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My husband has congestive heart failure. The doctor says it is caused by his age, and that there is no treatment. I read about a new discovery that age-related heart failure can be reversed in mice. Could that help my husband?
There are different kinds of congestive heart failure, and there are effective treatments for many. Your husband may have a common kind called age-related diastolic dysfunction. There is no specific treatment that prevents or reverses this condition. But you are right that a remarkable treatment was recently reported for a similar condition in mice.
Congestive heart failure occurs when the heart cannot pump efficiently enough to meet the body’s need for blood. In a young, healthy heart, when blood enters the main pumping chambers (the ventricles), their walls stretch and the chambers expand to receive all the blood.
In age-related diastolic dysfunction, the heart muscle becomes thicker and stiffer. As a result, when blood enters the heart, the heart muscle can’t stretch enough to accept all the blood. The blood backs up into the lungs, causing breathing difficulty. Blood also backs up into the rest of the body, causing fatigue and swelling — particularly of the legs and feet.
We don’t know what causes age-related heart failure in humans, and because of that, we don’t know how to prevent or reverse it. A similar condition occurs in mice, and we may now have figured out how to treat it.
A group of my colleagues at Harvard Medical School conducted the research in mice that you read about. They were led by Dr. Richard Lee, co-editor-in-chief of the Harvard Heart Letter, and professor Amy Wagers.
Dr. Lee and Dr. Wager’s team joined the blood circulation of an old mouse to that of a young mouse. Suddenly, the arteries and veins of the two animals shared the same blood. After four weeks of a shared circulation, the thickened, stiff heart muscle of the old mouse became dramatically less thick and stiff. The experiment was repeated on many pairs of old and young mice, with the same results.
This indicated that some substance was present in the blood of the young mice that rejuvenated the heart muscle of the old mice. Most likely, that substance had been in the blood of the old mice when they were younger, but the substance had decreased as the mice aged.
The team then identified a substance, called GDF11, which was present at high levels in the blood of young mice but not old mice. They treated old mice with enough GDF11 to raise their blood levels of GDF11 to the same levels as it was present in young mice. Again, the thickened, stiff heart muscle of the old mice became thinner and more flexible.
This discovery in mice may one day lead to effective treatments to prevent or reverse this common type of heart failure in humans. Although it will take many more years of research to determine if this discovery will help us, recent advances in aging research gives me hope that it will.
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