Led by University College London professors Juan Pablo Casas, Aroon Hingorani, and Daniel Swerdlow, the researchers sought to better understand the connection between inflammation and atherosclerosis, the buildup of fatty deposits on artery walls that causes the disease.
Specifically, the researchers focused on a signaling protein in the blood called the interleukin-6 receptor. They found that it increased inflammatory response -- until now, no one had identified an inflammatory agent responsible for the disease -- and that an existing anti-inflammatory drug was able to act on it.
"This study provides robust evidence that IL6R is implicated in coronary heart disease," said study co-author Brendan Keating. "Furthermore, our analysis showed that an existing anti-inflammatory drug, acting on this receptor, may offer a new potential approach for preventing CHD."
A companion study, also released today, found that a genetic variant in the IL6R gene reduces inflammation and subsequently lowers the risk of heart disease.
By analyzing more than 40 existing studies involving 133,500 participants from the U.S. and Europe with an array of tools (among them, Keating's IBC Human CVD BeadChip, nicknamed the "Cardiochip"), the scientists found that one type of DNA sequence variation -- a single-nucleotide polymorphism known as gene variant rs8192284 -- altered several biological markers associated with inflammation.
Their results were similar to those found in trials of tocilizumab, an anti-inflammatory drug currently used to treat the inflammation of rheumatoid arthritis.
In other works, participants carrying this gene variant had a lower risk of coronary heart disease -- and an IL6R-blocking drug like tocilizumab may help people who don't have the variant achieve similar results.
The next step: actually conducting the clinical trials to prove that anti-inflammatory drugs prevent heart disease.
Both studies were published online at The Lancet, a website of scientific journals.