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)

An analysis was undertaken to determine whether combined oral contraceptive (OC) use interacts with the effects of potential cardiovascular risk modifiers (age, body mass index, cigarette smoking, alcohol intake, exercise habit, family histories of heart disease or diabetes, number of pregnancies and duration of OC use) on blood pressure and lipid, lipoprotein, glucose and insulin risk markers for cardiovascular disease. Relationships between risk modifiers and risk markers were compared between non-users (n = 418) and users of low-estrogen dose OC (n = 925, categorised according to progestin content as monophasic levonorgestrel, triphasic levonorgestrel, norethindrone or desogestrel). OC use diminished the adverse effects of age on glucose tolerance. Aerobic exercise had a particularly beneficial effect on triglyceride levels and OGTT insulin response in OC users. The rise in HDL and HDL2 cholesterol concentrations with alcohol intake seen in non-users was diminished in OC users. Increasing duration of use of a desogestrel combination was associated with increasing HDL cholesterol concentrations. No adverse effects of risk modifiers on metabolic risk markers and blood pressure were augmented by OC use, and some were even diminished.
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PMID:Interaction of oral contraceptive use with the effects of age, exercise habits and other cardiovascular risk modifiers on metabolic risk markers. 863 Nov 92

The effects of consuming a soy protein isolate beverage powder (60 g/d for 28 d) vs. a casein supplement was evaluated in 20 male subjects who were randomly allocated into the two groups. A dramatic rise in plasma isoflavone concentrations was observed after supplementation in the soy protein group, the levels reaching 907 +/- 245 nmol/L for genistein (a 110-fold increase) and 498 +/- 102 nmol/L for daidzein (a 150-fold increase) as measured by isotope dilution gas chromatography - mass spectrometry. These concentrations are higher than previously reported for the plasma of Japanese subjects consuming a traditional diet (276 nmol/L and 107 nmol/L, respectively). No significant differences in collagen- or 9,11-dideoxy-11alpha, 9alpha-epoxymethanoprostaglandin F2alpha (U46619)-induced platelet aggregation were observed in platelet-rich plasma from the two groups; the increase in plasma isoflavonoids from soy protein supplementation is not sufficient to significantly inhibit platelet aggregation ex vivo. Similarly, plasma total and HDL-cholesterol were not affected by protein supplementation, possibly because the men were normocholesterolemic at entry. Analysis of plasma phospholipid polyunsaturated fatty acid composition showed no differences between soy protein and casein supplementation. Previous investigations reported a significant alteration in fatty acid status in animals fed soy protein relative to those fed casein. The present studies indicate that although soy protein supplementation to a typical Western diet can increase plasma concentrations of isoflavones, this may not necessarily be sufficient to counter heart disease risk factors such as high plasma cholesterol and platelet aggregation.
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PMID:A soy protein isolate rich in genistein and daidzein and its effects on plasma isoflavone concentrations, platelet aggregation, blood lipids and fatty acid composition of plasma phospholipid in normal men. 875 72

To determine the effect of a common mutation (Ser447-Ter) of the human LPL gene upon serum lipid and lipoprotein levels and coronary artery disease (CAD) within a representative adult male population, we analyzed subjects from the Caerphilly Prospective Heart Disease Study (n = 1273). The possession of this mutation associates with protective lipid and lipoprotein profiles. Subjects possessing the mutation have significantly higher HDL-C (p = 0.002) and apo AI (p < 0.04) levels, lower triglycerides (p = < 0.04) and total cholesterol/HDL-C ratios (p < 0.02); all established previously to reduce risk of CAD. We also find that this mutation is significantly less frequent amongst CAD subjects (p < 0.05). These associations provide evidence for a common mutation that appears to confer beneficial lipid and lipoprotein profiles amongst an adult male population with regard to risk of CAD.
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PMID:Identification of putative beneficial mutations for lipid transport. 876 63

Rapid economic growth in Taiwan is accompanied by changing lifestyles, and the mortality pattern has switched from predominantly infectious diseases to chronic diseases. Age-adjusted mortality from heart disease has increased slowly but steadily. However, mortality from heart disease in Taiwan remains low compared with many other countries. Mortality from the cerebrovascular diseases has decreased gradually. Current age- and sex-specific values of blood cholesterol low density lipoprotein cholesterol (LDL-C) and triglyceride (TG) are, in general, higher than values in mainland China, but lower than those in the NHANES III and PROCAM studies. From 1950 to 1987, percent dietary fat increased from 16% to 36% in Taiwan. However, a high polyunsaturated fat/saturated fat (P/S) ratio (1.3) maintained during this period may in part explain the favorable blood lipid status and low mortality from heart disease. Data from prospective studies are scarce. In case-control studies carried out in Chinese, significantly higher values of TG, CHOL LDL-C, but lower high density lipoprotein cholesterol (HDL-C) levels have often been found in coronary artery disease (CAD) patients than in controls. The percent differences in TG and HDL-C values (20%) were much greater than those of CHOL and LDL-C (3%). A few studies have identified the TG level as an independent risk factor for stroke and CAD in Taiwan, where a moderate to high fat diet with an advantageous P/S ratio is consumed.
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PMID:Plasma lipid profiles and epidemiology of atherosclerotic diseases in Taiwan--a unique experience. 877 Mar 22

