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

The significance of selenium deficiency was investigated in pigs that died suddenly of microangiopathy (MAP, mulberry heart disease). Hepatic selenium concentration (mean +/- SD) in pigs with MAP (1.04 +/- 0.47 micrograms/g dry weight) was lower than in healthy pigs (1.23 +/- 0.53 micrograms/g). The lowest hepatic selenium values were found in pigs with MAP and in 22.2% of MAP pigs hepatic selenium concentration was below 0.5 microgram/g which reflects selenium deficiency. Thus, pigs with a low selenium status are at risk of MAP. The low selenium status together with vitamin E deficiency increases oxidative stress and thus contributes to the development of oxidative damage.
 ...
PMID:Hepatic selenium concentration in pigs with microangiopathy (mulberry heart disease)--an animal model for the study of oxidative damage. 221 Sep 65

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.
 ...
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.
 ...
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

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.
 ...
PMID:Evidence for primary and secondary prevention of coronary artery disease in women taking oestrogen replacement therapy. 886 76

We investigated whether use of labetalol, a beta adrenoreceptor blocking antihypertensive agent commonly employed as an alternative to hydralazine, is independently associated with pulmonary edema in women with severe preeclampsia. We retrospectively evaluated women with severe preeclampsia who were given labetalol by intravenous bolus for MAP > 120 mm Hg. Outcome variables included: achieving MAP < 120 mm Hg with < 300 mg of labetalol, incidence of adverse effects of the drug, including pulmonary edema, hypotension, and maternal bradycardia. Total intravenous fluid intake exceeding output (+ delta I/O) and presence or absence of preeclamptic liver involvement were noted. Statistical analysis included unpaired t-tests and Fisher's exact test. Fifty-one women were studied, 7 (13.7%) of whom developed pulmonary edema. Demographic and pregnancy characteristics were not different between patients who did or did not develop pulmonary edema. No patient had detectable underlying heart disease. Patients with or without pulmonary edema did not differ as regards entry MAP (130 +/- 14 vs. 129 +/- 18 mm Hg), total dose of labetalol (209 +/- 83 vs. 193 +/- 39 mg/24 hours), incidence of bradycardia or hypotension (0/7 vs. 8/44), or presence of hepatic involvement (1/7 vs. 9/44). However, there was a significant difference in degree of positive fluid balance. Patients developing pulmonary edema had a net gain of 1,466 +/- 429 mL of fluid in the 24 hours in which they received labetalol than those who did not (659 +/- 1152 mL, P = .003). Initial central hemodynamic monitoring data revealed no impairment of cardiac performance (mean cardiac output 7.7 +/- 1.8 L/min, cardiac index 4.0 +/- 0.8 L/min/m2, left ventricular stroke work index 73 +/- 9 g.m.m-2) despite high pulmonary capillary wedge pressures (22 +/- 4 mm Hg). We conclude that the incidence of pulmonary edema in patients with severe preeclampsia who are treated with labetalol appears to be a result of an increase in third space fluid accumulation as a manifestation of the severity of their disease, not a direct effect of the drug on cardiac performance.
 ...
PMID:Does labetalol predispose to pulmonary edema in severe pregnancy-induced hypertensive disease? 964 12

The time course of intensive care for severe respiratory syncytial virus (RSV) lower respiratory tract illness may be predicted by the severity of gas exchange during the first 48 h of mechanical ventilation. To test this hypothesis, two studies were undertaken in RSV-positive mechanically ventilated patients who did not have chronic lung disease, congenital heart disease or immunodeficiency. First, a retrospective criteria-generating review of 45 infants was carried out. In these infants, more severe lower airway disease, as demonstrated by four-quadrant consolidation on chest X-ray, was associated with 'best' alveolar arterial oxygen gradients (AaDO2, torr) and mean airway pressure (MAP, cm H2O) values as follows: first 24h, AaDO2 > 400 and MAP > 10 (positive and negative predictive values 100% and 97%, respectively); second 24 h, AaDO2 > or = 300 and MAP > 10 (positive and negative predictive values 91% and 100%, respectively). The second study, a prospective, hypothesis-testing, analysis of length-of-stay in 44 infants stratified according to the above AaDO2 and MAP criteria demonstrated that the duration of intensive care was longer in the severe group: median (interquartile range in days) 17 (15-39) vs 7 (4-8) (p < 0.01). We suggest that, in mechanically ventilated infants with RSV, the time course of intensive care is predictable based on early clinical features and respiratory parameters. Therefore reports on the effectiveness of special therapies using intensive care stay as a measure of outcome should be interpreted with respect to these observations before drawing conclusions about efficacy.
 ...
PMID:Time course of severe respiratory syncytial virus infection in mechanically ventilated infants. 1097 23

