July 24, 2009 A new drug that targets a master disease-causing gene can dramatically reduce heart muscle damage after a heart attack and may lead to significantly improved patient outcomes, UNSW researchers have shown.
The drug, known as Dz13, specifically targets and neutralises the gene responsible for inflammation and muscle death in the aftermath of a heart attack, preclinical trials have found.
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 heart’s pumping action is protected by the drug, dramatically improving 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, from UNSW’s Centre for Vascular Research.
“It’s a targeted therapy that can be used to complement other procedures and improve chances of a normal recovery,” he said.
The heart muscle suffers damage at two distinct times during a heart attack, Professor Khachigian said: 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,” he said.
“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."
Co-author on the study, interventional cardiologist Dr Ravinay Bhindi from Royal North Shore Hospital, said the technique represents an important potential advance in the treatment of heart disease, which is Australia’s number one killer.
“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,” Dr Bhindi said.
Safety trials of Dz13 are now underway ahead of Phase 1 human trials. A paper outlining the animal study appears this month in the cardiovascular journal Arteriosclerosis, Thrombosis and Vascular Biology.
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