Systemic Blood Pressure, Arterial Stiffness and Pulse Waveform Analysis at Altitude

Rhodes, Helen; Chesterman, K.; Chan, Colin; Collins, Peter; Kewley, E; Pattinson, Kyle T. S.; Myers, Stephen D.; Imray, Christopher; Wright, Alexander D.

doi:10.1136/jramc-157-01-18

Cited by 28 publications

(24 citation statements)

References 16 publications

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“…In a very recently published field study (n = 17) to 4770 m, Rhodes et al failed to demonstrate a consistent change in arterial SI with high altitude exposure, but did observe an ACUTE HYPOBARIC HYPOXIA initial significant fall in RI, as in our study. However, as with all of the above studies assessment of diastolic function and PAP were not performed (Rhodes et al, 2011). Our data appears to suggest that hypoxia leads to differential haemodynamic effects along the arterial tree.…”

contrasting

confidence: 61%

“…The endothelium is also a principle regulator of arterial stiffness (Wilkinson et al, 2002;Boos et al, 2007). There have been very few studies that have investigated the effects of hypoxia on arterial stiffness and its relationship to endothelial function under hypoxic conditions and the findings have been inconsistent (Vedam et al, 2009;Rhodes et al, 2011). This has clinical implications as changes in arterial stiffness influence diastolic function and left ventricular (LV) filling (London et al, 2004;Chung CM et al, 2010;Erdogan et al, 2007).…”

Section: Introductionmentioning

confidence: 92%

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The Effects of Acute Hypobaric Hypoxia on Arterial Stiffness and Endothelial Function and its Relationship to Changes in Pulmonary Artery Pressure and Left Ventricular Diastolic Function

Boos

Hodkinson²,

Mellor

et al. 2012

High Altitude Medicine & Biology

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This study investigated, for the first time, the effects of simulated high altitude, following acute hypobaric hypoxia (HH), on simultaneous assessment of large artery stiffness and endothelial function and its inter-relationship to left ventricular (LV) diastolic function, pulmonary artery systolic pressure (PASP), and estimated PA vascular resistance (PVR). Ten healthy subjects were studied at baseline pre and following acute HH to 4800 m for a total of 180 minutes. Assessments of LV diastolic function, mitral inflow, estimated LV filling pressure (E/e'), PVR, and PASP were undertaken using transthoracic echocardiography. Simultaneous assessments of arterial stiffness index (SI), systemic vascular resistance (SVR), vascular tone, and endothelial function (reflective index [RI]) were performed using pulse contour analysis of the digital arterial waveform. Acute hypoxia led to a fall in SpO₂ (98.1±0.7 vs. 71.8±7.1%; p=0.0002), SVR (1589.1±191.2 vs. 1187.8±248.7; p=0.004), and RI (50.8±10.3 vs. 33.0±6.5%; p=0.0008) with an increase in PASP (24.3±2.2 to 35.0±5.3 mmHg; p=0.0001) and estimated PVR (116.40±19.0 vs. 144.6±21.5; p<0.001). There was no rise in either SI (p=0.13), mitral early annular early e' filling velocity or E/e'. There was a significant inverse correlation between SpO₂ and PASP (r=-0.77; p<0.0001), PVR (r=-0.57; p=0.008) and between the fall in SpO₂ and change (Δ) in RI (baseline vs. 150 min, r=-0.52; p<0.001). There was a modest inverse correlation between ΔRI (lower ΔRI=worsening endothelial function) and ΔPAP (r=-0.55; p=0.10) and a strong inverse correlation between ΔRI and ΔPVR (r=-0.89; p=0.0007). Acute hypobaric hypoxia does not significantly alter large artery stiffness or cause overt LV diastolic function. However, the degree of hypoxia influences both the systemic endothelial and pulmonary vascular responses. This noted association is intriguing and requires further investigation.

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contrasting

confidence: 61%

Section: Introductionmentioning

confidence: 92%

The Effects of Acute Hypobaric Hypoxia on Arterial Stiffness and Endothelial Function and its Relationship to Changes in Pulmonary Artery Pressure and Left Ventricular Diastolic Function

Boos

Hodkinson²,

Mellor

et al. 2012

High Altitude Medicine & Biology

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“…In addition, systolic blood pressure also significantly increased after high-altitude exercise [6]. Significant rise in systolic and diastolic blood pressure in the initial phase of exposure to altitude was also reported in other studies [7,8].…”

Section: Cardiac Systemsupporting

confidence: 54%

Cardiovascular Adaptation to High-Altitude Hypoxia

Ji¹,

Wang²,

Xiao³

2017

Hypoxia and Human Diseases

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High-altitude exposure has been well recognized as a hypoxia exposure that significantly affects cardiovascular function. However, the pathophysiologic adaptation of cardiovascular system to high-altitude hypoxia (HAH) varies remarkably. It may depend on the exposed time and oxygen partial pressure in the altitude place. In short-term HAH, cardiovascular adaptation is mainly characterized by functional alteration, including cardiac functional adjustments, pulmonary vascular constriction, transient pulmonary hypertension, and changes in cerebral blood flow (CBF). These changes may be explained mainly by ventilatory acclimatization and variation of autonomic nervous activity. In long-term HAH, cardiovascular adaptation is mainly characterized by both functional and structural alterations. These changes include right ventricle (RV) hypertrophy, persistent pulmonary hypertension, lower CBF and reduced uteroplacental and fetal volumetric blood flows.

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“…The muscular arteries are much more sensitive than elastic arteries to sympathetic nervous system activity, and, therefore, the weak and insignificant increase in carotid-radial PWV with altitude suggests that other factors, in addition to sympathetic activation, may 26,27 hemoconcentration with consequent increase in blood viscosity, 28 and interstitial edema 29 of the arterial wall, may have an important role in determining the changes in arterial distensibility observed in this condition. Acute exposure to HA has indeed been reported to impair both endothelial 5,30 and vascular smooth muscle-cell function, 5 as shown in a previous study by our group which demonstrated a link between the altitude-induced increase in pulmonary artery pressure and an increase in plasma and urinary endothelin-1 levels. 31 All these changes might contribute to explain the hypoxia-related increase in arterial stiffness at altitude, although their possible role in this regard is mostly based on speculative considerations which remain to be supported by further experimental studies.…”

Section: Arterial Stiffness At Very Hamentioning

confidence: 62%

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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Systemic Blood Pressure, Arterial Stiffness and Pulse Waveform Analysis at Altitude

Abstract: We conclude that acute exposure temporarily affected endothelial function as measured by a change in vascular tone but this did not predict the development of AMS. The rise in arterial BP was not related to changes in arterial stiffness or tone.

Cited by 28 publications

References 16 publications

The Effects of Acute Hypobaric Hypoxia on Arterial Stiffness and Endothelial Function and its Relationship to Changes in Pulmonary Artery Pressure and Left Ventricular Diastolic Function

The Effects of Acute Hypobaric Hypoxia on Arterial Stiffness and Endothelial Function and its Relationship to Changes in Pulmonary Artery Pressure and Left Ventricular Diastolic Function

Cardiovascular Adaptation to High-Altitude Hypoxia

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

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