Abstract 13889: Impact Of Acute Hypoxia On Left Ventricular Relaxation Time In Healthy Men

Abstract

Introduction: The oxygen-dependence of myocardial contractility is known but it is not the case for ventricular distension in humans. It has been shown that acute ischemia causes incomplete and retarded relaxation through the decrease in intracellular pH and ATP content. Purpose: to verify whether hypoxemia changes the left ventricular relaxation time (LVRT). Methods: Overall, 37 physically active normotensive men (age 19-42 years, 20.4±2.3 yrs., M±SD) constituted the study sample. The LVRT was derived from aortic pulse wave analysis (SphygmoCor) and measured as difference between the end of systole (ejection duration point, ED, corresponding to the closure of aortic valve) and the time of peak pressure (T1), generated by LV in the aortic root and corresponding to the first incisura [LVRT,%=(ED-T1)/length of cardiac cycle*100]. Subjects inhaled hypoxic mixture with 10%O2 over 10 min for mean blood SpO2 of 80%. Associations were assessed by partial correlation (age, SBP=const.), multiple linear regression analyses (GLM option in SPSS), and t-test for dependent samples. Results: At baseline, the longer length of LVR was associated with lower end systolic blood pressure (r=-0.56, p<0.001). The regression model combining heart rate, augmentation pressure, and aortic-to-radial pulse pressure amplification explained 98.6% of total LVRT variation with significant effects of all covariates. Hypoxia increased LVRT from 19.0±2.8% to 23.1±4.2%, p<0.001. The response of LVRT to hypoxic exposure (range for Δ, -0.7%, +9.1%) was directly correlated with the extent of blood oxygen desaturation (r=0.53, p=0.016). Conclusion: The results show that cardiomyocytes retard their relaxation in hypoxic conditions. Cardiomyocytes happened to be quite sensitive to hypoxemia since even 10-min hypoxia was sufficient for elongation of the ventricular relaxation.