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Study raises hopes for aortic stenosis sufferers

A molecule that causes inflammation plays a key role in the development of a heart valve disease called aortic stenosis, new research shows. The findings, published in the journal Circulation, suggest that anti-inflammatory medicines could be used to slow the progress of the c...

A molecule that causes inflammation plays a key role in the development of a heart valve disease called aortic stenosis, new research shows. The findings, published in the journal Circulation, suggest that anti-inflammatory medicines could be used to slow the progress of the condition. When blood flows from the heart to the aorta (the major blood vessel leading from the heart to the rest of the body), it must pass through the aortic valve. Aortic stenosis arises when this valve does not open fully, effectively decreasing the blood flow from the heart. It is the most common disease of the heart valves. The condition is most common among the elderly, where a build-up of calcium deposits narrows the valve. However, some people are born with the problem and others develop the condition following a bout of rheumatic fever. It is more common in men than women. Symptoms of aortic stenosis include breathlessness, chest pain, fainting and weakness, and heart palpitations. Currently the only treatment is surgery to replace the diseased valve. If left untreated, the prognosis for patients who have developed symptoms is poor. The race is therefore on to find drugs that could slow or even halt the progress of the disease. Aortic stenosis shares many features in common with atherosclerosis (in which the arteries become calcified). However, although statins are good at treating atherosclerosis, tests have shown that they are not effective at preventing the calcification of the aortic valve. In this study, researchers from Karolinska Institutet in Sweden investigated the underlying causes of another hallmark of aortic stenosis, namely inflammation. They were particularly interested in the role of inflammatory substances called leukotrienes. They studied in great detail the heart valves of 68 people (including both aortic stenosis patients and people with other conditions) whose aortic valves had been removed during surgery. Their analyses allowed them to differentiate between healthy, thickened and calcified areas of the valve. The team found that high levels of leukotrienes were produced in thickened tissue, and even higher levels were found in calcified tissue. The most serious inflammation was also seen in patients whose valves appeared narrowest on ultrasound. Furthermore, studies of cell cultures demonstrated that leukotrienes stimulate the calcification of heart valve cells. 'In summary, we provide evidence that [leukotriene]-synthesizing enzymes are upregulated in thickened tissue from stenotic aortic valves and that their local expression levels correlate significantly with severity of stenosis,' the researchers write. Associate Professor Magnus Bäck of the Karolinska Institutet's Department of Medicine, who led the research team, commented: '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.'For more information, please visit: Karolinska Institute:http://ki.se Circulation:http://circ.ahajournals.org

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