Atherosclerosis pathophysiology describes the complex biological processes that lead to the hardening and narrowing of arteries due to the accumulation of lipid-rich plaques within the vessel walls. This chronic inflammatory process is initiated by endothelial dysfunction, often exacerbated by metabolic imbalances and hormonal shifts. The condition represents a critical nexus between lipid metabolism, inflammation, and vascular health, directly impacting longevity and vitality. Recognizing this underlying mechanism is essential for clinical practitioners aiming to mitigate cardiovascular risk in patients managing hormonal changes.
Origin
The term combines “athero,” derived from the Greek word for gruel or paste, referring to the soft, fatty material in the plaque, and “sclerosis,” meaning hardening. Pathophysiology is a compound term from Greek roots pathos (suffering/disease) and physis (nature/origin), denoting the functional changes associated with disease. The clinical understanding of this disease process has been refined over centuries, with modern endocrinology highlighting the role of insulin resistance and sex hormone decline in accelerating its progression.
Mechanism
The process begins with injury to the endothelial lining, which promotes the infiltration of low-density lipoproteins into the arterial intima. Macrophages engulf these lipids, transforming into foam cells that form the fatty streak, the earliest lesion. Chronic inflammation and smooth muscle cell migration contribute to the formation of a fibrous cap, creating an unstable plaque susceptible to rupture, leading to acute cardiovascular events. Hormones like estrogen and testosterone influence the inflammatory cascade and lipid profile, thus modulating the rate of atherosclerotic development.
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