How hardened arteries cause heart attacks

Coronary heart disease (CHD) is the leading cause of death in Australia. However, many people don't know they have the disease until they have angina or a heart attack.

In 2018, an average of two people died of CHD each hour. That’s 48 Australians every single day.

It’s a tricky disease and you may not know that you’re living with growing plaque buildup in the walls of your coronary arteries because you have no symptoms.

An international team of scientists recently reported that 11 genes contribute to the hardening of the heart’s arteries – and eight of those genes had not previously been identified.

One of the study’s authors, Professor Jason Kovacic, CEO and Director of the Victor Chang Cardiac Research Institute, says understanding the biological mechanisms is important for future treatment.

“Coronary heart disease … is the biggest driver of heart attacks, so if we can get in early and stop its progression in the first place, we could save tens of thousands of lives each year,” he said.

Coronary arteries harden because of the build-up of calcium, which can take place over many years. It is caused by fatty plaque which eventually hardens (or calcifies), causing the arteries to narrow.

This can affect the heart’s ability to pump blood to move oxygen and nutrients around the body. If a piece of the calcified plaque breaks off, it can cause a heart attack.

The new study, of 35,000 people, is the largest yet conducted to understand the genetic basis of coronary artery calcification. Unlike many medical studies, it contained a large proportion of participants of non-Caucasian backgrounds, including 8,867 individuals of African ancestry.

The team identified 11 genes, eight of which were new, and the role they played in coronary artery calcification.

The study also confirmed that another gene called PHACTR1 plays a big role in the calcification process.

PHACTR1 is known to be a major driver of SCAD heart attacks. These happen when an inner layer of one of the blood vessels in the heart tears and blood seeps between the artery layers forming a blockage causing angina, heart attack, abnormalities in heart rhythm, or sudden death.

It is also a driver in fibromuscular dysplasia, which affects more than one in 20 Australian women.

The study findings mean scientists can work to develop drugs or repurpose existing ones that can target the genes or encode proteins to reduce calcification, before heart disease can take hold.

That could be a game-changer for treating a disease responsible for more than 17 million deaths annually around the world.