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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The issue whether a postpartum woman should take oral contraceptives can be expressed as 3 questions: has she any contraindications? would the pill affect her coagulation, lactation or psychologic state? when should she start taking the pill? The same risks and contraindication apply to postpartum women as to any others: smoker age 35, hypertension, thrombophlebitis or thromboembolism, arterial vascular disease, heart disease, liver disease, estrogen-dependent tumors, hypertriglyceridemia, and previous non-compliance. While high-dose estrogens commonly given to block lactation do increase existing hypercoagulability in the immediate postpartum period, there is no evidence that current low-dose pills further increase blood clotting. Combined pills decrease milk production, and have been prescribed in the immediate postpartum to help inhibit lactation. Progestin-only pills and injectables do not compromise lactation. It is unknown whether oral contraceptives effect postpartum mood disorders. Low-dose oral contraceptives can be started immediately postpartum if the woman has no risk of thromboembolism. It is standard practice to start 3 weeks after delivery if she does not intend to breastfeed.
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PMID:Oral contraceptives in the puerperium. 167 22

5 major criteria are used to evaluate family planning methods: efficacy, both theoretical and practical; acceptability as measured by continuation of use; safety; reversibility; and cost, including the cost of treatment, follow-up, and screening for contraindications. Traditional family planning methods are mostly based on periodic abstinence during the presumed fertile period. The calendar, temperature, Billings or cervical mucus, and symptothermal methods are based on observation of different symptoms of ovulation and fertility. Their advantages are that they do not require intervention by health personnel, their costs of use are nil, and they are morally acceptable to some couples. Their efficacy is lower than that of other methods and they should be viewed as methods to space rather than limit births. The withdrawal method, also less effective, requires active cooperation by the male partner. Among mechanical methods, the use of condoms has increased recently because of the protection they offer against HIV infection and other sexually transmitted diseases. Their efficacy depends on correct use, regular use, and the quality of the condom. The Pearl index varies from 93099 per 100 woman-years. The diaphragm must be individually measured and should be used with spermicides. The Pearl index ranges from 85095 per 100 woman-years. Spermicides, generally either nonoxynol-9 or benzalkonium chloride, are surfactants that have a Pearl index of 83-97 per 100 woman-years. They are available as creams, jellies, foams, suppositories, tablets, or impregnated sponges. Most failures appear due to errors of utilization. The mechanism of action of the IUD is imperfectly understood, but it is known to prevent nidation of the fertilized egg. Copper devised have higher rates of efficacy and tolerance. Pearl indices range from 95-99.5. Contraindications include genital infection, uterine anomalies, valvular cardiopathy, and coagulation problems. The IUD is relatively contraindicated if there is history of ectopic pregnancy or upper genital tract infections. The combined oral contraceptive is the most widely utilized method in France. The Pearl index is nearly 100 in the absence of forgetting, vomiting, or drug interactions. The contraindications are basically those of estrogens: history of thrombosis, prolonged bedrest, hypertension, hyperlipidemia, hepatic disorders, hormonodependent cancers, or smoking after age 35. Progestin-only methods are available in 3 forms: low-dose pills which must be taken at the same time each day, higher-dosed progestins taken for 20 days each month, and injectable progestins providing contraception for 8-12 weeks. Postcoital contraception using OCs or IUDs is possible but not well known among women or physicians. The Neuwirth law authorizing use of contraception in France was passed in 1967. Amendments in 1974 improved access and provided for reimbursement for some methods, but some newer forms are not reimbursed.
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PMID:[Family planning. Objectives, measures, regulations, structures]. 185 35

The cardiovascular effects of oral contraceptives, as predicted by studies on serum lipid changes in users, are based on the progestin dose, androgenic potency and biologic effect of the estrogen in the pill. Women suffer 250,000 deaths per year in the U.S. resulting from cardiovascular disease, almost half as many as men. They have the same risk factors: high cholesterol, high blood pressure and smoking, and also have more risk from diabetes than men do. The serum HDL, especially HDL2, correlates closely and inversely with heart disease risk. Exogenous estrogens raise HDL and HDL2, and lower LDL, conferring protection against coronary disease, in direct proportion to dose. Progestins usually have adverse effects, in proportion to dose, but progestin potency and type also determine their effects. The estrane progestins norethindrone, norethindrone acetate and ethynodiol diacetate are less potent and much less androgenic, while the gonanes norgestrel and especially levonorgestrel are 5-20 times as potent and androgenic. Each pill needs to be considered as a unit. Several comparative studies are reviewed, corroborating the prediction that pills with higher progestin potency have adverse effects on serum lipids, compared to those with higher estrogen effect. For new lower dose multiphasics, the effects either way are minimal, but HDL2 is still significantly lowered by pills containing levonorgestrel. Progestin-only pills lower HDL2 17- 21%. It is prudent to follow and treat the long-term effects of oral contraceptives on blood lipids.
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PMID:Oral contraceptives and cardiovascular risk. Taking a safe course of action. 220 2

