Mitral Valve Endocardiosis (MVE) Research
R(D)SVS University of Edinburgh, Scotland & Department of Anatomy, University College Galway, Ireland
MVE is the single most important acquired cardiac disease in dogs and is probably the single most important disease of any type in the Cavalier King Charles Spaniel. We know a lot about this disease and over the years there have been major advances in our understanding of how this disease presents, how it affects heart function, how it affects quality of life and survival and how it can be managed medically. We also know a reasonable amount about what happens to the heart valve of affected dogs but we know nothing about why it occurs.

Research strategies in the past have concentrated on increasing our understanding of the clinical aspects of this disease, improving treatment with new approaches and drugs, and attempting to develop breeding strategies to reduce the disease incidence. While these have all been valuable developments they do not provide information on the fundamental underlying cause of the disease.

We are pursuing an alternative research approach in which we will use powerful molecular biology tools in an attempt to explain what is happening to the valves at the cellular level. We suspect the reason dogs develop MVE is because a cell type, known as a valvular interstitial cell, within the valve structure is malfunctioning and failing to produce normal structural components. These components are crucial to maintaining the valves structural rigidity, its shape and function, and so prevent it from leaking.

The work is being carried out at the University of Edinburgh in collaboration with University College Galway. The study is looking at the structure and appearance of the valve cells using electron microscopy, thereby enabling us to characterise the differences between normal and abnormal cells. In conjunction with that work we are setting up the procedures that will hopefully enable us to isolate normal and abnormal cells and grow them in culture. This will allow us to carry out more detailed and specific investigation of the function of these cells in a controlled laboratory environment. For example, we will be able to monitor the biochemical reactions going on within the cell and determine if there are particular biochemical pathways that are not functioning normally. Such abnormalities might then be amenable to drug therapy. Furthermore, we will be able to check gene function in the cells, and if differences between normal and abnormal cells can be detected, this would open a wide area of research that could lead to genetic testing and therapy.

However, the immediate aim of our studies is to first prove these cells are abnormal, in what way they are abnormal and why they are abnormal. Such work in itself will require significant research input. Whether or not this work leads on to development of new treatments, or new methods of detecting the disease before damage had occurred, or genetic testing and gene therapy, remains to be seen, but the consensus among veterinary cardiologists is that effort should be directed at trying to find the cause of MVE, and we believe we have a research strategy that will help us achieve that aim.
Dr B M Corcoran
Head Cardiopulmonary Service
University of Edinburgh
22"' March 2002
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