Heart failure is a global pandemic affecting more than 64 million people worldwide. It is a debilitating disease with a greater than 50% mortality within 5 years and few effective treatments.

It has been known for many years that failing hearts switch their ‘fuel source’ from burning fats for energy to increasing their use of glucose. New research, led by Professor Mike Shattock from the School of Cardiovascular Medicine & Sciences, has found that this switch in fuel utilisation can be triggered by simply increasing sodium levels in the cardiac muscle cell.

In the study, researchers from London, Glasgow, Dundee, Birmingham and Texas, have shown that whether this elevation of sodium is induced acutely by drugs, or more long-term by heart failure or genetic mutation, they share a common ‘metabolic fingerprint’ shifting the energy supply away from fatty acids towards the use of other energy sources.

These findings provide unique insights not only into the mechanisms behind heart failure, but also identify potential novel therapeutic targets.

The research suggests that in a healthy heart this change in fuel supply can be switched on and off by simply changing the sodium concentration inside the cell. If this process is truly reversible, researchers hope that developing drugs that lower the sodium elevation in failing hearts will not only treat the electrical and contractile problems but may also improve their energy supply.

Read the paper published in Nature Communications.