Progesterone receptors are present in the arterial wall and it is, therefore, likely that the arterial effects of progestins are mediated through progesterone receptors as well as through down-regulation of the estradiol receptor. Progestin therapy affects arterial function, as it can stabilize arteries in a state of vasomotor instability, but may also induce vasoconstriction of estrogenized vessels. Thus, the cardiovascular effects of progestins may influence the cardioprotective effect of estrogens. There has been some concern that a combined estrogen-progestogen therapy may attenuate some of estrogen's beneficial effects on cardiovascular health. This is a reflection of the past epidemiologic studies which have used primarily unopposed estrogen. The PEPI trial is the only large-scale, long-term study to compare directly the effects of different combined hormone replacement therapy regimens upon plasma lipids in healthy women. This study has shown that the adjunctive clinical impact of different progestogens on the beneficial effect of estrogen replacement therapy is trivial. It has never been proved that in normocholesterolemic women, e.g., those included in the PEPI trial, the increase in HDL reduces cardiovascular mortality or morbidity. Based on the results of PEPI, hormone replacement therapy has positive effects on key heart disease risk factors and endometrial tissue, and the magnitude of those effects does not differ significantly across the hormone replacement therapy regimens used. At present there are only few and inconclusive data available on the vascular effect of progestins in menopausal women. Some studies found that progestins reduced the beneficial effect of estrogens, while others did not. Our group has recently shown that different estrogen-progestin treatments have different effects upon vascular reactivity and that a careful selection of the progestin to be added to estrogen is of capital importance to preserve, or even enhance the positive vascular effects of estrogens. Few epidemiological studies have investigated the effect of adding a progestin to estrogen therapy upon cardiovascular mortality and morbidity, and all have suggested that hormone replacement therapy may be more effective than estrogen replacement alone in reducing cardiovascular events in primary prevention. The results of the recently published Heart and Estrogen/progestin Replacement Study (HERS) have added some critical data on the effect of hormone replacement therapy for secondary prevention in women with coronary artery disease. The study, however, is affected by several important methodological and statistical problems, which make its interpretation difficult and its conclusions useless for clinical practice. The results of the study should be evaluated with caution by physicians who give advice on hormone replacement therapy, and no woman should be taken off hormone replacement therapy because of HERS. Of importance, the results of HERS should not be used to suggest alternative forms of treatment, especially the selective estrogen receptor modulators (SERMs), for cardiovascular protection in postmenopausal women.
 ...
PMID:Comparative cardiovascular effects of different progestins in menopause. 1172 Jan 97

Hormonal replacement therapy (HRT) has shown to be efficacious in treatment and preventing of heart disease, osteoporosis and reducing mortality in postmenopausal and ovariectomized females. Several attempts to utilize the native estrogen and its analogs such as Depo-Provera, conjugated estrogen and estrogen benzoate have shown different physiological responses. In addition, the route of administration and its mode of action is lacking in the literature. The specific objective of this study was to investigate the role of sustained delivery of estrogen on the functional and structural capacity of the kidney using adult female rats as a model. A total of 24 adult female rats were subdivided into four equal groups. Groups I and II were ovariectomized (OVX) by following standard laboratory surgical procedures. Each rat in groups II and III (intact) were implanted with tricalcium phosphate lysine (TCPL) drug delivery system loaded with 40 mg of estrogen. Rats in group IV were unimplanted and untreated to be served as a control group. At the end of 45 days post treatment the animals were sacrificed by using overdose of Halothane and assured by cervical dislocation. Vital and reproductive organs were retrieved, weighed and subjected to H&E staining procedure. The results of this investigation suggest: (i) TCPL delivery system released estrogen at a sustained level for 45 days without any untoward response, (ii) the wet weights of kidneys (normalized to body weight) were increased (p < 0.05) in intact rats treated with estrogen compared to control, (iii) sustained delivery of estrogen resulted in a maintenance of kidney weights compared to the control level, however, the lack of estrogen treatment resulted in a remarkable regression in the kidney weights of OVX rats, (iv) the ratio of renal arteries-diameter (normalized to arterial wall thickness) was significantly increased in intact rats treated with estrogen compared to the control and other experimental groups, (v) histopathological evolutions of renal tubules revealed tubular epithelial damage in intact rats received estrogen treatment compared to the control and other groups. In conclusion, this study suggests that exogenous estrogen therapy could lead profound tubular damage and consequently major renal insufficiency. HRT also could lead to hypertensive renal damage.
 ...
PMID:Histomorphometric evaluation of renal glomeruli exposed to sustained delivery of estrogen using adult ovariectomized rats. 1272 40

