Stories about: heart failure

Seeking a way to keep organs young

Images of mouse hearts with fibrosis
These mouse hearts show differing levels of fibrosis (blue) resulting from cardiac stress. New Boston Children’s Hospital research suggests certain therapies could prevent or reduce fibrosis, like we see in the center and right images.

The wear and tear of life takes a cumulative toll on our bodies. Our organs gradually stiffen through fibrosis, which is a process that deposits tough collagen in our body tissue. Fibrosis happens little by little, each time we experience illness or injury. Eventually, this causes our health to decline.

“As we age, we typically accumulate more fibrosis and our organs become dysfunctional,” says Denisa Wagner, PhD, the Edwin Cohn Professor of Pediatrics in the Program in Cellular and Molecular Medicine and a member of the Division of Hematology/Oncology at Boston Children’s Hospital and Harvard Medical School.

Ironically, fibrosis can stem from our own immune system’s attempt to defend us during injury, stress-related illness, environmental factors and even common infections.

But a Boston Children’s team of scientists thinks preventative therapies could be on the horizon. A study by Wagner and her team, published recently by the Journal of Experimental Medicine, pinpoints a gene responsible for fibrosis and identifies some possible therapeutic solutions.

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Soft robot could aid failing hearts by mimicking healthy cardiac muscle

heart-failure

Every year, about 2,100 people receive heart transplants in the U.S., while 5.7 million suffer from heart failure. Given the scarcity of available donor hearts, clinicians and biomedical engineers from Boston Children’s Hospital and Harvard University have spent several years developing a mechanical alternative.

Their proof of concept is reported today in Science Translational Medicine: a soft robotic sleeve that is fitted around the heart, where it twists and compresses the heart’s chambers just like healthy cardiac muscle would do.

Heart failure occurs when one or both of the heart’s ventricles can no longer collect or pump blood effectively. Ventricular assist devices (VADs) are already used to sustain end-stage heart failure patients awaiting transplant, replacing the work of the ventricles through tubes that take blood out of the heart, send it through pumps or rotors and power it back into a patient’s bloodstream. But while VADs extend lives, they can cause complications.

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First six months of life are best for stimulating child heart growth

heart-regeneration-study2
In these sample sections of mouse heart, the color blue signifies scar tissue. Damage from scarring was minimized by early administration of the drug neuregulin.

Developing a child-centric approach to treating heart failure is no easy task. For one thing, the underlying causes of decreased cardiac function in children vastly differ from those in adults. While most adults with heart failure have suffered a heart attack, heart failure in children is more likely the result of congenital heart disease (CHD), or a structural defect present at birth that impairs heart function. And most therapies designed for adults haven’t proven equally effective in children.

Stimulating heart muscle cells to regenerate is one way cardiac researchers at Boston Children’s Hospital’s Translational Research Center hope to restore function to children’s ailing hearts. In this area, children actually have an advantage over adults: their young heart cells are better suited for regrowth.

Reporting in the April 1 Science Translational Medicine, Brian Polizzotti, PhD, and Bernhard Kuhn, MD, demonstrate that not only does the drug neuregulin trigger heart cell regeneration and improve overall heart function in newborn mice, but its effects are most potent for humans within the first six months of life.

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‘Heart on a chip’ suggests a surprising treatment for a rare genetic disease

heart chip BarthIt was the variability that intrigued pediatric cardiologist William Pu, MD, about his patient with heart failure. The boy suffered from a rare genetic mitochondrial disorder called Barth syndrome. While he ultimately needed a heart transplant, his heart function seemed to vary day-to-day, consistent with reports in the medical literature.

“Often patients present in infancy with severe heart failure, then in childhood it gets much better, and in the teen years, much worse,” says Pu, of the Cardiology Research Center at Boston Children’s Hospital. “This reversibility suggests that this is a disease we should really be able to fix.”

Though it needs much more testing, a potential fix may now be in sight for Barth syndrome, which has no specific treatment and also causes skeletal muscle weakness and low white-blood-cell counts. It’s taken the work of multiple labs collaborating across institutional lines.

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A regenerative approach to heart failure in children?

A heart muscle cell from an 8-year-old beginning the process of mitosis: The cell nucleus is preparing to divide. (Courtesy Bernhard Kühn)

For more than 100 years, people have been debating whether human hearts can grow after birth by generating new contractile muscle cells, known as cardiomyocytes. Recently, Bernhard Kühn, MD, at Boston Children’s Hospital and his colleagues added fuel to the debate—and hope for regenerative therapies for diseased hearts—with their findings that infants, children and adolescents are indeed capable of generating new cardiomyocytes.

Research in the 1930s and 1940s suggested that cardiomyocyte division may continue after birth, and recent investigations in zebrafish and newborn mice presented the possibility that some young animals can regenerate heart muscle through muscle cell division. Still, for many years, the accepted dogma among physicians and researchers was that human hearts grow after birth only through existing cells growing larger.

“This is a very sticky subject in cardiology,” says Kühn. Not only do long-held scientific beliefs die hard, but the ability to directly study heart cell growth in humans has been limited. “Healthy human hearts are hard to come by,” he says.

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Could nanotechnology improve treatment of heart attack and heart failure?

People who have had a heart attack or have coronary artery disease often sustain damage that weakens their heart. Milder forms of heart failure can be treated with medications, but advanced heart dysfunction requires surgery or heart transplant. A team of physicians, engineers and materials scientists at Children’s Hospital Boston and MIT offers two alternative ways to strengthen weakened, scarred heart tissue — both involving nanotechnology.

One approach blends nanotechnology with tissue engineering to create a heart patch laced with gold whose cells all beat in time – as shown in the above video.

The other uses minute nanoparticles that can find their way to dying heart tissue, carrying stem cells, growth factors, drugs and other therapeutic compounds.

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