Medroxyprogesterone acetate (MPA; Provera) was given orally to 449 women from the 5th to 7th week of pregnancy until at least the 18th week. Data are recorded from two treatment groups (recurrent abortion and threatened abortion) and are compared to a matched series. A total of 1,016 pregnancies are included in the study, and all patients were recruited from a subfertile population conceiving from a range of infertility treatments. Early pregnancy wastage was high throughout the groups and was significantly elevated (43%; P less than .001) in those women who had vaginal bleeding in early pregnancy. The study focuses on the question of potential teratogenicity of progestagens administered in the first trimester. There were 15/366 (4.1%) infants with congenital abnormalities in the MPA-treated group and 15/428 in the untreated group (3.5%). The difference was not significant, and MPA is considered to have no embryopathic risk, nor is it likely to retain an abnormal fetus that might otherwise abort. It appears that MPA is a safe drug to use in pregnancy although the question of efficacy has not been addressed in this report. Considering other recent negative epidemiologic studies with regard to teratogenicity, we add to the conclusion that MPA cannot be demonstrated to have a measurable teratogenic risk and certainly does not present a risk for congenital heart disease and limb reduction defects.
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PMID:Medroxyprogesterone acetate therapy in early pregnancy has no apparent fetal effects. 317 47

Male Balb/c mice inoculated with a heart-adapted variant of coxsackievirus, group B, type 3 (CVB3M) develop severe myocarditis characterized by extensive focal lesions of inflammatory cells and necrosis of the myocardium. Females generally develop minimal myocarditis except when infected during the first and third trimesters of pregnancy. Enhanced myocarditis is usually accompanied by elevations in virus concentrations in the heart, virus-specific antibody titers, and lymphocyte mediated cytolytic activity to both uninfected and CVB3M-infected myocytes in vitro. As previously shown in males, T-lymphocyte-depleted pregnant female mice inoculated with the virus do not develop significant myocarditis indicating that immune rather than virus-mediated myocyte damage is important in myocarditis. Progesterone increases during gestation reaching maximum concentrations during the third week when heart disease is most severe. Administration of progesterone to castrated male and female mice prior to virus inoculation resulted in increased virus concentrations, cellular and humoral CVB3M-specific immunity, and myocarditis. Two hypotheses for exacerbation of the disease with elevated progesterone concentrations have been postulated: the hormone either indirectly increases cellular immune responses by enhancing virus replication, or independently enhances both T-cell responses and virus replication.
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PMID:Aggravation of coxsackievirus, group B, type 3-induced myocarditis and increase in cellular immunity to myocyte antigens in pregnant Balb/c mice and animals treated with progesterone. 608 88

A protective effect of estrogen is the most obvious reason for the substantial and consistent favored status of women vs. men with regard to coronary heart disease (CHD). This paper briefly reviews the history of studies of the estrogen-heart disease hypothesis, the reason why clinical trials of postmenopausal estrogen are necessary (despite the strength, consistency, and plausibility of the 'protection' seen in observational studies), and the status of the 'Postmenopausal Estrogen/Progestin Interventions' (PEPI) trial results and ongoing trials. The potential for nonhormonal primary prevention is emphasized.
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PMID:Postmenopausal estrogen and heart disease. 882 60

The increasing use of oestrogen replacement therapy in women has focussed attention on the cardioprotective properties it has demonstrated. Historically, it has been shown that women enjoy a certain protection from heart disease, a phenomenon, however, which has not been studied extensively. Women at every age have less coronary artery disease (CAD) than men, even when various risk factors are accounted for, although the presence of diabetes carries equal mortality for both sexes. However, women who do develop CAD have a greater risk of mortality than men with CAD. Other gender differences include a later age of onset of CAD for women, and a difference in the type of atherosclerotic lesions developed. Most striking is the fact that, in women, high-density lipoprotein (HDL) seems to be a more potent predictor of major cardiovascular events than low-density lipoprotein (LDL), or total cholesterol. The Postmenopausal Oestrogen and Progesterone Interventions (PEPI) Trial looked at changes in HDL, fibrinogen, blood pressure and serum insulin resulting from oestrogen use. Four regimens were compared against placebo in 875 women. The results showed that HDL was increased significantly, LDL decreased significantly, fibrinogen levels decreased significantly, and blood pressure and serum insulin levels were essentially unaffected by oestrogen and oestrogen/progestin interactions. The Heart and Oestrogen/Progestin Replacement (HERS) Study, currently underway, is a secondary prevention trial testing the protective effect of hormone therapy in women with documented CAD. This trial may definitively answer the question of whether hormones protect against CAD. After HERS, it may be unethical to continue conducting placebo-controlled trials in a therapy that has such documented cardioprotective benefit.
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PMID:Evidence for primary and secondary prevention of coronary artery disease in women taking oestrogen replacement therapy. 886 76

