Effects of estrogen on the vascular wall: vasomotor function and inflammation
2002; Oxford University Press; Volume: 55; Issue: 4 Linguagem: Inglês
10.1016/s0008-6363(02)00487-x
ISSN1755-3245
Autores Tópico(s)Atherosclerosis and Cardiovascular Diseases
Resumoly diseased arteries and coronary mortality may not just be related to the number of arteries with 70% or greater Far from being only an anatomic barrier to prevent the stenosis, but may also be tied to the amount of minor influx of circulating blood into the vessel wall, the plaque disease in other vessels [7].These observations endothelium is a metabolically active organ system that have driven a search for other mechanisms, including the maintains vascular homeostasis.The endothelium modu-potential association of endothelial dysfunction and associlates vascular tone, regulates local cellular growth and the ated inflammation with plaque rupture, and the activation deposition of the extracellular matrix, protects the vessel of platelets and coagulation with thrombus formation.from the potentially harmful consequences of substances Advances in research in this area are particularly and cells circulating in the blood, and mediates the relevant to the health of older women, since cardiovascular hemostatic, inflammatory, and reparative responses to local disease (CVD) results in more deaths in women in the injury.Nitric oxide (NO) produced by the endothelium United States than any other disease.Several prospective, plays a pivotal role in maintaining vascular health and observational studies have suggested that postmenopausal protecting against vascular injury.women who do not have documented cardiovascular Conditions such as hypercholesterolemia [1], systemic disease and who take estrogen replacement therapy (ERT) hypertension [1], and estrogen deficiency [2] have been or hormone replacement therapy (HRT-estrogen plus a associated with impaired functions of the endothelium.As progestin) have a reduced risk of major coronary events a result of impairment, the vessel wall may promote compared with untreated women [8-10].In contrast, the inflammation, oxidation of lipoproteins, smooth muscle Heart and Estrogen / progestin Replacement Study (HERS) cell proliferation, extracellular matrix deposition or lysis,[11], a randomized controlled trial among older women accumulation of lipid-rich material, the activation of with established heart disease, found an increased risk of platelets (which promote clotting), and thrombus forma-cardiovascular events in the first year of treatment in this tion.All of these consequences of endothelial dysfunction at-risk cohort.This result, in part, has led the American may contribute to the development and clinical expressionHeart Association [12] to advise against the initiation of of atherosclerosis and coronary heart disease [3,4].HRT for the secondary prevention of CVD, or for the sole This hypothesis is supported by serial angiographic purpose of the primary prevention of CVD until the results studies carried out before and after a myocardial infarction, of ongoing randomized trials are reported and analyzed.which indicate that the underlying plaque responsible forThe potential atheroprotective effects of estrogen have unstable angina and myocardial infarction usually produces been attributed principally to the hormone's effects on an arterial narrowing of less than 50% before the acute serum lipid concentrations [13,14].However, estrogenevent [5,6].Indeed, a recent angiographic study suggests induced alterations in serum lipids account for only that the positive correlation between the number of severe-approximately one-third of the observed reduction in risk of mortality from CVD among ERT or HRT users [15].
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