Stephen Spurgin still remembers the first time he peered through the microscope at pulmonary artery cells starved of their natural rhythm. As a researcher at UT Southwestern (UTSW), he was unraveling a mystery that has long haunted pediatric cardiology: why children born with single-ventricle hearts—though saved by the Glenn procedure—often develop fragile, malformed lung blood vessels years later. The answer, his team discovered, lies not just in anatomy but in motion. Pulsatile blood flow, that rhythmic surge once thought to be a mere byproduct of a beating heart, is in fact a vital signal that keeps lung vessels strong and structured.
For decades, the Glenn procedure—a surgical rerouting of blood flow directly from the superior vena cava to the lungs—has been a cornerstone of care for infants with complex congenital heart defects. It bypasses the heart’s missing or underdeveloped ventricle, allowing oxygenation to continue. But in doing so, it eliminates the pulse in pulmonary circulation. Clinicians noticed a troubling pattern: many patients later developed pulmonary vascular disease, marked by thinning vessel walls and poor cellular communication. What remained unclear was why.
Spurgin and his colleagues at UTSW pieced together the puzzle using a three-pronged approach. They analyzed clinical data from pediatric patients, studied human pulmonary artery cells grown in the lab, and tested their findings in animal models. The results were consistent: pulsatile flow activates molecular signals—particularly in the TGF-β pathway—that maintain the integrity of blood vessel walls. Without that rhythmic push, those signals dim, cells lose their structural cues, and vessels begin to deteriorate.
The implications are profound. This study, published in JCI Insight (2026), suggests that the mechanical force of pulsation is not passive plumbing but active biology. It’s a revelation that could reshape how surgeons and engineers think about heart-lung support systems. For the roughly 1,500 children in the U.S. who undergo the Glenn procedure each year, the future might include devices that reintroduce controlled pulsatility, preserving lung health long before complications arise.
"We’ve been treating blood flow like a steady stream," said Dr. Mary Leonard, a pediatric cardiologist not involved in the study, "but the body clearly reads it as a message—one we’ve been silencing." The UTSW team is now collaborating with bioengineers to design pulsatility-enhancing modifications to existing shunts and assist devices. While still in early development, the goal is clear: to give these children not just longer lives, but healthier ones. As research moves from the lab to the clinic, the pulse—once lost—may soon be restored.