Infiltrative cardiomyopathy, like amyloidosis, causes thickening and decreased compliance of the heart. Thought of another way, this increases the elasticity of the heart wall. This presents as increased "contractility" because of Frank-Starling mechanisms, but there isn't an intrinsic positive ionotropy. It's a mechanical effect.
Infiltrative cardiomyopathy, like amyloidosis, causes thickening and decreased compliance of the heart. Thought of another way, this increases the elasticity of the heart wall. This presents as increased "contractility" because of Frank-Starling mechanisms, but there isn't an intrinsic positive ionotropy. It's a mechanical effect.
Sure, it's not really critical to understanding this, and I could have done without it, but the way I view it, Frank-Starling is based on the sarcomere. If you stretch a sarcomere to a certain length, within reason, (i.e. increase preload), then you increase contraction and therefore stroke volume. I only brought it up to say that with increased elasticity, you would expect whatever volume you put into the LV to be ejected.