Heart failure is a changing paradigm. The hemodynamic model, which served our needs
well from the 1950s through the early 1980s, has now been largely abandoned, except for
the management of decompensated patients in the hospital. The pathophysiology is
exceedingly complex and involves structural changes, such as loss of myofilaments,
apoptosis and disorganization of the cytoskeleton, as well as disturbances in Ca2+
homeostasis, alteration in receptor density, signal transduction, and collagen synthesis. A …