Effects of hypobaric hypoxia exposure at high altitude on left ventricular twist in healthy subjects: data from HIGHCARE study on Mount Everest

Osculati, Giuseppe; Revera, Miriam; Branzi, Giovanna; Faini, Andrea; Malfatto, Gabriella; Bilo, Grzegorz; Giuliano, Andrea; Gregorini, Francesca; Ciambellotti, Francesca; Lombardi, Carolina; Agostoni, Piergiuseppe; Mancia, Giuseppe; Parati, Gianfranco

doi:10.1093/ehjci/jev166

Cited by 29 publications

(35 citation statements)

References 34 publications

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“…We observed major changes in LV twist mechanics at high altitude. In accordance with recent studies (Osculati et al., ; Stembridge et al., ), we observed a greater diastolic apical rotational rate (but not basal rotational rate) and untwisting rate at high altitude compared with sea level. Moreover, the increase in untwisting rate followed the twist behaviour, because we found a correlation between these two parameters ( r = 0.64, P < 0.001).…”

Section: Discussionsupporting

confidence: 93%

“…Few data are available regarding the relative differences of function between the inner and outer layers of the LV wall at high altitude. Using the TSR, an indirect index of subendocardial dysfunction (Van Der Toorn et al., ), recent findings indicated that subendocardial fibres were more affected by hypoxia than subepicardial ones (Osculati et al., ). In the present study, we observed no alterations in the TSR after high‐altitude trekking, suggesting no subendocardial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

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Medex 2015: The key role of cardiac mechanics to maintain biventricular function at high altitude

Maufrais

Rupp

Bouzat

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?This study is the first to investigate the effects of high‐altitude trekking on biventricular mechanics, including measurements of left ventricular subendocardial and subepicardial function. What is the main finding and its importance?We provide new evidence that an increased contractility and untwisting efficiency, a key element of diastolic function, probably plays a key role in preservation of cardiac function during high‐altitude trekking. Persistent increased loading conditions during several weeks at high altitude might have a key role in the appearance of left or right ventricular dysfunction. Abstract Cardiac responses to acute hypoxic exposure have been thoroughly investigated. We analysed the effects of high‐altitude trekking (i.e. prolonged hypoxic exposure) on biventricular function, including the evaluation of subendocardial and subepicardial function in the left ventricle (LV). Resting evaluations of LV and right ventricular (RV) function and mechanics were assessed by speckle tracking echocardiography on 20 subjects at sea level and at high altitude (5085 m, after a 10 day ascent). Pulmonary artery systolic pressure was increased at high altitude (sea level, 13.1 ± 5.9 mmHg; high altitude, 26.6 ± 10.8 mmHg; P < 0.001). Left ventricular volumes were decreased, whereas RV volumes were increased at high altitude. Alterations in pulmonary artery systolic pressure and cardiac volumes were correlated with hypoxaemia. We observed neither RV nor LV systolic dysfunction, including analysis of LV subendocardial and subepicardial function. Left ventricular systolic strain rates were enhanced at high altitude. Transmitral and transtricuspid diastolic filling ratios were decreased at high altitude. Diastolic apical rotational rate, untwisting rate and untwisting rate/peak twist ratio (i.e. untwisting efficiency) were enhanced at high altitude. We observed no echocardiographic signs of LV and RV pathological dysfunction at rest at high altitude. In contrast, our data highlighted major changes in the LV mechanics, with an increased LV contractility and a higher untwisting efficiency at high altitude. Biventricular interaction, alterations in loading conditions and an increase in plasma catecholamine concentration might partly explain these modifications. Thus, we demonstrated that LV mechanics (i.e. increased strain rates and untwisting efficiency) have a key role in preservation of cardiac function during high‐altitude trekking.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Medex 2015: The key role of cardiac mechanics to maintain biventricular function at high altitude

Maufrais

Rupp

Bouzat

et al. 2019

Experimental Physiology

View full text Add to dashboard Cite

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“…Details on the cardiac ultrasound examination are described elsewhere. 21 Leftventricular diastolic pressure was evaluated by echocardiography using the Nagueh formula, 1.24 E/e'+1.91. 22 Systolic pressure-time index is considered as an estimate of myocardial needs of oxygen and represents the area under the aortic pressure curve in systole: systolic The area corresponding to isovolumic contraction time, assessed by echocardiography, was also taken into account in the evaluation of systolic pressure-time index.…”

