An experimental treatment for heart patients has been found to change the scar tissue that pigs form after heart attacks. Although the extent of scarring remains the same, the structure changes, allowing greatly improved recovery in an animal considered an excellent proxy for humans for conditions like this.
Heart muscle is damaged in heart attacks, leading to the formation of scar tissue. As a result, even when people survive the attack, their capacity to pump blood can be reduced thereafter, helping make heart attacks the leading cause of death worldwide.
Existing medical responses rely on trying to restore blood flow, and therefore oxygen, to the heart as quickly as possible after an attack. This reduces scarring, but since attacks seldom strike where medical technology is close to hand, it often comes too late to prevent long-term harm. Heart failure occurs within a year of almost a quarter of patients' first attack.
Dr James Chong of the University of Sydney synthesised the growth factor rhPDGF-AB (naturally produced in small quantities by human platelets) and gave 36 pigs either a seven-day intravenous infusion, or a sham procedure. A month later, the pigs that received the growth factor had better heart function, and a 40 percent increase in survival rate, Chong reported in Science Translational Medicine.
Chong told IFLScience the team were initially surprised by the results, because while heart function was clearly improved, the volume of scar tissue hadn't changed. “So we thought if it is not quantity, maybe it is quality,” he said. Using advanced microscopy techniques the team found the control pigs' scar tissue had “chaotic and disorganized” collagen fibers. For the pigs that got the rhPDGF-AB, the fibers were aligned.
Although the team are not yet certain why the aligned scar tissue works so much better, Chong told IFLScience the thinking is that “it aids transmission of viable heart muscle on either side, and also assists blood vessel formation.” Together these allow the heart to go on performing relatively normally, even in the face of induced shocks.
The work was not a total surprise, since Chong's collaborators had found similar results in mice, but Chong said: “Regulatory bodies usually want evidence from a clinically relevant large animal” before allowing clinical trials in humans. Unlike mice, pigs' hearts are of similar size and beat rate to humans.
Moving to clinical trials will be expensive, and the university is seeking commercial partners, as well as needing to complete some specific safety tests before this can occur.
The major outstanding question, however, is how quickly after a heart attack occurs treatment needs to start to be effective. The pigs in the study received treatment that began immediately after induced attacks. Since that won't be possible with people, the delay time could prove the crucial factor.
