( Researchers at the University of Leeds ...)Breakthrough for Treatment of Fatal Heart Condition,Health

Researchers at the University of Leeds have found a mechanism to prevent a potentially fatal heart condition that can strike without warning.

Dr Lezanne Ooi, a postdoctoral researcher in the Faculty of Biological Sciences, has found that the progression of cardiac hypertrophy can be halted by increasing one of the bodys naturally occurring proteins. This is a significant discovery because whilst the symptoms can be managed, the cause of heart hypertrophy cannot yet be treated. This research provides a first step in the search for a possible treatment. says Dr Ooi.

Cardiac hypertrophy is a relatively common condition often caused by high blood pressure, or can be the result of a genetic predisposition, resulting in an abnormal thickening of the heart muscle. It is known to affect 1 in 500 people in the UK and US and can lead to heart failure, arrhythmias and sudden death. The condition varies in its manifestation, with some people suffering severe symptoms such as breathlessness, fatigue and chest pain - and others being entirely asymptomatic. In those not displaying any symptoms, death can be its first presentation, therefore the scale of the problem is not fully known. It is also the most common cause of sudden cardiac death in athletes, as hypertrophic hearts are unable to cope with intense physical activity.

Dr Oois study is the first to identify the mechanism behind specific changes in protein levels that impact upon cardiac cell size. Levels of two proteins, known as ANP and BNP, are naturally higher in fetal hearts and the hearts of babies and children, but should drop as an individual matures. However, in adults with cardiac hypertrophy these levels increase to become abnormally high.

Dr Ooi has found that an increase in a third protein in the body, known as REST, can halt the rise of the proteins causing cardiac hypertrophy, which, for the first time, offers an approach to treating the cause of heart h
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