While the exact mechanisms by which ECP produces clinical improvement remains unknown, here are two primary hypotheses that have been discussed in the clinical literature.

Postulated Mechanism of Action #1:

Raised transmyocardial pressure gradients open “latent” conduits
Both arteriogenesis and angiogenesis occur
Increased shear forces stimulate growth factor release, capillary sprouting and
  endothelial migration
Nitric oxide levels are increased while endothelin levels diminish
Restoring flow reserve

Postulated Mechanism of Action #2:

35 hour-long periods of cardiac assist rest the myocardium
Myocyte metabolism switches back from free fatty acid energy supply toward
  glucose utilization
Neurohumoral signals are “normalized,” permitting improved arterial compliance
  and arteriolar reactivity
Oxygen demand is reduced as oxygen efficiency is improved