Abstract 17879: A Decrease in Cardiac Energy Metabolism Precedes a Reduction in Mass and Function in the The Hypoxic Human Heart
Background: Hypoxia impairs cardiac contractile function, yet the cellular mechanisms are unknown.
Objective: To determine if decreased cardiac high energy phosphate metabolism underlies hypoxia-induced changes in cardiac function.
Methods: Normal healthy volunteers were studied before and after a) 20 h (short-term) normobaric hypoxia in a chamber, or b) a trek to Mt Everest base camp (long-term hypoxia). In the chamber, subjects (n = 12, age 24 ± 2) has an estimated partial pressure of arterial oxygen between 50 and 60 mmHg. Different subjects (n = 14, age 38 ± 3 years) were studied immediately before, and within four days of return from, 17 days exposure to hypobaric hypoxia whilst trekking to and from Mount Everest Base Camp (17388 feet, 5300 m). Cardiac function and mass were measured using magnetic resonance imaging (MRI) and echocardiography. High energy phosphate metabolism was measured as the ratio of phosphocreatine to ATP (PCr/ATP) by 31Phosphorus magnetic resonance spectroscopy (MRS) before and after hypoxia.
Results: Cardiac PCr/ATP was decreased by 15% after short-term hypoxia (p < 0.01, Figure), with no changes in cardiac function or mass. Following long-term hypoxia, cardiac PCr/ATP had decreased by 17%, left ventricular mass and left and right ventricular stroke volumes had decreased by 11% and mitral inflow E/A ratio had fallen by 24%l (all p < 0.05).
Conclusions: Short term hypoxia altered cardiac PCr/ATP alone, whereas long-term hypoxia decreased, not only PCr/ATP, but cardiac volumes, mass and diastolic function, suggesting that impaired high energy phosphate metabolism may underlie to cardiac dysfunction after hypoxic exposure, whether in health or disease.
- © 2010 by American Heart Association, Inc.