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updated by
Christopher Spry
2 May 2014

University of London, St. George's Hospital Medical School

The Chair of Cardiovascular Immunology

Held by: Prof. Christopher J.F. Spry MA DPhil FRCP FRCPath FESC


(1) why, and how the inner part of the heart may become severely damaged in some patients with a blood disease called eosinophilia (their heart disease is called endomyocardial fibrosis or EMF) and

(2) the cause of another disease, which is not associated with a blood disorder but which results in a widespread failure of the heart muscle to work properly. This second type of heart disease is called dilated cardiomyopathy or DCM.We have found that EMF is caused by an alteration in one of the blood cells called the eosinophil. Most people have very few of these in their blood, but they can increase in number. It is not the total number of eosinophils that is important in the development of their heart disease, but the fact that they have been stimulated to become activated. Activated eosinophils have a vastly greater capacity to cause heart damage. We have developed some special methods to assess this and in the last year we have shown how activation comes about, using some sophisticated laboratory measurements on patients’ eosinophil. We are now looking closer at why activation occurs in only some patients, and how this might be prevented.The cause, or causes of DCM has proved rather more difficult to define. We have tried hard to detect a change in the proteins that are used by heart cells to contract and enable the heart beat strongly. This does not’t happen in DCM so we suspected that some of the proteins might be abnormal. We are in the process of developing a number of very precise ways of detecting abnormalities in these proteins. So far we have had no luck in finding anything abnormal, but we have every hope that this approach will lead us to understanding more about this type of heart disease as it seldom improves on treatment even when it is detected early. We look after many patients with eosinophilia and various types of heart disease. It is therefore a pleasure to acknowledge publicly the fine support that all of them have given to our research programme by giving up their valuable time and allowing us to take extra samples of their blood, bone marrow and other tissues for this work.

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