoxie provoque une vasoconstriction pulmonaire, qui peut être cause d’hypertension pulmonaire et donc de défaillance cardiaque droite.
La vasoconstriction pulmonaire hypoxique varie considérablement. L’exposition à l’altitude s’accompagne d’une augmentation de la pression artérielle pulmonaire en proportion de la vasoconstriction initiale. Des échocardiographies réalisées en altitude montrent que la pression artérielle pulmonaire moyenne s’y établit généralement à 20 mmHg, soit la limite supérieure de la normale normoxique. La postcharge du ventricule droit n’est alors que modérément augmentée, avec quelques perturbations fonctionnelles démontrées par imagerie, mais préservation d’une adaptation aux contraintes de l’effort physique. Dans moins de 1 % des cas, il y a hypertension pulmonaire hypoxique franche avec ou sans défaillance cardiaque droite.
L’impact pronostique de l’hypertension pulmonaire et des altérations associées de la fonction cardiaque en altitude n’est pas défini. Le traitement de l’hypertension pulmonaire hypoxique repose empiriquement sur une évacuation à une altitude inférieure, sur l’administration d’oxygène et sur la prise de vasodilatateurs pulmonaires. Ces stratégies thérapeutiques ne sont pas rigoureusement validées.
Une défaillance cardiaque droite peut survenir lors d’une exposition à l’altitude. Cette complication rare devrait faire l’objet d’études épidémiologiques et interventionnelles prospectives.
Altitude is associated with a decrease in partial pressure of oxygen. Hypoxia induces pulmonary vasoconstriction with subsequent fixed increase in pulmonary artery pressure, and eventual right heart failure.
High altitude exposure is associated with an increase in pulmonary artery pressure that is proportional to initial vasoconstriction. Echocardiographic evaluations on a large number of subjects show that the altitude-induced increase in pulmonary pressure is generally modest and does not exceed the 25 mmHg that are diagnostic of pulmonary hypertension. This does not greatly increase right ventricular afterload, so that imaging of the right ventricle only shows some alterations of indices of systolic or diastolic function, but preserved contractile reserve during exercise. In less than 1% of cases, hypoxic vasoconstriction is strong and may be a cause of severe pulmonary hypertension and right heart failure.
The prognostic relevance of altitude-induced pulmonary hypertension and associated cardiac function alterations is not known. Treatment of hypoxic pulmonary hypertension relies on evacuation to a lower altitude, oxygen and pulmonary vasodilators. These treatment strategies have not been rigorously evaluated.
Altitude may be a cause of right heart failure. This uncommon complication of altitude exposure requires further epidemiological and therapeutic studies.
Altered Left Ventricular Geometry and Torsional Mechanics in High Altitude-Induced Pulmonary Hypertension: A Three-Dimensional Echocardiographic Study
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Changes in left ventricular (LV) torsion have been related to LV geometry in patients with concomitant long-standing myocardial disease or pulmonary hypertension (PH). We evaluated the effect of acute high altitude-induced isolated PH on LV geometry, volumes, systolic function, and torsional mechanics.
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At high altitude, oxygen saturation decreased by 15%–20%, heart rate and cardiac index increased by 15%–20%, and TRPG increased from 21 ± 2 to 37 ± 9 mm Hg (P < .01). LV volumes, preload, ejection fraction, multidirectional strains, and sphericity remained unaffected, but diastolic (1.04 ± 0.07 to 1.09 ± 0.09 on D3/D4, P < .05) and systolic (1.00 ± 0.06 to 1.08 ± 0.1 [D3] and 1.06 ± 0.07 [D4], P < .05) eccentricity slightly increased, indicating mild septal flattening. LV torsion decreased from 2.14 ± 0.85 to 1.34 ± 0.68 (P < .05) and 1.65 ± 0.54 (P = .08) degrees/cm on D3/D4, respectively. Changes in torsion showed a weak inverse relationship to changes in systolic (r = −0.369, P = .013) and diastolic (r = −0.329, P = .032) eccentricity but not to changes in TRPG, heart rate or preload.
High-altitude exposure was associated with mild septal flattening of the LV and reduced ventricular torsion at unchanged global LV function and preload, suggesting a relation between LV geometry and torsional mechanics.

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: This work was supported by the Foundation of Cardiac Surgery and by Fonds de la Recherche Scientifique Médicale (Grant 3.4551.05), Brussels, Belgium. Dr. Huez was fellow of Fonds National de la Recherche Scientifique, Brussels, Belgium.

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MiscellaneousEchocardiographic and Tissue Doppler Imaging of Cardiac Adaptation to High Altitude in Native Highlanders Versus Acclimatized Lowlanders

Section snippets

Methods

Results

Discussion

Acknowledgments

J Am Coll Cardiol

Am J Cardiol

J Am Soc Echocardiogr

J Am Coll Cardiol

Chest

Sildenafil for enhanced performance at high altitude

Ann Intern Med

Sildenafil increased exercise capacity during hypoxia at low altitudes and at Mount Everest base camp: a randomized, double-blind, placebo-controlled crossover trial

Ann Intern Med

The physiologic basis of high-altitude diseases

Ann Intern Med

The heart and pulmonary circulation at high altitudesHealthy highlanders and chronic mountain sickness

Circulation

Miscellaneous
Echocardiographic and Tissue Doppler Imaging of Cardiac Adaptation to High Altitude in Native Highlanders Versus Acclimatized Lowlanders