New Insights into Molecular Mechanisms and Radiomics in Non-Contrast CT for Aortic Dissection: A Case Report and Literature Review

Abstract

Background: Computed tomography (CT) angiography is widely regarded as the gold standard for diagnosing acute aortic dissection. However, in patients with contraindications to iodinated contrast media, such as those with renal insufficiency or hemodynamic instability, non-contrast CT may offer a viable alternative for initial evaluation. Understanding the molecular mechanisms underlying aortic dissection, including extracellular matrix degradation, smooth muscle cell apoptosis, and inflammatory pathways, is crucial for developing novel diagnostic and therapeutic approaches. This report describes a single case of acute Stanford type A aortic dissection initially detected on non-contrast CT. Case Presentation: We describe a 74-year-old man who presented to the emergency department with fever and suspected infection, but without chest pain. An incidental finding on non-contrast CT revealed ascending aortic dilatation, pericardial effusion, and a suspected intimal flap. Subsequent CT angiography confirmed a Stanford type A aortic dissection. Conclusions: This case highlights the potential value of non-contrast CT in the early detection of aortic dissection, particularly when CT angiography cannot be performed. Recent advances in artificial intelligence (AI) and radiomic analysis have shown promise in augmenting the diagnostic capabilities of non-contrast CT by identifying subtle imaging features that may correlate with underlying molecular pathology and elude human observers. Emerging evidence suggests that radiomic features may reflect molecular alterations in the aortic wall, including metalloproteinase activity, collagen degradation, and inflammatory cell infiltration. Incorporating AI-assisted interpretation alongside insights into molecular mechanisms could facilitate earlier diagnosis, improve risk stratification, and guide personalized treatment strategies in critically ill patients. Although non-contrast CT has limited sensitivity for aortic dissection, it may still reveal crucial findings in selected cases and should be considered when contrast-enhanced imaging is not feasible. Ongoing progress in AI, radiomics, and molecular biomarker research may further expand the clinical applications of non-contrast CT in emergency cardiovascular care and bridge the gap between imaging phenotypes and molecular endotypes. These findings are hypothesis-generating and require validation in larger cohorts before clinical generalization.

Keywords: aortic dissection; computed tomography angiography; intima flap; non-contrast computed tomography.

Figure 1

Computed tomography (CT) findings of Stanford type A aortic dissection in this patient. (A,B) Axial non-contrast CT images at different levels of the ascending aorta demonstrate marked aortic dilatation and an obvious intimal flap (red arrowheads) with associated high-attenuation density, consistent with acute dissection. Hounsfield unit (HU) values of both the suspected inner membrane (HU up to 70–80). (C) The presence of the intimal flap is further confirmed by contrast-enhanced CT angiography (red arrowheads). (D) An axial CT slice reveals massive fluid accumulation in the pericardial space (yellow arrowheads), compatible with hemopericardium. (E,F) Sagittal reconstructions from both non-contrast CT (E) and contrast-enhanced CT angiography (F) show the extent of ascending aortic dilation and the eccentric intimal flap (red arrowheads) coursing along the aortic wall.

Figure 2

Prior surveillance axial non-contrast CT images and CTA images for ascending aortic aneurysm. (A) Image obtained two years prior and (B) five years prior demonstrate progressive ascending aortic dilatation over time. No obvious high-attenuation calcification intimal flap or signs of acute aortic pathology were noted at either time point. Retrospective review revealed mild dilatation at the aortic root (yellow arrowheads).

Figure 3

Aortic dissection pathogenesis. Injured vascular smooth muscle cells secrete chemokines, promoting inflammatory cell infiltration into the aortic wall, including T lymphocytes and monocytes. Activated dendritic cells release chemotactic mediators that recruit macrophages and CD4⁺ T cells. These immune cells secrete proinflammatory cytokines, resulting in elastic fiber fragmentation and medial degeneration. Imbalance between proteases and their inhibitors enhances proteolytic activity, impairing extracellular matrix remodeling. The TGF-β signaling pathway regulates cell proliferation, apoptosis, and matrix homeostasis through the Smad2/3-Smad4 complex, while its noncanonical pathways (ROCK and MAPK) also participate in aortic aneurysm progression and dissection pathogenesis, ultimately leading to structural deterioration of the aortic wall. (Figure 3 is an original schematic based on published literature).