08:26pm Monday 25 September 2017

Inflammation behind heart valve disease

Magnus Bäck Photo: Ulf Sirborn

Aortic stenosis is the most common heart valve disease, which is caused by calcium deposits and a narrowing of the aortic valve. This is typically seen in the elderly, but can also be caused by a congenital defect. Aortic stenosis is currently treated by surgical replacement of the diseased valve, but research is on-going for identifying medicines which can delay the progress of the disease.

In a new study presented in the scientific journal Circulation, researchers from Karolinska Institutet show that specific pathways of inflammation are important underlying factors in the development of aortic stenosis.

By studying heart valves from patients undergoing surgery for various valve diseases, the researchers have shown that immune cells and a group of inflammatory substances called leukotrienes can be found in calcified heart valves. The most significant inflammation was seen in patients with the narrowest valves on ultrasound examination. The researchers have also shown in cell cultures that leukotrienes stimulate the calcification of heart valve cells.

There are similarities between atherosclerosis (calcification of the arteries) and aortic stenosis. However, lipid-lowering medicines known as statins which are capable of preventing atherosclerosis have proved ineffective in preventing calcification of the aortic valve.

 

“The results suggest that anti-inflammatory medication could be a future treatment for aortic stenosis, and it would mean a lot to these patients, most of whom are elderly, if we could slow the disease to the extent that they do not need surgery”, says associate professor and cardiologist Magnus Bäck, one of the researchers behind the study.

Publication:

Nagy E, Andersson DC, Caidahl K, Eriksson MJ, Eriksson P, Franco-Cereceda A, Hansson GK and Bäck M

Upregulation of the 5-lipoxygenase pathway in human aortic valves correlates with severity of stenosis and leads to leukotriene-induced effects on valvular myofibroblasts

Circulation 14 mars 2011

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