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Scientists discover gout drugs can help prevent heart attacks

A recent discovery by Sydney’s Heart Research Institute has suggested that heart attacks could be prevented by simple commonly available drug.

A cheap, commonly available drug used to treat gout could help heart attack survivors live longer healthier lives, say Australian researchers at Sydney’s Heart Research Institute.

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A study by the Heart Research Institute, published today in the highly regarded Journal of the American Heart Association, has revealed that an anti-inflammatory medication used to treat gout and combat arthritis also improves the heart health of people who have suffered a heart attack or other major heart event.

The discovery paves the way for a new treatment regime that may protect thousands of Australian heart patients from future attacks that could either kill them or further damage their already impaired hearts.

The researchers, led by Dr Sanjay Patel, says they have proved that the widely available drug is both safe and profoundly effective in reducing local cardiac inflammation.

The discovery was made during an investigation into new treatment for acute coronary syndrome, a sudden and life-threatening condition in which the coronary blood vessel is blocked, triggering a heart attack or severe chest pain associated with unstable angina.

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The condition, most commonly caused by atherosclerosis (thickened arteries) is often diagnosed on the operating table after a major heart trauma.

Dr Patel hypothesised that the drug colchicine, with its anti-inflammatory qualities, could combat the inflammation that plays a strong role in cardiovascular disease.

HRI collaborated with researchers from Royal Prince Alfred Hospital, the University of Sydney, Catholic University School of Medicine, Santiago, the Paris-Cardiovascular Research Centre and the University of Cambridge to test out the hypothesis in 83 patients.

Two doses of the drug were given the day before a coronary angiogram, a common procedure to investigate the state of a patient’s heart vessels. When the angiogram was carried out the researchers tested levels of key inflammatory cytokines, substances that drive inflammation and disease progression.

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“Patients with acute coronary syndrome will have higher levels of these cytokines that work to trigger the dangerous inflammation around the heart,” Dr Patel says. “We discovered that colchicine has a striking ability to suppress the release of these cytokines, effectively stopping inflammation in its tracks.”

Specifically, researchers saw a rapid and significant drop in levels of interleukin-1 and interleukin-18 within the coronary arteries, as well as a drop in interleukin-6, a key downstream cytokine strongly associated with artery-thickening inflammation.

Exactly how colchicine inhibits the production of inflammatory cytokines is not completely understood but the team believes the drug works by blocking the NLRP3 inflammasome, a protein complex within immune cells responsible for the production of active IL-1 and IL-18.

This is the first time the effects of colchicine on cardiac cytokine release have been studied in humans or animals, making the findings all the more important.

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“The next step will be to prove clinical effect through rigorous multi-centre clinical trials,” says Dr Patel. “If it works we have a cheap yet potent treatment with very important therapeutic implications for heart patients.”

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