Australian researchers have demonstrated how a single injection of HDL cholesterol could stop heart cells dying following a heart attack.

Australian scientists believe HDL cholesterol has the potential to significantly reduce the the number of people who die prematurely of heart failure caused by heart attack.

A pre-clinical trial conducted at the Baker Heart & Diabetes Institute demonstrated a single injection of the 'good' cholesterol administered to mice in the hours immediately after a heart attack stopped heart cells and tissue dying and improved heart function.

The HDL works by increasing glucose uptake in the heart muscle, says lead researcher Professor Bronwyn Kingwell.

She says it's critical the heart has access to glucose in the early stages of a heart attack to ensure the survival of heart cells.

"Basically the heart cells are starved of oxygen and glucose when the heart attack is happening and this HDL is a way to get the glucose into the cells and stops them from dying," explained Prof Kingwell.

"In a nutshell what we're doing is preserving heart cells in the context of a heart attack and minimising heart damage so that the heart functions better and then doesn't deteriorate to heart failure."

The findings are published in journal Science Translational Medicine and builds on a previous finding in 2009 that showed HDL modulated glucose metabolism in skeletal muscle.

While there has been significant development of drugs over the past few decades to reduce cardiovascular disease such as the introduction of statins to clinical practice, Prof Kingwell says there are few therapeutic options to reduce the impact of heart attack.

Currently when a person having a heart attack presents to hospital they are taken straight up to a cardiac catheter lab and their coronary arteries are opened with a balloon angioplasty. This provides a window of opportunity to deliver a drug like HDL, says Prof Kingwell.

What makes this discovery "exciting" is that there are already HDL preparations available, Prof Kingwell.