This term describes the pathological accumulation of cellular debris, lipids, calcium, and fibrin within the intima of medium and large arteries. Clinically, it represents a critical stage in the progression toward chronic vascular compromise. We observe this process as a measurable risk factor impacting long-term cardiovascular homeostasis. Understanding its genesis is key to modulating systemic wellness.
Origin
The term derives from Greek roots, ‘athere’ meaning gruel or porridge, referencing the soft, fatty core of the lesion, and ‘skleros’ meaning hard, referring to the fibrous cap that often forms over the lesion. Its origin is rooted in gross pathology observations of arterial disease progression. This accumulation process occurs within the subendothelial space of the arterial vasculature.
Mechanism
The initiation involves endothelial dysfunction, often influenced by metabolic or hormonal shifts, allowing for LDL particle infiltration. Macrophages subsequently engulf these lipids, transforming into foam cells, which form the fatty streak precursor. Over time, this lesion matures through smooth muscle cell migration and extracellular matrix deposition, resulting in a fibroatheroma that can narrow the vessel lumen.
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