Plaque volume is a quantitative metric, typically measured via advanced imaging techniques like Intravascular Ultrasound (IVUS) or Coronary Computed Tomography Angiography (CCTA), that represents the total spatial extent of atherosclerotic material accumulated within the lumen of an artery. This measurement is a direct, tangible indicator of the burden of cardiovascular disease and a critical prognostic factor for future cardiac events. Increased plaque volume signifies chronic endothelial injury and lipid deposition, processes often exacerbated by hormonal imbalances, insulin resistance, and systemic inflammation. Reducing this volume is a primary clinical goal in longevity and cardiovascular health management.
Origin
The concept of quantifying plaque burden evolved from early pathological and angiographic studies that merely assessed the degree of stenosis. The clinical utility of volume quantification emerged with the development of high-resolution, cross-sectional imaging, allowing for a more accurate, three-dimensional assessment of the disease process. This metric shifted the clinical focus from just the narrowest point of the artery to the total disease burden.
Mechanism
Plaque formation is initiated by endothelial dysfunction, which allows oxidized lipoproteins to accumulate in the sub-endothelial space, triggering a localized inflammatory response. Macrophages engulf these lipids, becoming foam cells, which aggregate to form the atherosclerotic plaque. Hormonal factors, such as low estrogen in post-menopausal women or low testosterone in men, can accelerate this process by promoting dyslipidemia and chronic vascular inflammation. Plaque volume increases as more smooth muscle cells migrate and a fibrous cap forms over the lipid core.
Hormonal optimization can halt cardiovascular damage progression and restore vascular function by targeting its root metabolic and inflammatory causes.
Concurrent hormone and peptide use may alter atherosclerosis by modulating the interplay of vascular inflammation, metabolic health, and cellular repair.
Testosterone therapy's cardiovascular implications differ by sex, with men facing specific risks at higher doses while women's lower-dose therapy shows less established cardiac impact.
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