RESUMO
Withdrawal of oral estrogen therapy is associated with a deterioration in endothelial function in postmenopausal women with coronary artery disease. Our data also suggest that withdrawal of estrogen results in enhanced hyperemic flow, although this observation will require validation with further study.
Assuntos
Doença das Coronárias/fisiopatologia , Endotélio Vascular/efeitos dos fármacos , Estradiol/sangue , Terapia de Reposição de Estrogênios , Estrogênios Conjugados (USP)/farmacologia , Pós-Menopausa/sangue , Síndrome de Abstinência a Substâncias/fisiopatologia , Administração Oral , Idoso , Artéria Braquial/diagnóstico por imagem , Artéria Braquial/efeitos dos fármacos , Artéria Braquial/fisiologia , Endotélio Vascular/diagnóstico por imagem , Endotélio Vascular/fisiologia , Feminino , Nível de Saúde , Humanos , Nitroglicerina/farmacologia , Pós-Menopausa/fisiologia , Síndrome de Abstinência a Substâncias/diagnóstico por imagem , Ultrassonografia , Vasodilatação/efeitos dos fármacos , Vasodilatadores/farmacologiaRESUMO
We studied endothelial function using the brachial artery ultrasound model in 100 subjects from the Armed Forces Regression Study, a placebo-controlled, angiographic regression trial in subjects with normal or modestly elevated low-density lipoprotein (LDL) cholesterol and low levels of high-density lipoprotein (HDL) cholesterol treated for 30 months with gemfibrozil and (if necessary) niacin and/or cholestyramine to raise HDL by 25% and lower LDL to < 110 mg/dl. Although the treatment group had highly significant improvements in LDL and HDL cholesterol, there was no difference between the 2 groups in flow-mediated dilation (treatment vs control 6.9 +/- 6.5% vs 6.3 +/- 7.3%) or nitroglycerin-induced dilation (12.4 +/- 9.6% vs 11.9 +/- 7.4%, all p = NS). Treatment and control subjects without a history of hypertension had flow-mediated dilation similar to that of a normal reference population (10.6 +/- 8.3% vs 8.4 +/- 4.5%), whereas subjects with a history of systemic hypertension had markedly impaired flow-mediated dilation that was not significantly improved with treatment (treatment vs control, 6.0 +/- 5.5% vs 4.3 +/- 5.9%, p = 0.2). Thus, nonhypertensive subjects with angiographic coronary disease and low HDL cholesterol had normal endothelial function in the brachial artery model. Patients with a history of hypertension had marked endothelial dysfunction despite blood pressure treated to normal levels, and this dysfunction is not attenuated by pharmacologic therapy for dyslipidemia.
