Inflammation and cardiovascular research

For most of the twentieth century, heart attacks were explained mainly as a plumbing problem: cholesterol built up in the artery walls until blood could no longer flow. That picture is still partly true, but research since the 1980s has added an important piece. Atherosclerosis, the disease behind most heart attacks and strokes, is also a chronic inflammatory disease.

A note on this domain: ceric.se was once used by a Stockholm research centre for inflammation and cardiovascular disease. This site is an independent information site and has no connection to that centre or to any university. Old links to the centre's research pages lead here. For current research, see the websites of the universities and research groups themselves.

Atherosclerosis as inflammation

When LDL cholesterol gets trapped in the wall of an artery, it is modified and treated by the immune system as something foreign. White blood cells called monocytes move into the wall, turn into macrophages and swallow the cholesterol. Over time they become so-called foam cells, the core of a plaque. T cells and other immune cells join in, and the inflamed area releases signalling molecules that keep the process going.

In 1999, the American pathologist Russell Ross summed up decades of work in a widely cited article with the title "Atherosclerosis: an inflammatory disease". Inflammation also helps explain why plaques sometimes rupture: an inflamed plaque has a thinner, weaker cap, and when it breaks a blood clot can form and block the artery.

Lipid mediators and the immune response

Swedish researchers played a central role in discovering the lipid signalling molecules that control inflammation. Prostaglandins and leukotrienes, studied intensively at Karolinska Institutet, were recognised with the Nobel Prize in Physiology or Medicine in 1982. Later work showed that these molecules are active in the artery wall, and that the body also produces substances that help inflammation resolve.

From theory to treatment

For a long time it was unclear whether treating inflammation itself would prevent heart attacks. Two lines of research changed that:

• CRP studies showed that people with slightly raised levels of the inflammation marker CRP have a higher risk of cardiovascular events, even when their cholesterol is normal. Read more in CRP and inflammation.
• Clinical trials tested anti-inflammatory drugs. In the CANTOS trial, published in 2017, an antibody that blocks the inflammatory signal interleukin-1 beta reduced repeat cardiovascular events. Later trials found that low-dose colchicine, an old drug for gout, lowered the risk in people with heart disease, and it has since been approved for this use in some countries.

Inflammatory diseases and the heart

The link also works the other way. People with chronic inflammatory diseases such as rheumatoid arthritis, psoriasis or inflammatory bowel disease have a higher risk of heart disease. Good control of the underlying disease, together with attention to blood pressure, cholesterol and smoking, is part of protecting the heart.

What it means for you

Most of the inflammation-related risk can be influenced by familiar measures: not smoking, regular physical activity, a healthy weight and an anti-inflammatory diet. Statins, the most common cholesterol-lowering drugs, also have anti-inflammatory effects. Specific anti-inflammatory drugs for heart disease are prescribed by specialists for selected patients.