Almost every drug on the market for heart disease targets cholesterol. So it was major news on Aug. 27 when a group of cardiologists from around the world announced they’d discovered a drug that reduces inflammation—and currently used to treat juvenile arthritis—successfully prevented heart attacks, strokes, and other kinds of cardiac death in a recent trial.
The drug is called canakinumab and sold under the brand name Ilaris by the Swiss company Novartis, which funded the study. It works to treat juvenile arthritis by reducing the number of inflammatory chemicals in the blood called interleukin-1β.
The new study, published in the New England Journal of Medicine, involved over 10,000 patients living in 39 countries who were at a higher risk of heart disease. Each had a history of heart attacks and high levels of interleukin-1β in their blood; 40% of the patients also had diabetes. Patients were randomly put in four groups and received either a placebo, 50 milligrams, 150 milligrams, or 300 milligrams of canakinumab every two weeks of the first month, and then once every three months through an injection for up to four years after.
Throughout the study, researchers also kept track of heart attacks, strokes, and death resulting from heart failure. By the end of the study, there were just over 1,400 reported incidents of these events; the patients receiving the highest dose of canakinumab had 14% fewer of them than the placebo group.
For years, cholesterol was thought to be the hormonal villain associated with heart disease. The idea was that it would clog up arteries by clumping against the sides of blood vessels, making it impossible for blood to squeeze through. Doctors were hugely excited when cholesterol-lowering statins were invented back in 1994; these drugs are now prescribed to tens of thousands of Americans with the hope that they will keep heart disease at bay.
But lowering cholesterol doesn’t seem to prevent heart disease in every patient. So now experts believe high interleukin-1β blood levels can also be responsible for raising heart attack risk. The general thinking is that these inflammatory chemicals end up preventing the heart from healing from damage from previous heart heart attacks. This extra stiffening and swelling may put an extra strain on it in the future, too.
Interleukin-1β isn’t all bad; we need it to survive injury or other infections. The chemical works by forcing damaged tissue to swell up with extra fluid from blood vessels, in order to isolate potential pathogens before they make their way all over the body. But interleukin-1β tends to be a little trigger-happy, and can sometimes cause inflammatory reactions that are more harmful than helpful, especially in certain chronic diseases like arthritis, and now, possibly, heart disease.
Interestingly, different results from the same trial suggesting that this therapy may even work to extend the lives of patients living with lung cancer were published in a paper the same day in The Lancet. That said, Barnett Kramer, the director of the Division of Cancer Prevention at the National Cancer Institute who was not associated with the work, told the Washington Post that these effects may be coincidental.
The drug itself is not likely to be a miracle cure. In both papers, those taking canakinumab were at a higher risk of dying from infections—suggesting that there are risks associated with decreasing the body’s immune response. Canakinumab is also really expensive: a year’s supply for heart disease treatment would cost $64,000. But, this trial opens the door for future treatments for patients for whom controlling cholesterol isn’t enough to improve heart health.