Thrombo-inflammation as a missing variable in thoracic aortic intervention timing: toward a biology-informed threshold.

Aortic dissection and aneurysm have long been framed as mechanical failures of a degenerating wall. A growing body of evidence suggests that they may also reflect a shared thrombo-inflammatory process, in which coagulation and innate immunity are increasingly proposed to contribute actively to wall destruction rather than merely to indicate it. This review synthesizes that shift across the dissection and aneurysm spectrum. We first delineate the core machinery, including tissue-factor-driven coagulation, platelet and leukocyte interactions, neutrophil extracellular traps, inflammasome signaling, and complement activation. We, then connect these mediators to the proteolytic and phenotypic events that remodel the aortic wall: matrix metalloproteinase activation, elastin and collagen degradation, smooth muscle cell phenotype switching, apoptosis, and ferroptosis. We contrast disease-specific biology, the acute thrombo-inflammatory storm and false-lumen dynamics of dissection against the intraluminal thrombus and complement consumption that characterize aneurysm. A dedicated section examines the endothelial interface on which these processes depend, integrating junctional integrity, membrane-channel function, and cyclic-nucleotide microdomain regulation as the permissive substrate linking a compromised barrier to leukocyte engagement and maladaptive remodeling. We evaluate candidate circulating biomarkers, reinterpret endovascular therapy through a thrombo-inflammatory lens by addressing post-implantation inflammatory responses and false-lumen thrombosis, and outline how multi-omics and computational integration of the inflammatory, remodeling, and endothelial axis may refine preoperative risk assessment. The aim of our study is a mechanistically coherent framework connecting molecular drivers to clinical strategy.