The pattern of ripples above is a telltale sign of a broken heart. Or at least a sign that a transplanted heart is being rejected by its host. This cross-section of a blood vessel illustrates a condition called chronic allograft vasculopathy (CAV), a major factor limiting long-term survival following heart transplants. The recipient’s immune system has reacted to the new heart, or allograft. The reaction has ultimately changed—and damaged—blood vessels in the transplanted organ.
CAV manifests as thickening of the vessel walls, which eventually reduces blood flow. The thickening is due to the formation of concentric lesions, which consist of smooth muscle cells, fibroblasts, immune cells and extracellular matrix deposits, as shown here. Collagen—the major component of scar tissue—is stained pink.
“This is a representative image of blood vessel structural changes that occur in CAV,” says Nathalie Accart-Gris, who works in Analytical Sciences and Imaging at the Novartis Institutes for BioMedical Research (NIBR). “At this stage of the rejection process, we can clearly see concentric collagen layers around the center of the vessel.”
Accart-Gris and her colleagues in NIBR’s Autoimmunity, Transplantation & Inflammatory Disease group use images such as this cross-section to study the chronic rejection process in animal models. They are evaluating possible therapeutic strategies to prevent the development of CAV and prolong graft survival.