Scientists have identified a new drug that can dramatically reduce heart muscle damage after a heart attack and may lead to significantly improved patient outcomes.
Researchers at University of New South Wales say that pre-clinical trials have shown that the drug, known as Dz13, specifically targets and neutralises the gene responsible for inflammation and muscle death in the aftermath of a heart attack.
The drug also reduces incidental cell and tissue death resulting from life-saving interventions such as balloon angioplasty and stent placements used to open blocked arteries, or from the delivery of clot-busting drugs.
Significantly, the drug protects the heart's pumping action and dramatically improves the patient's chances of a full recovery after a heart attack.
"While this drug doesn't prevent the heart attack, it does reduce the damaging effects of the blockage on the heart once it's happened," said lead investigator Professor Levon Khachigian.
"It's a targeted therapy that can be used to complement other procedures and improve chances of a normal recovery," he said.
Khachigian said that the heart muscle suffers damage at two distinct times during a heart attack- first when the initial blockage occurs causing the chest pain and second, when the patient undergoes a "revascularisation" intervention, such as angioplasty or stenting, to reopen the blocked artery.
"At both these times a range of potentially damaging coordinated molecular responses kick in. We have been able to develop a drug to silence a disease-triggering gene. The drug improves heart function, regardless of whether it's administered at the time of the heart attack, or at the time of the revascularisation process," he said.
"This drug not only structurally reduces heart attack size but it protects heart muscle function. Both those things in combination improve outcomes and give hope to patients," said Dr Ravinay Bhindi, a co-author of the study.
Safety trials of Dz13 are underway, ahead of Phase 1 human trials.
The findings of the study will be published in an upcoming issue of high-impact cardiovascular journal Arteriosclerosis, Thrombosis and Vascular Biology.