Steven Weiss is working on a drug that will reduce
the amount of cellular damage heart attacks
cause.
Image: Belinda Pratten

It is a rapid way to die.

First the heart lurches into a strange rhythm and stops pumping. The flow of blood around the body is halted.

Consciousness shuts down at the 15 second mark. After three minutes the brain starts to die. Another ten minutes and the body has followed suit.

Then that’s it. You’re gone.

Sudden cardiac arrest – heart attack – is part of a group of conditions called Ischaemic heart disease (IHD), where blood supply to the heart muscle is restricted. This is the single largest cause of death in Australia, and in most Western nations. In 2006, year of the most recent snapshot from the Australian Bureau of Statistics, more than 22,000 Australians lost their lives due to IHD.

Many more suffer a heart attack and survive, but must live with reduced heart, brain and body function because of the damage done.

Dr Steven Weiss is developing a new use for a known drug that could prevent the abnormal heart rhythms that arise from heart attacks, and reduce the amount of cellular damage such rhythms and heart attacks cause.

Weiss is working towards his second PhD, this time at the John Curtin School of Medical Research (JCSMR). His credentials in developing medical instruments, patents and financial management helped him win $25,000 as part of Innovation ANU – a new program established to support research commercialisation at the University.

“During a heart attack you get a blockage or a spasm in an artery that supplies the heart muscle with blood and oxygen,” Weiss explains. “The heart cells on the other side of the blockage don’t receive any oxygen. They become what’s called ‘hypoxic’.”

In the 1990s, Dr David Saint working with Professor Peter Gage at JCSMR discovered that hypoxic cells admit more sodium than normal ones. Weiss hypothesised in 1994 that during a heart attack, cells becoming hypoxic can admit sufficient sodium to cause the heart to beat more rapidly and irregularly (arrhythmia), potentially leading to cardiac arrest. “That’s when the patient falls over, loses consciousness and dies,” Weiss says.

He says too much sodium entering a cell can also reverse the normal sodium-calcium exchange process, leading to an excess of calcium being admitted. This can cause more arrhythmia and calcification – a cellular death sentence.

Weiss believes an existing pharmaceutical compound can be used to block the sodium overflow from occurring in hypoxic cells, which means that irregular beating is reduced and cells on the wrong side of a blockage remain viable for longer. For people experiencing a heart attack, this would mean less damage to overcome once normal heart function is restored, and a reduced risk of arrhythmia in future.

This drug, which can’t be named until further progress is made, could potentially be offered to two patient groups: people who are in the throes of a heart attack or undergoing heart surgery, known as the acute group; and a chronic group including people who are at risk of heart arrhythmia, including those who have survived an attack.

Weiss says if the treatment is successful in clinical trials, it could help millions of people and generate billions of dollars. To this end he is setting up a company called Neoviva partnering with Saint, who made the initial discovery about sodium admittance in hypoxic cells.

Getting to market could be up to a decade down the road – a timescale that might deter the weak hearted. But not Weiss.

“I persist because every type of experiment I throw at it, the drug comes out with startlingly beneficial results,” he says. “I’m in it for the long haul.”