Assessment of Cardiac Function Using Pressure-Volume Loops as Cardiac Hypertrophy Develops from Iron Deficiency

Abstract

Aims: Cardiac hypertrophy develops from prolonged, severe iron deficiency (ID), but little is known about its function. We hypothesized that 4 weeks of ID would result in enhanced cardiac function, but would transition to loss by 9 weeks. Study Design: 38 rats were fed either control or ID diets for 4, 6, or 9 weeks, then subjected to a pressure-volume loop protocol to assess cardiac function. Place and Duration of Study: Biology Department, Western Wyoming College, between January 2013 and December 2013. Methodology: Rats were anesthetized with ketamine/xylazine, catheters placed in femoral and jugular veins. A pressure-conductance microcatheter was inserted through the right carotid artery, to the left ventricle. Baseline data was collected for 10 minutes, followed by occlusion of the inferior vena cava to reduce venous return. Hypertonic saline was infused through the jugular vein to allow for parallel conductance subtraction. Rats were sacrificed, and hearts and blood collected for mass and volume calibration, respectively. Results: Cardiac output was increased (P = .01) with ID after 4 weeks, but was not increased after 6 or 9 weeks. The increase was due to enhanced stroke volume (P = .02), but not heart rate (P = .48). Stroke volume was increased due to enhanced contractility with ID (P = .03), along with a decrease in the pressure at which ejection begins (afterload, P = .001). By 9 weeks, contractility was decreased (P = .01), but afterload remained lower. Cardiac efficiency was enhanced after 4 weeks (P = .002), which was lost by 9 weeks of ID. No diastolic parameters of cardiac function were altered by ID. Conclusion: An adaptive compensation of cardiac function develops within 4 weeks of severe ID, but is lost within weeks, at which time, the ID heart is in a state of pathological decompensation.