Diagnostic testing in patients with congenital heart disease is usually performed supine and at rest, conditions not representative of their typical hemodynamics. Upright exercise measurements of blood flow may prove valuable in the assessment of these patients, but data in normal subjects are first required. With the use of a 0.5-T open magnet, a magnetic resonance-compatible exercise cycle, and cine phase-contrast techniques, time-dependent blood flow velocities were measured in the right (RPA), left (LPA), and main (MPA) pulmonary arteries and superior (SVC) and inferior (IVC) vena cavae of 10 healthy 10- to 14-yr-old subjects. Measurements were made at seated rest and during upright cycling exercise (150% resting heart rate). Mean blood flow (l/min) and reverse flow index were computed from the velocity data. With exercise, RPA and LPA mean flow increased 2.0 +/- 0.5 to 3.7 +/- 0.7 (P < 0.05) and 1.6 +/- 0.4 to 2.9 +/- 0.8 (P < 0.05), respectively. Pulmonary reverse flow index (rest vs. exercise) decreased with exercise as follows: MPA: 0.014 +/- 0.012 vs. 0.006 +/- 0.006 [P = not significant (NS)], RPA: 0.005 +/- 0.004 vs. 0.000 +/- 0.000 (P < 0.05), and LPA: 0.041 +/- 0.019 vs. 0.014 +/- 0.016 (P < 0.05). SVC and IVC flow increased from 1.5 +/- 0.2 to 1.9 +/- 0.6 (P = NS) and 1.6 +/- 0.4 to 4.9 +/- 1.3 (P < 0.05), respectively. A 56/44% RPA/LPA flow distribution at both rest and during exercise suggests blood flow distribution is dominated by distal pulmonary resistance. Reverse flow in the MPA appears to originate solely from the LPA while the RPA is in relative isolation. During seated rest, the SVC-to-IVC venous return ratio is 50/50%. With light/moderate cycling exercise, IVC flow increases by threefold, whereas SVC remains essentially constant.
 ...
PMID:Blood flow conditions in the proximal pulmonary arteries and vena cavae: healthy children during upright cycling exercise. 1503 Nov 21

The assessment of anger has received increasing attention because of growing evidence that anger and hostility are related to heart disease. Research on anger assessment has also been stimulated by the development of psychometric measures for evaluating different aspects of anger. First, we review the major self-report scales used to assess anger and hostility. The scales appeared to have been constructed without explicit definition of anger and there is little differentiation between the experience and expression of anger. The factor-derived STAXI-2 is a 57-item measure of the expression of anger, and is comprised of the state-trait anger scale [Spielberger CD, Jacobs G, Russell JS, Crane RS. Assessment of anger: the state-trait anger scale. In: Butcher JN, Spielberger CD, editors. Advances in personality assessment, 2. Hillside, NJ: Erlbaum; 1983] and the anger expression scale (AX; Spielberger et al., 1985). The state anger scale (SAS) includes three subscales: feeling angry, feeling like expressing anger verbally, and feeling like expressing anger physically. The trait anger scale (TAS) consists of two subscales: angry temperament and angry reaction. The AX deals with the direction of both anger expression and anger control, resulting in four revised AX subscales: anger expression/out (verbal and physical, aggressive behavior directed toward other persons or objects), and anger expression/in (anger suppression), anger control/out (attempts to monitor and prevent the outward expression of anger) and anger control/in (active attempts to calm down and reduce angry feelings). The aim of this work was to examine the factor structure and the psychometric properties of the French adaptation of STAXI-2. A sample of 1085 French subjects, 546 female and 539 male, between 18 and 70 years old participated in the study. The 57 items of the three original subscales (SAS, TAS, and AX scale) were analyzed separately by sex and by subscale, using exploratory factor analyses (principal axis analysis, followed by promax rotations). For the first part of the questionnaire (SAS), factor analysis suggested the presence of three factors with eigenvalues >1.0; but the factor structure obtained for males and females differed and was difficult to interpret. Moreover, the explained variance of Factors 2 and 3 was low. Velicer's MAP criteria and screen test established that one solution factor was more relevant. Confirmatory factor analysis suggested that the three factor solution was acceptable, but the unifactorial solution adjusted better to the data. For the second part of the questionnaire (TAS) factor analysis was conducted following the same procedure, and two factors were extracted. The explained variance of Factor 2 was very low. Velicer's MAP criteria and screen test suggested that the solution factor was more relevant. Moreover, the adjustment parameters of the original two-factor structure were not satisfactory. Finally, the analyses of the 32 items of anger expression and control yielded four factors with eigenvalues >1.0. All items loaded higher than 0.38 on the corresponding factor and lower than 0.30 in other factor. The factor structure of the AX scale was fairly robust, both for males and females. Internal consistency and test-retest reliability of the subscales were acceptable except for the SAS. The correlations of the six subscales with four criterion variables (Buss Durkee hostility inventory, Cook and Medley Ho scale, NEO PI-R Ho scale and Courtauld emotions control scale) were in the expected direction, establishing their convergent validity. In summary, the analysis reported in this study checked the factor structure of the STAXI-2 translated into French. The state anger dimension was also essentially confirmed, but no distinction was found between the three components: feeling angry, feeling like expressing anger verbally, and feeling like expressing anger physically. Moreover, the distinction between angry temperament and angry reaction was not confirmed because of gender differences, but we established a robust and valid trait anger factor. Finally, we confirmed the factor structure of the original anger expression scale without gender differences. Some practical and theoretical perspectives for the use of the French adaptation of the STAXI-2 are suggested.
 ...
PMID:[The French adaptation of the STAXI-2, C.D. Spielberger's State-trait anger expression inventory]. 1855 45


1 2 Next >>