Efforts to understand cardiac disease progression and develop therapeutic tissues that can repair the human heart are just a few areas of focus for the Feinberg research group at Carnegie Mellon University. The group's latest dynamic model, created in partnership with collaborators in the Netherlands, mimics physiologic loads on engineering heart muscle tissues, yielding an unprecedented view of how genetics and mechanical forces contribute to heart muscle function.
"Our lab has been working for a long time on engineering and building human heart muscle tissue, so we can better track how disease manifests, and also create therapeutic tissues to one day repair and replace heart damage," said Adam Feinberg, a professor of biomedical engineering and materials science and engineering. "One of the challenges is that we have to build these small pieces of heart muscle in a petri dish, and we've been doing that for many years. What we've realized is that these in vitro systems do not accurately recreate the mechanical loading we see in the real heart due to blood pressure."
Hemodynamic loads, or the preload (stretch on heart muscle during chamber filling) and afterload (when the heart muscle contracts), are important not only for healthy heart muscle function, but also can contribute to cardiac disease progression. Preload and afterload can lead to maladaptive changes in heart muscle, as is the case of hypertension, myocardial infarction and cardiomyopathies.
