Key result
Acute hypobaric hypoxia significantly increased pulmonary artery systolic pressure (24.3 to 35.0 mmHg; p=0.0001) and decreased endothelial function, without altering large artery stiffness.
Why the study?
Does acute hypobaric hypoxia alter arterial stiffness, endothelial function, LV diastolic function, and pulmonary artery pressure in healthy subjects?
Does acute hypobaric hypoxia alter arterial stiffness, endothelial function, LV diastolic function, and pulmonary artery pressure in healthy subjects?
Absolute Event Rate: 35% vs 24.3%
p-value: p=0.0001
Acute hypobaric hypoxia significantly influences systemic endothelial and pulmonary vascular responses without overtly altering large artery stiffness or LV diastolic function.
Acute hypoxia may impair endothelial function and raise pulmonary pressure in healthy subjects; leaves open long-term cardiovascular risks or chronic exposure effects.
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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Boos et al. (2012) studied Healthy (n=10). Acute hypobaric hypoxia vs. Baseline was evaluated on Pulmonary artery systolic pressure (PASP) (p=0.0001). Acute hypobaric hypoxia significantly increased pulmonary artery systolic pressure (24.3 to 35.0 mmHg; p=0.0001) and decreased endothelial function, without altering large artery stiffness.
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