Heart attacks, even when not fatal, cause irreparable damage. After a heart attack, the healthy tissue dies and is replaced with scar tissue, which greatly reduces the heart’s ability to pump blood effectively.
Recently, there have been a variety of research experiments completed around the world to combat the detrimental effects of heart attacks. Scientists hope to provide solutions that will help patients return their heart functions back to pre-heart attack levels.
Karen Christman, a Bioengineering professor at UCSD, and her team are working on developing a hydrogel that would serve as a scaffold for new heart tissue to grow on.
Unlike other similar technologies, the hydrogel could be injected using a catheter, eliminating any need for surgery or anesthesia.
The hydrogel is made from connective tissue from the heart. The muscle cells are removed, and the remaining tissue is crushed into powder. From there, an enzyme is used to liquefy the powder. When this liquid is injected into a patient, it reaches body temperature and turns into gel.
Throughout its research, Christman’s team has performed numerous animal trials using the hydrogel. The team reports that when the gel was injected into pigs with heart damage, it partially solidified and the pigs saw an improvement in heart function.
Scientists at the University of Toronto are leading another research effort to combat heart damage. They have bioengineered an asymmetrical, 2D protein mesh that actually has the ability to attach to itself like Velcro.
The material, formed from flexible polymer, has microscopic posts that mimic the small hooks on Velcro strips.
Milica Radisic, the lead researcher, explains that when the meshes make contact with one another, they start to beat. When electrical field stimulation is applied, the meshes even beat in synchrony.
This Bioengineered “Velcro” could be grafted onto the heart, promoting new tissue growth in a matter of months.
Over time, the mesh structures would be absorbed by the body, leaving only a repaired heart.
Pilar Ruiz-Lozano, a professor from Stanford University, began his research endeavor by examining the heart’s epicardial cells. Through careful study, his team discovered that these cells actually cause existing muscle cells within the heart to multiply.After narrowing down the 300 proteins found in the epicardial cells, the Follistatin-like 1 (FSTL1) protein was identified as the one responsible for causing the muscle cell growth. FSTL1 was then incorporated into a collagen patch that can be attached to the heart. The patch slowly releases the protein over time, stimulating tissue generation.
In animal trials, pigs’ pumping capacities were increased from 30% after a heart attack to 40%. This improvement was seen over the course of the first week. The Stanford team expects to transition to human trials in 2017.
Above: From left to right, Karen Christman, Milica Radisic, and Pilar Ruiz-Lozano.