Researchers from Virginia Tech University (VT) have developed a variant of the compound alphaCT1, which can improve heart attack recovery if administered during, or soon after, a heart attack.

In a study on perforated mouse hearts published in the Journal of theAmerican Heart Association, the variant alphaCT11 showed a more robust injury-reducing effect than the original alphaCT1 even 20 minutes after theloss of blood flow that causes an ischemic heart attack.

Therefore, this keeps the injury to the heart muscle as limited and localised as possible.

Lead author of the study and VT Center for Heart and Reparative Medicine Research’s Fralin Biomedical Research Institute director Robert Gourdie said: “Cardiologists say that when a heart attack occurs, time is muscle.

“The problem is that the area of dying tissue is not quarantined.

“Damaged heart cells start to send out signals to otherwise healthy cells, and the injury becomes much bigger.

“AlphaCT11 seems to be even more effective than the original peptide in protecting hearts from ischemic injury similar to those occurring during a heart attack.

“AlphaCT11 could provide the basis for a new way to treat heart attacks and prevent the spread of damage that occurs immediately after a heart attack.”

Gourdie co-discovered alphaCT1 a decade ago and found it was responsible for controlling key channels related to the bystander affect, which is known to play a role in the spread of injury signals in situations like a heart attack.

In order to further understand the mechanism of action of alphaCT1, the VT team chemically altered it to create variants, including alphaCT11.

Gourdie and his team are planning to test alphaCT11 in live mice and then focus on a safe way to administer the compound to humans in preparation for clinical trials in patients who have suffered a heart attack.

AlphaCT1 is currently being studied in Phase III clinical trials for skin wound healing by a spin-out created by Gourdie and his co-discoverer Gautam Ghatnekarcalled FirstString Research.