Section: Central Bpmentioning

confidence: 99%

Renin–Angiotensin–Aldosterone System Is Not Involved in the Arterial Stiffening Induced by Acute and Prolonged Exposure to High Altitude

et al. 2017

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T he exposure to hypobaric hypoxia at high altitude (HA) is responsible for complex modifications in both systemic and pulmonary circulation. Activation of the peripheral chemoreflex leads to a sympathetic nervous system activation, which increases blood pressure (BP), heart rate, and cardiac output counteracting the direct systemic vasodilator effect of hypoxia. [1][2][3][4] Previous studies have shown that systemic vascular dysfunction both in lowlanders during acute HA exposure 5 and in native highlanders 6,7 is related to increased sympathetic nervous system activity, increased oxidative stress, and decreased nitric oxide bioavailability. However, until now, there is no data supporting a role of the renin-angiotensin-aldosterone system (RAAS) in this setting. Hypoxia may also have a direct effect on RAAS, and retention of fluid and sodium has been proposed as one of the mechanisms involved in the pathogenesis of acute mountain sickness and possibly also of HA pulmonary edema. 8Although most available HA studies focused on pathophysiology of HA pulmonary hypertension, 9 only few data are available on changes in cardiac function and in systemic circulation, and in particular, in arterial wall properties, primarily when explored in relation to changes in sympathetic and RAAS activity.HIGHCARE Himalaya project (HA cardiovascular research) was designed to fill-in this gap, based on a randomized, double-blind, parallel group, placebo-controlled study design, and focusing on changes in several cardiovascular variables related to systemic circulation in response to acute Abstract-This randomized, double-blind, placebo-controlled study was designed to explore the effects of exposure to very high altitude hypoxia on vascular wall properties and to clarify the role of renin-angiotensin-aldosterone system inhibition on these vascular changes. Forty-seven healthy subjects were included in this study: 22 randomized to telmisartan (age, 40.3±10.8 years; 7 women) and 25 to placebo (age, 39.3±9.8 years; 7 women). Tests were performed at sea level, pre-and post-treatment, during acute exposure to 3400 and 5400-m altitude (Mt. Everest Base Camp), and after 2 weeks, at 5400 m. The effects of hypobaric hypoxia on mechanical properties of large arteries were assessed by applanation tonometry, measuring carotid-femoral pulse wave velocity, analyzing arterial pulse waveforms, and evaluating subendocardial oxygen supply/demand index. No differences in hemodynamic changes during acute and prolonged exposure to 5400-m altitude were found between telmisartan and placebo groups. Aortic pulse wave velocity significantly increased with altitude (P<0.001) from 7.41±1.25 m/s at sea level to 7.70±1.13 m/s at 3400 m and to 8.52±1.59 m/s at arrival at 5400 m (P<0.0001), remaining elevated during prolonged exposure to this altitude (8.41±1.12 m/s; P<0.0001). Subendocardial oxygen supply/demand index significantly decreased with acute exposure to 3400 m: from 1.72±0.30 m/s at sea level to 1.41±0.27 m/s at 3400 m (P<0.001), remaining significantl...

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“…Speckle tracking echocardiography performed during the HIGH CARE STUDY on Mt. Everest demonstrates, however, an increase of the left ventricular twist (LVT) and torsion to shortening ratio in healthy trekkers at 5400 m (Osculati et al, 2015). Both parameters allow assessing predominantly the function of the subendocardial myocardium, which is most sensitive to inadequate oxygen supply.…”

Section: Speckle Tracking Echocardiography Suggests ''Subclinical'' Ementioning

confidence: 99%

Sightings, edited by Erik R. Swenson and Peter Bärtsch

2015

High Altitude Medicine & Biology

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Effects of hypobaric hypoxia exposure at high altitude on left ventricular twist in healthy subjects: data from HIGHCARE study on Mount Everest

Cited by 29 publications

References 34 publications

Medex 2015: The key role of cardiac mechanics to maintain biventricular function at high altitude

Medex 2015: The key role of cardiac mechanics to maintain biventricular function at high altitude

Renin–Angiotensin–Aldosterone System Is Not Involved in the Arterial Stiffening Induced by Acute and Prolonged Exposure to High Altitude

Sightings, edited by Erik R. Swenson and Peter Bärtsch

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