By Clifton Leaf
August 28, 2017

There was a bit of breathlessness over a clinical trial report published this weekend in The New England Journal of Medicine and presented at the European Society of Cardiology Congress in Barcelona.

The trial, called CANTOS (for “Canakinumab Antiinflammatory Thrombosis Outcome Study”) investigated the use of a man-made antibody called canakinumab in patients who’d previously suffered a heart attack to see if that drug reduced the risk of future heart attacks and death. Canakinumab, which is made by Novartis and already approved by the FDA to treat a form of juvenile rheumatoid arthritis and other rare diseases, targets interleukin 1-beta, a protein involved in the process of inflammation.

What had the cardio world abuzz was that the CANTOS trial seemed to offer the first substantial evidence—and in a giant (10,061 patients), double-blind, randomized controlled trial to boot—that targeting inflammation alone (as opposed to lowering blood cholesterol and other fats) could reduce the risk of heart attack.

This is important because, despite our very good efforts over the past half-century to lower blood lipids (largely through the use of statins and changes in diet), heart disease remains the No. 1 killer in the U.S., and continues to claim millions of lives each year around the world.

Jolting the excitement factor, a separate report, published in The Lancet, looked at whether this same anti-inflammatory agent could lower the risk of lung cancer, too. (In that study, patients who received the highest tested dose of canakinumab, in fact, did appear to have a significant reduction in both lung cancer mortality and death from all cancers compared with the control group.)

The notion that the process of inflammation is involved in the development of human disease is a venerable one. In the case of cancer, a Scotsman named Sir Alexander Haddow introduced the idea in the early 1970s, suggesting that inflammation—a core process of wound healing—could go badly wrong, leading to tumor development in some cases. That theory was later resurrected by Harold Dvorak in a now-famous paper entitled, “Tumors: Wounds That Do Not Heal.”

In the case of heart disease, inflammation has been found to both increase atherosclerosis (the hardening and narrowing of blood vessels) as well as weaken plaque-lined tissue, which can then rupture. So doctors routinely look for blood markers of systemic inflammation—notably c-reactive protein—when evaluating cardiovascular health.

In the current New England Journal study, patients who received a 150-mg injection of canakinumab every three months had a 15% reduction in risk of having, um, a bad event. (The “primary end point” for the trial wasn’t one specific outcome, but rather a curious amalgam of three: a nonfatal heart attack, a nonfatal stroke, or a cardiovascular-related death.) Those getting the drug had 3.86 of these events per 100 person-years versus 4.50 for those in the placebo group.

But volunteers in the drug arm also had more fatal infections and, well, the drug is hellza-pricey, too. An accompanying editorial in the NEJM by Robert Harrington, a leading interventional cardiologist at Stanford Medicine, concluded: “…the modest absolute clinical benefit of canakinumab cannot justify its routine use in patients with previous myocardial infarction until we understand more about the efficacy and safety trade-offs and unless a price restructuring and formal cost-effectiveness evaluation supports it.”

And, importantly, there’s an awfully cheap, mostly safe (in the majority of people) alternative drug that has been brilliantly targeting inflammation for somewhere on the order of two millennia. It’s called aspirin. Study after study after study after study has shown it to be effective at lowering the risk for—get this—heart disease and cancer.

So why isn’t aspirin getting more buzz these days? It needs a better marketing department.

This essay appears in today’s edition of the Fortune Brainstorm Health Daily. Get it delivered straight to your inbox.

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