Newborns with life-threatening congenital heart disease often undergo open-heart surgery with cardiopulmonary bypass, which carries a risk of damaging the brain. Critically ill newborns who are placed on ECMO are at even higher risk for brain injury. Hypothermia, or cooling the body, can improve neurologic outcomes, but has limitations.
A new study in a large animal model suggests that adding a dash of hydrogen to the usual mix of respiratory gases could further protect babies’ brains.
the heart is fully formed, the cells that make up heart muscle, known as cardiomyocytes,
have very limited ability to reproduce themselves. After a heart attack, cardiomyocytes
die off; unable to make new ones, the heart instead forms scar tissue. Over
time, this can set people up for heart failure.
New work published last week in Nature Communications advances the possibility of reviving the heart’s regenerative capacities using microRNAs — small molecules that regulate gene function and are abundant in developing hearts.
In 2013, Da-Zhi Wang, PhD, a cardiology researcher at Boston Children’s Hospital and a professor of pediatrics of Harvard Medical School, identified a family of microRNAs called miR-17-92 that regulates proliferation of cardiomyocytes. In new work, his team shows two family members, miR-19a and miR-19b, to be particularly potent and potentially good candidates for treating heart attack.
Scientists around the world have been trying to replace damaged heart tissue using lab-made heart-muscle cells, either injecting them into the heart or applying patches laced with the cells. But results to date have been underwhelming.
“If you make cardiomyocytes in a dish from pluripotent stem cells, they will engraft in the heart and form muscle,” says William Pu, MD, director of Basic and Translational Cardiovascular Research at Boston Children’s Hospital. “But the muscle doesn’t work very well because the myocytes are stuck in an immature stage.” …
While engineered heart tissues can replicate muscle contraction and electrical activity in a dish, many aspects of heart disease can only adequately be captured in 3D. In a report published online yesterday by Nature Biomedical Engineering, researchers describe a scale model of a heart ventricle, built to replicate the chamber’s architecture, physiology and contractions. Cardiac researchers at Boston Children’s Hospital think it could help them find treatments for congenital heart diseases. …
For decades, cardiac researcher James McCully, PhD, has been spellbound by the idea of using mitochondria, the “batteries” of the body’s cells, as a therapy to boost heart function. Finally, a clinical trial at Boston Children’s Hospital is bringing his vision — a therapy called mitochondrial transplantation — to life.
Mitochondria, small structures inside all of our cells, synthesize the essential energy that our cells need to function. In the field of cardiac surgery, a well-known condition called ischemia often damages mitochondria and its mitochondrial DNA inside the heart’s muscle cells, causing the heart to weaken and pump blood less efficiently. Ischemia, a condition of reduced or restricted blood flow, can be caused by congenital heart defects, coronary artery disease and cardiac arrest.
For the smallest and most vulnerable patients who are born with severe heart defects, a heart-lung bypass machine called extracorporeal membrane oxygenation (ECMO) can help restore blood flow and oxygenation to the heart. But even after blood flow has returned, the mitochondria and their DNA remain damaged.
“In the very young and the very old, especially, their hearts are not able to bounce back,” says McCully.
Ischemia can be fatal for the tiniest patients
After cardiac arrest, for instance, a child’s mortality rate jumps to above 40 percent because of ischemia’s effects on mitochondria. If a child’s heart is too weak to function without the support of ECMO, his or her risk of dying increases each additional day spent connected to the machine.
But what if healthy mitochondria could come to the rescue and replace the damaged ones? …
Pulmonary vein stenosis (PVS) is a rare disease in which abnormal cells build up inside the veins responsible for carrying oxygen-rich blood from the lungs to the heart. It restricts blood flow through these vessels, eventually sealing them off entirely if left untreated. Typically affecting young children, the most severe form of PVS progresses very quickly and can cause death within a matter of months after diagnosis.
Until recently, treatment options have been limited to keeping the pulmonary veins open through catheterization or surgery. Yet this approach only removes the cells but does nothing to prevent their regrowth. Now, a clinical trial shows that adding chemotherapy to a treatment regimen including catheterization and surgery can deter abnormal cellular growth and finally give children with PVS a chance to grow up.
“Through this approach, we’ve created the first-ever population of survivors who are living with severe PVS,” saysChristina Ireland, RN, MS, FNP, who has managed enrolling patients in the trial and treating new patients since the trial ended. “We’ve changed this disease from an acute killer to a chronic, manageable condition.” …
Children can be at risk for compromised breathing after surgery or from conditions like asthma, congestive heart failure or sleep apnea. Opioid therapy and sedation for medical procedures can also depress breathing. Unless a child is sick enough to have a breathing tube, respiratory problems can be difficult to detect early. Yet early detection can mean the difference between life and death.
“There is currently no real-time objective measure,” says Viviane Nasr, MD, an anesthesiologist with Boston Children’s Hospital’s Division of Cardiac Anesthesia. “Instead, respiratory assessment relies on oximetry data, a late indicator of respiratory decline, and on subjective clinical assessment.”
A new device, recently cleared by the FDA for children 1 year and older in medical settings, provides an easy, noninvasive way to tell how much air the lungs are receiving in real time. It can signal problems as much as 15-30 minutes before standard pulse oximetry picks up low blood oxygenation, according to one study. …
Everything from food aspiration to an asthma attack to heart failure can cause a patient to die from asphyxia, or lack of oxygen. For more than a decade, the Translational Research Laboratory (TRL) of Boston Children’s Hospital’s Heart Center has been pursuing a dream: tiny, oxygen-filled bubbles that can be safely injected directly into the blood, resuscitating patients who can’t breathe.
The lab’s first generation of bubbles were made with a fatty acid, but the lipid shells weren’t stable enough for long-term storage or clinical use. The bubbles popped open too easily. …
Soft robotic actuators, which are pneumatic artificial muscles designed and programmed to perform lifelike motions, have recently emerged as an attractive alternative to more rigid components that have conventionally been used in biomedical devices. In fact, earlier this year, a Boston Children’s Hospital team revealed a proof-of-concept soft robotic sleeve that could support the function of a failing heart.
Despite this promising innovation, the team recognized that many pediatric heart patients have more one-sided congenital heart conditions. These patients are not experiencing failure of the entire heart — instead, congenital conditions have caused disease in either the heart’s right or left ventricle, but not both.
“We set out to develop new technology that would help one diseased ventricle, when the patient is in isolated left or right heart failure, pull blood into the chamber and then effectively pump it into the circulatory system,” says Nikolay Vasilyev, MD, a researcher in cardiac surgery at Boston Children’s.
Now, Vasilyev and his collaborators — researchers from Boston Children’s, the Harvard John A. Paulson School of Engineering and Applied Sciences and the Wyss Institute for Biologically Inspired Engineering at Harvard University — have revealed their soft robotic solution. They describe their system in a paper published online in Science Robotics today. …
Placed near the heart, the device can potentially predict life-threatening cardiac arrest in critically ill heart patients, according to tests in animal models. The technology was developed through a collaboration between Boston Children’s Hospital and device maker Pendar Technologies (Cambridge, Mass.).
“With current technologies, we cannot predict when a patient’s heart will stop,” says John Kheir, MD, of Boston Children’s Heart Center, who co-led the study. “We can examine heart function on the echocardiogram and measure blood pressure, but until the last second, the heart can compensate quite well for low oxygen conditions. Once cardiac arrest occurs, its consequences can be life-long, even when patients recover.”
In critically ill patients with compromised circulation or breathing, oxygen delivery is often impaired. The new device measures, in real time, whether enough oxygen is reaching the mitochondria, the organelles that provide cells with energy. …