This thesis investigates how extracellular matrix architecture determines the mechanical behavior of vascular tissue, with a focus on collagen organization in the arterial wall. Using high-resolution optical microscopy and atomic force microscopy (AFM), it quantifies microstructural and biomechanical changes in healthy and diseased tissue. The findings show that loss of collagen network organization, rather than collagen quantity alone, drives mechanical weakening in aneurysmal tissue, while crosslinking contributes to plaque stability. The work also demonstrates that immune-cell mediated matrix remodeling is a key mechanism in disease progression and a relevant target for future interventions.