Acute afterload elevations shifted the diastolic pressure-volume relation upward by 2.2 to 12.1 mmHg depending on preload, demonstrating that load is an acute determinant of the ED P-V relation.
Afterload-induced changes in myocardial relaxation are a mechanism for diastolic dysfunction when afterload is elevated beyond certain limits. The present study investigated the effects of acute afterload and preload changes on the position of the end-diastolic (ED) pressure-volume (P-V) relation. Beat-to-beat afterload elevations were induced in seven open-chest rabbits by gradually occluding the ascending aorta to increase peak left ventricular pressure (LVP) from baseline to isovolumetric level. Afterload elevations were performed at three ED LVP: 2.0 +/- 0.2 (low), 5.7 +/- 0.2 (mid), and 9.6 +/- 0.6 (high) mmHg. Preload was altered with caval occlusions and/or intravenous dextran. Afterload elevations induced an upward shift of the diastolic P-V relation, which became more important as afterload and/or preload increased. For instance, maximal afterload elevations shifted this relation upward 2.2 +/- 0. 5, 5.1 +/- 0.8, and 12.1 +/- 1.7 mmHg at low, mid, and high preload, respectively. These effects were partially due to changes in relaxation rate and time available to relax. In conclusion, load is an acute determinant of the ED P-V relation, which, therefore, does not provide a load-independent assessment of diastolic function.
Leite‐Moreira et al. (Mon,) conducted a other in Diastolic function (n=7). Acute afterload and preload changes vs. Baseline was evaluated on Position of the end-diastolic (ED) pressure-volume (P-V) relation. Acute afterload elevations shifted the diastolic pressure-volume relation upward by 2.2 to 12.1 mmHg depending on preload, demonstrating that load is an acute determinant of the ED P-V relation.