Innovative Heart Failure Discovery: Heart Failure’s Effects in Cells May be Reversed Via Rest

Our hearts might not be so different from our skeletal muscles after all. Researchers at the Imperial College London  have found that structural changes in heart muscle cells after heart failure can be reversed by allowing the heart to rest. Findings from a study conducted on rats published today in the European Journal of Heart Failure show that the condition’s effects on heart muscle cells are not permanent, as has conventionally been believed by scientists and physicians. The discovery could open the door to new treatment strategies and procedures.

Heart failure means the heart can no longer pump enough blood to meet your body’s needs. It is commonly the result of a heart attack; it can occur with other disorders; or it can occur as a result of simply aging. Around 750,000 people in Britain are living with heart failure and it is estimated that it affects nearly 5 million Americans. Severe heart failure carries a substantial risk of death within one year, which is worse than the prognosis associated with most cancers. Clearly we need new heart failure treatments and preventive measures.

In 2006, researchers at Imperial College led by Professor Magdi Yacoub showed that in some individuals resting the heart using an LVAD (Left Ventricular Assist Device) fitted for a limited time can help the heart muscle to recover. The LVAD is a small pump that boosts the function of the heart and reduces strain on the left ventricle, the most important pumping chamber of our heart. The new study is a major step in understanding the mechanisms for improving muscle recovery at the level of heart muscle cells.

The Imperial researchers studied whether “unloading” the demands on heart muscle cells can reverse the changes and damage that occurs during heart failure in rats.

“If you injure a muscle in your leg, you rest it and this allows it to recover,” said Dr Cesare Terracciano, from the National Heart and Lung Institute (NHLI) at Imperial, who supervised the study. “The heart can’t afford to rest – it has to keep beating continuously. LVADs reduce the load on the heart while maintaining the supply of blood to the body, and this seems to help the heart recover. We wanted to see what unloading does to heart muscle cells, to see how this works.”

Researchers transplanted a failing heart from one rat into another rat alongside that rat’s healthy heart, so that it received blood but did not have to pump. After the heart was able to rest, several changes in heart structure that impair heart contraction were reversed in the damaged heart.

“This is the first demonstration that this important form of remodelling of heart muscle cells induced by heart failure is reversible,” said Michael Ibrahim, also from the NHLI at Imperial, who conducted the research for his PhD funded by the British Heart Foundation. “If we can discover the molecular mechanisms for these changes, it might be possible to induce recovery without a serious procedure like having an LVAD implanted.”

The most profound cellular effects observed in this study concerned structures called t-tubules. These allow electrical signals to travel deep into the muscle cells so that all of the fibers contract simultaneously. T-tubules become sparse and irregular after heart failure. Unloading the heart led to the t-tubules returning to normal.

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