In atherosclerosis, inflammation and an overreacting immune system is involved - the same as in rheumatoid arthritis. When fat is stored in blood vessels and becomes rancid, the body tries to rid itself of the fat by calling in white corpuscles. But the reaction is often too powerful, so the inflammatory cells start to break down the walls of the vessels in the same way they break down joint cartilage and bone in rheumatoid arthritis.

A central role in inflammation in rheumatoid arthritis is played by a signal molecule called TNF-alpha. Heart scientist Stefan Jovinge can now show that TNF-alpha is also involved in atherosclerosis. His research team first developed a special breed of mice that was prone to develop this disease, whereupon they knocked out the gene for TNF-alpha and found that the mice developed less atherosclerosis. The same result was achieved by giving these atherosclerosis-conditioned mice a drug that impedes the effect of TNF in the body.

Working with rheumatology units in southern Sweden, rheumatologist Lennart Jacobsson at Malmö University Hospital has studied at the same time the use of new TNF-inhibiting drugs on patients with chronic rheumatic arthritis. In some 1,500 patients, the symptoms of the joint disorder were substantially alleviated, and at the same time the risk of coronary disease, which otherwise is higher among these patients, fell to nearly half.

The two research teams are now carrying on their collaboration. Already roughly a fifth of all patients with rheumatoid arthritis in Malmö are treated with a TNF inhibitor, and Stefan Jovinge hopes to be able to test the medicine on special groups of heart patients in about a year.

MEDICA.de; Source: Lund University