Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen deficiency in the postmenopausal woman results in numerous symptomatic and asymptomatic manifestations, including vasomotor symptoms, osteoporosis, heart disease, bladder and vaginal symptoms, and cardiovascular disease. Estrogen replacement therapy is associated with amelioration of these problems but has attendant risks. A newer class of drugs, the selective estrogen receptor modulators, provides both estrogen agonist and antagonist properties, depending on the target tissue. This article discusses the mechanism by which selective estrogen receptor modulators may vary in their end-organ effects and reviews the clinical studies associated with these compounds. Phytoestrogens are widely used in the United States, but little information is available regarding their potential long-term effects.
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PMID:Selective estrogen receptor modulators and phytoestrogens: new therapies for the postmenopausal women. 1037 37

Cardiovascular disease (CVD), and in particular coronary artery heart disease (CAHD), is the leading cause of morbidity and mortality in women. Until recently, most of our knowledge about the pathophysiology of CVD in women - and, subsequently, management guidelines - were based on studies conducted mostly in men. While similar mechanisms operate to induce CVD in women and men, gender-related differences exist in the anatomy and physiology of the myocardium, and sex hormones modify the course of disease in women. Women, more than men, have their initial manifestation of CAHD as angina pectoris; are likely to be referred for diagnostic tests at a more advanced stage of disease, and are less likely than men to have corrective invasive procedures. The overall morbidity and mortality following the initial ischaemic heart event is worse in women, and the case fatality rate is greater in women than in men. Also, the relative impact of impaired vasoreactivity of the coronary artery, increased viscosity of the blood and dysregulation of automaticity and arrhythmia, is greater in women than in men. The most effective means of decreasing the impact of CVD on women's health is by an active approach from childhood to proper principles of healthcare in order to modify the contribution of specific risk factors. The latter include obesity, abnormal plasma lipid profile, hypertension, diabetes mellitus, cigarette smoking, sedentary lifestyle, increased blood viscosity, augmented platelet aggregability, stress and autonomic imbalance. The use of lipid-lowering drugs has not been adequately studied in women but reports from studies conducted mostly in men do predict an advantage also to women. Oestrogen deficiency after spontaneous or medically induced menopause is an important risk factor for CVD and CAHD. Observational and mechanistic data suggest a role for oestrogen replacement after menopause for primary, and possibly secondary, prevention of CVD. However, two recent prospective trials suggest that treatment de novo with hormone replacement of older post-menopausal women after an acute coronary event may not confer cardiovascular protection and may increase the risk of thromboembolic disease. Results of ongoing long-term studies may determine the beneficial role of hormone replacement versus potential risks involved with this treatment.
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PMID:Update on cardiovascular disease in post-menopausal women. 1209 66

1. Oestrogen deficiency causes progressive reduction in endothelial function. Despite the benefits of hormone-replacement therapy (HRT) evident in earlier epidemiological studies, recent randomized trials of HRT for the prevention of heart disease found no overall benefit. Instead, HRT users had higher incidences of stroke and heart attack. Most women discontinue HRT because of its many side-effects and/or the increased risk of breast and uterine cancer. This has contributed to the development of selective oestrogen receptor modulators (SERMs), such as tamoxifen and raloxifene, as alternative oestrogenic agents. 2. A SERM is a molecule that binds with high affinity to oestrogen receptors but has tissue-specific effects distinct from oestrogen, acting as an oestrogen agonist in some tissues and as an antagonist in others. Clinical and animal studies suggest multiple cardiovascular effects of SERMs. For example, raloxifene lowers serum levels of cholesterol and homocysteine, attenuates oxidation of low-density lipoprotein, inhibits endothelial-leucocyte interaction, improves endothelial function and reduces vascular smooth muscle tone. 3. Available evidence suggests that raloxifene and tamoxifen are capable of acting directly on both endothelial cells and the underlying vascular smooth muscle cells and cause a multitude of favourable modifications of the vascular wall, which jointly contribute to improved local blood flow. The outcome of the Raloxifene Use for the Heart (RUTH) trial will determine whether raloxifene, currently approved for the treatment of post-menopausal osteoporosis, could substitute for HRT in alleviating cardiovascular symptoms in post-menopausal women.
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PMID:Raloxifene, tamoxifen and vascular tone. 1760 May 63