Key result
Acute hypoxic breathing in HAPE-susceptible subjects induced a paradoxical myocardial performance, significantly impairing right ventricular function (RV Tei index increased from 0.34 to 0.47, p=0.008) while enhancing left ventricular function.
Why the study?
Does acute hypoxic breathing alter myocardial performance (Tei index) in subjects susceptible to high-altitude pulmonary edema compared to resistant subjects?
Case-Control (n=20)
Single-blind
No
Does acute hypoxic breathing alter myocardial performance (Tei index) in subjects susceptible to high-altitude pulmonary edema compared to resistant subjects?
Acute hypoxia induces a paradoxical myocardial performance with augmented LV and attenuated RV function in HAPE-susceptible subjects, which may contribute to HAPE pathogenesis.
OBJECTIVE: A recent study concerning high-altitude pulmonary edema (HAPE), a non-cardiogenic pulmonary edema, suggested that it is initially a hydrostatic-type pulmonary edema. We suspect that some extent of cardiac insufficiency may likely relate to the mechanism of the development of this disease. METHODS: By Doppler echocardiography, the Tei index (a new quantitative index proposed for the evaluation of global myocardial performance) and the systolic pulmonary artery pressure (sPAP) were measured before and after 30 minutes of hypoxic breathing. PATIENTS: Eleven HAPE-susceptible subjects (HAPE-s) and nine HAPE-resistant subjects (HAPE-r). RESULTS: The results of Tei index indicated an enhanced left myocardial performance but an impaired right performance in HAPE-s during hypoxic breathing. The sPAP of HAPE-s was significantly increased after hypoxic breathing, which was not correlated with the heart functions such as right ventricular (RV) Tei index, cardiac index (CI), percent ejection fraction (EF%) and percent fractional shortening (FS%) under hypoxic condition. Comparatively, the HAPE-r subjects did not show such significant changes of Tei index after hypoxic breathing. The results suggested that a paradoxical myocardial performance, in a format of an augmented left ventricular (LV) in contrast to an attenuated RV, was observed in the HAPE-s exposed to acute hypoxia. CONCLUSION: The responses of the left and right myocardial performances to hypoxia may be involved in the pathogenesis of HAPE.
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Hanaoka et al. (2011) conducted a case-control in High-Altitude Pulmonary Edema (HAPE) susceptibility (n=20). Acute hypoxic breathing vs. Normoxia (room air) was evaluated on Right ventricular (RV) Tei index (p=0.008). Acute hypoxic breathing in HAPE-susceptible subjects induced a paradoxical myocardial performance, significantly impairing right ventricular function (RV Tei index increased from 0.34 to 0.47, p=0.008) while enhancing left ventricular function.
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