Similar to how protein clumps build up in the brain in people with some neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, protein clumps appear to accumulate in the diseased hearts of mice and people with heart failure, according to a team led by Johns Hopkins University researchers.

In experiments described in the May 11 issue of the journal Circulation Research, the investigators report identifying in diseased hearts the form of the protein that tends to clump, and visualizing it in the heart using a noninvasive positron emission tomography (PET) scan could, they say, lead to advances in monitoring disease progression and testing new therapies.

Heart failure is a chronic condition in which the heart doesn't fill or pump blood as well as it should, leading to excessive fatigue. About 5.7 million people in the U.S. have heart failure, and about half of people diagnosed will die within five years, according to the U.S. Centers for Disease Control and Prevention.
"From a molecular standpoint there's not a unified, clear mechanism for why the heart goes into failure," says Giulio Agnetti, Ph.D., assistant professor of medicine at the Johns Hopkins University School of Medicine and University of Bologna. "But by figuring out this mechanism, we may be able to devise better treatments and diagnostic tools."

Current drugs used to treat heart failure -- such as those that lower blood pressure by relaxing blood vessels -- reduce stress on the heart and symptoms associated with heart failure without necessarily fixing the underlying cause. Once the heart fails to pump, the only treatment in the end is a heart transplant.

Previous work by this team, published in 2014, showed that the protein desmin accumulates in clumps called amyloid in the hearts of dogs with heart failure. Desmin is a protein found in the cell's "skeleton," or supporting structure, and is known as intermediate filaments. Why it clumps in diseased heart cells isn't known, Agnetti says.

To see if desmin protein clumps are also found in human heart failure, the researchers studied the proteins from heart tissue biopsies from people with or without heart failure. They used a fluorescent antibody commonly used in Alzheimer's disease research and a new fluorescent stain for amyloid developed by Agnetti to visualize and quantify the desmin protein clumps. They observed twice as many desmin clumps in heart failure patients than those without heart failure.

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