Testosterone and atherosclerosis.

摘要: Abstract Hypoandrogenemia in men and hyperandrogenemia women are associated with increased risk of coronary artery disease but also visceral obesity, insulin resistance, low high-density lipoprotein (HDL) cholesterol, elevated triglycerides, low-density (LDL) cholesterol plasminogen activator inhibitor (PAI-1). These gender differences confounders render the precise role endogenous androgens atherosclerosis unclear. Exogenous androgens, on other hand, induce both apparently beneficial deleterious effects cardiovascular factors by decreasing serum levels HDL-C, PAI-1 (apparently deleterious), Lp(a), fibrinogen, insulin, leptin fat mass beneficial) as well women. However, androgen-induced declines circulating HDL-C should not automatically be assumed to pro-atherogenic, since it may reflect accelerated reverse transport instead. Short-term application supraphysiological doses exogenous T can reduce severity frequency angina pectoris improve electrocardiographic signs myocardial ischaemia; long-term have been investigated. Nonetheless, interpretations pharmacological arterial compliance flow-mediated dilatation particular must treated circumspection because at physiological concentrations, beneficial, neutral, detrimental vascular reactivity observed. Testosterone exerts ‘pro-atherogenic’ macrophage function facilitating uptake modified lipoproteins an ‘anti-atherogenic’ effect stimulating efflux cellular HDL. In majority animal experiments, testosterone exerted neutral or development atherosclerosis. conclusion, overall administration cardiovascular-disease is difficult assess such extraordinary array vivo. When dealing a complex multifactorial condition CAD, premature assume that clinical benefits derived from manipulation sex steroid milieu – even when these assumptions based biologically plausible mechanisms or, indeed, cross-sectional risk-factor observational data. Neither needs therapeutic use restricted concerns regarding side effects.