Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible role of oestrogens in modifying the occurrence of ischaemic heart disease and cardiovascular disease (CVD) in general in postmenopausal women has long been controversial. Analysis of the literature indicates a difference between the epidemiological studies published before 1980 and those published recently. In the former, the risk in women using oestrogen replacement therapy (ERT) was either unchanged or increased when compared with those women who did not use ERT. In the latter the trend has changed and a clear protective effect of ERT has been shown. These contradictory results might be explained by a change in prescribing habits, using lower oestrogen doses and selecting women with no risk factor for CVD as candidates for long-term ERT.
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PMID:[Estrogens and cardiovascular risk in postmenopausal women. I. Epidemiologic data]. 214 74

The possible role played by oestrogens in modifying the occurrence of ischaemic heart disease (IHD) in particular and cardiovascular disease (CVD) in general in post-menopausal women has long been controversial. Analysis of the literature reveals a difference between the findings of epidemiological studies published before 1980 and those published more recently. In the former, it was reported that the risk in women using oestrogen replacement therapy (ERT) either remained unchanged or increased in relation to that in non-users. In the latter, the trend changed and ERT was shown to have a definite protective effect. These contradictory results might be explained by a change in prescribing habits, involving the use of lower oestrogen doses and the selection of women with no CVD risk factors as recipients of long-term ERT. The protective effects of ERT have been attributed to metabolic changes induced by oestrogens, namely the increase in high density lipoprotein (HDL) cholesterol observed after oral therapy. Recently, long-term studies using non-oral oestrogens delivered either by implant, or the percutaneous or transdermal routes have indicated the same favourable changes in lipid profiles as seen with oral ERT, provided follow-up is maintained for at least 6 mth. Factors other than lipids that are involved in CVD should also be evaluated in order to clarify the mechanism via which ERT affords cardiovascular protection in post-menopausal women.
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PMID:Oestrogen replacement therapy and cardiovascular disease in post-menopausal women. A review. 269 14

Estrogens are known as potent mammary mitogen substances and are the major stimulus for the growth of hormone-dependent tumors and clearly implicated in the pathogenesis of breast cancer. Therefore it is a general belief that hormone replacement therapy (HRT) after breast cancer will increase the risk of developing recurrences, though there are no clear data available to support this suggestion. No prospective study with a large number of patients and a long treatment period was performed concerning this issue. On the other hand it may not be justifiable to withhold hormone replacement therapy from low-risk patients after menopause, knowing the benefits of this therapy concerning osteoporosis and cardiovascular advantages. Nevertheless, until appropriate clinical trials help to resolve this problem, non hormonal alternatives constitute the standard of care. One possible approach is to treat menopausal women who have had breast cancer symptomatically and avoid ERT unless absolutely necessary. The risk of cardiovascular diseases can be reduced with lifestyle. Tamoxifen has a beneficial effect on serum lipids and the intake for 5 years leads to a 50% reduction in the incidence of fatal myocardial infarction and a decrease in morbidity associated with ischaemic heart disease. Low doses of progestogen is effective for menopausal hot flushes. Tibolone reduces vasomotoric symptoms such as hot flushes and offers benefit on osteoporosis and has shown a significant reduction in high-density lipoprotein cholesterol. Whether replacing of estrogens is safe for patients after breast cancer remains uncertain. There is a need for a large controlled clinical trial to evaluate the safety and advantages of long time estrogen replacement in women treated for breast cancer.
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PMID:Estrogen replacement therapy in women with a history of breast cancer. 1046 73

Review oral modified release drug forms of beta-adrenoblocker metoprolol which is used in arterial hypertension and ischemic heart disease is presented. Metoprolol has salts such as tartrate which is used for production of immediate release (IR) and sustained release (SR) forms and succinate used for production of controlled release form (CR/XL). Metoprolol SR has monolith matrix type, metoprolol CR/XL-system of multiple pellets. Effect of metoprolol tartrate (IR) on mortality was demonstrated in a number of studies in patients with arterial hypertension (AH) (MAPHY), myocardial infarction (SMT, GMT, MIAMI), dilated cardiomyopathy and heart failure (MDC). Studies of efficacy of metoprolol SR are scarce. Antihypertensive efficacy of metoprolol SR in patients with AH did not exceed that of a metoprolol IR or CR/XL. First retrospective analysis of efficacy of metoprolol tartrate and succinate (CR/XL) in patients after myocardial infarction allowed to obtain comparable results of 34% mortality lowering. In a prospective study in patients with chronic heart failure (COMET) metoprolol tartrate IR was not superior to carvedilol when mortality lowering was concerned. At the same time administration of controlled release metoprolol (CR/XL) in 2 large clinical trials (RESOLVD, MERITAHF) was advantageous in patients with chronic heart failure relative to lowering of mortality and rate of hospitalizations. A novel controlled release form of metoprolol has been created as a tartrate salt on the basis of pellet technology (CD/ERT) and its bioequivalence to metoprolol CR/XL has been proved.
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PMID:[Evolution of oral drug forms of metoprolol: advantages of long acting modified release forms with modified release]. 2159 98