Several studies have reported an association between hormone replacement therapy (HRT) in postmenopausal women and increased risk of idiopathic venous thromboembolic events (VTEs). Given the widespread use of HRT, it is important to identify factors that may predispose women on HRT to VTEs. To address this concern, we examined potential risk factors for VTEs in women assigned to HRT in the Postmenopausal Estrogen/Progestin Interventions (PEPI) study, a three-year, double-blinded, placebo-controlled trial of 875 postmenopausal women designed to assess the effects of HRT on heart disease risk factors (HDL cholesterol, fibrinogen, blood pressure, and insulin). Women with a history of estrogen-associated VTEs were excluded from the trial. Ten women, all assigned to HRT, had a VTE during PEPI. Only baseline fibrinogen varied significantly between those who did (mean = 249.0 mg/dl) and did not (mean = 280.8 mg/dl) have a VTE while assigned to HRT (P < 0.03). Adjusting for covariates including age, smoking, body mass index, lipid levels, blood pressure, alcohol, exercise, and prior HRT or oral contraceptive use did not affect this finding. The significantly lower fibrinogen levels seen among women subsequently reporting VTEs may be a marker for a specific, but as yet undefined, coagulopathy that is magnified in the presence of exogenous hormones. However, larger studies are needed to confirm this finding.
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PMID:Low fibrinogen level: A predisposing factor for venous thromboembolic events with hormone replacement therapy. 1044 Sep 16

The Heart and Estrogen/Progestin Replacement Study (HERS) was the first randomised, double-blind, placebo-controlled study to evaluate the outcome of hormone replacement therapy (HRT) on subsequent cardiac events in postmenopausal women with established coronary heart disease (CHD). Of the 2763 women enrolled, 1380 were randomised to receive 0.625mg of conjugated equine estrogens plus 2.5mg of medroxyprogesterone daily (Prempro) and 1383 were randomised to receive a placebo. The results were surprising: 179 women in the hormone group and 182 women in the placebo group experienced either a nonfatal myocardial infarction or CHD death (relative hazard 0.99, 95% confidence interval 0.81 to 1.22). This occurred despite a net 11% reduction in low density lipoprotein (LDL) and a net 10% increase in high density lipoprotein (HDL) after 1 year of follow-up (p < 0.001 for LDL and HDL). Also, there were no differences between the 2 treatment groups in any secondary cardiovascular outcomes. The overall null effect may have been the result of an unexpected early adverse effect of the HRT regimen that offset a later reduction in risk. Clearly, the use of HRT for secondary prevention of heart disease is more complex than was initially believed. More data are needed from other clinical trials concerning the risks and benefits of HRT to confirm or refute the puzzling HERS results. HERS also underscores the need for trials with clinical end-points to evaluate both the safety and efficacy of drug therapy. Although observational studies are useful, they cannot provide definitive answers regarding treatment recommendations. Until further data are available, clinicians should not use estrogen plus medroxyprogesterone for the sole purpose of secondary prevention of CHD.
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PMID:The Heart and Estrogen/Progestin Replacement Study: what have we learned and what questions remain? 1064 52

In the premenopausal period, the risk of heart disease is considerably lower in women than in men; however, in the postmenopausal period, when estrogen levels are considerably lower, women's risk of heart disease increases dramatically and approaches that of men. Numerous animal studies, using a variety of models, also confirm estrogen's cardioprotective effect. Although the results of numerous population-based, observational studies have demonstrated a lower risk of heart disease in women who receive estrogen replacement therapy, evidence from prospective, randomized clinical trials is scant. The Postmenopausal Estrogen/Progestin Intervention (PEPI) trial evaluated cardiovascular risk factors, not events, in a large, prospective, randomized trial and found that estrogen improved lipid profiles and other known risk factors. In addition, the PEPI trial compared several estrogen/progestogen treatment regimens, including both medroxyprogesterone acetate (MPA) and micronized progesterone (MP), and found that combined hormone replacement therapy regimens including MP attenuated the beneficial effects of estrogen less than those containing MPA. In the Heart and Estrogen/Progestin Replacement Study (HERS), however, which prospectively evaluated whether estrogen and MPA use reduced the number of nonfatal myocardial infarctions and cardiovascular events, no effect was seen. Although HERS was a null trial, the vast literature base showing a cardioprotective effect should not be discounted. Further research will be required before blanket recommendations on the cardioprotective effects of hormone therapy can be made.
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PMID:Preserving cardiovascular benefits of hormone replacement therapy. 1075 7


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