The purpose of this double-blind study was to investigate the influence of dietary supplementation with an algae source of docosahexaenoic acid [DHA; 22:6(n-3)], devoid of any eicosapentaenoic acid [EPA; 20:5(n-3)], on serum/platelet DHA status, the estimated retroconversion of DHA to EPA, and risk factors for heart disease in vegetarian subjects. Healthy vegetarians (12 male, 12 female) consumed nine capsules daily of either DHA (1.62 g/d) or corn oil for 6 wk. Consumption of DHA capsules increased DHA levels in serum phospholipid by 246% (from 2.4 to 8.3 g/100 g fatty acids) and in platelet phospholipid by 225% (from 1.2 to 3.9 g/100 g fatty acids). EPA levels increased in serum phospholipid by 117% (from 0.57 to 1.3 g/100 g fatty acids) and in platelet phospholipid by 176% (0.21 to 0.58 g/100 g fatty acids) via metabolic retroconversion; the estimated extent of DHA retroconversion to EPA was 11.3 and 12.0%, based on the serum and platelet analyses, respectively. Arachidonic acid [AA; 20:4(n-6)] levels in serum and platelet phospholipids decreased moderately during the trial period (DHA group) as did both docosapentaenoic acids [22:5(n-6) and 22:5(n-3)]. Although no significant changes were found in the total and LDL-cholesterol levels with DHA supplementation, the total cholesterol:HDL-cholesterol ratio showed a moderate decrease over time as did the LDL-cholesterol:HDL-cholesterol ratio and serum triglyceride concentrations. DHA supplementation did not alter the various thrombogenic factors measured. In conclusion, DHA supplementation markedly enhanced the DHA status (of serum and platelets), provided for the formation of substantial EPA, and lowered the total and LDL-cholesterol:HDL-cholesterol ratios.
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PMID:Supplementation with an algae source of docosahexaenoic acid increases (n-3) fatty acid status and alters selected risk factors for heart disease in vegetarian subjects. 900 71

Overwhelming evidence indicates that the Western diet plays a major role in atherogenesis. Clinicians are only now beginning to tease out the precise components of the diet that are harmful or beneficial. With respect to fat intake, it remains unclear whether it is the amount or type of fat that promotes atherosclerotic disease. There appears to be a consistent positive association of cholesterol, saturated fat, and possibly trans-fatty acid intake and atherosclerotic disease. Although there is general agreement that reducing intake of these dietary components would be beneficial, controversy remains on what should replace these harmful fats. Some researchers advocate massive reductions in total fat consumption with replacement with carbohydrates for everyone, whereas others recommend a Mediterranean-style diet, which replaces saturated animal fats with vegetable fats. Very low-fat diets have been shown to lower the chance of a heart attack among those with severe coronary artery disease, but for the majority of Americans who do not have obvious artery disease, there is no convincing evidence that a very low-fat diet is optimal. There may be other adverse health effects of this Asian diet, such as increased rates of hemorrhagic stroke. Further research is required to refine thinking on the optimal composition of fats in diet. The effects of alcohol consumption on chronic diseases are complex. The strength and consistency of the observational and experimental evidence strongly suggests a causal link between light to moderate alcoholic beverage consumption and reduced risks of CHD. These reductions in risk of CHD appear to be mediated largely by raising HDL cholesterol levels, although additional mechanisms remain possible and do not appear to be beverage specific. Maximal benefit in terms of CHD appears to be at the level of one drink per day. From a public policy standpoint, whether the benefits for CHD persist at heavy drinking levels or are attenuated is moot because clear harm of heavy drinking in terms of overall mortality outweighs any benefits in the reduction of heart disease. Although the association of alcohol and CHD is likely to be causal, any individual or public health recommendations must consider the complexity of alcohol's metabolic, physiologic, and psychological effects. With alcohol, the differences between daily intake of small to moderate and large quantities may be the difference between preventing and causing disease. A discussion of alcohol intake should be a part of routine preventive counseling. Given the complex nature of alcohol disease relationships, alcohol consumption should not be viewed as a primary preventive strategy; also, it should not necessarily be viewed as an unhealthy behavior. Based on the totality of available evidence, antioxidants represent a possible but as yet unproven means to reduce risks of cardiovascular disease. Although it remains unclear whether supplementation of diet with antioxidant vitamins will reduce risks of atherosclerotic disease, most researchers agree that consumption of fruits and vegetables is an important part of a healthy diet. The U.S. Department of Agriculture recommends two to four servings of fruit and three to five servings of vegetables per day.
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PMID:Diet and heart disease. The role of fat, alcohol, and antioxidants. 907 92

Gender-specific differences in heart disease have long been known but it has only been since the advent of molecular biology that it has become possible to investigate the molecular mechanisms. Most biochemical work in the last 50 years has focused on the characterization of the steroid hormones involved in gender specificity. More recently, the cloning of the steroid receptors and characterization of the signaling pathways through these proteins has given new insights into the mechanisms underlying the mode of action of steroid hormones. It has also become clear that the steroid receptors can be classified into families (receptors for thyroid hormone, glucocorticoids, estrogens, androgens, retinoic acid, and so called orphan receptors of mostly unknown function). The structures of these receptors show very close resemblance and all are DNA-binding proteins acting as transcription factors. Some (if not all) act as repressors of transcription of some genes in the native state and are converted to activators (or perhaps repressors of other genes) upon binding of the cognate hormone. Naturally, classical target tissues for estrogens and androgens have been studied first and only in very recent years has it been recognized that estrogens and androgens act on a much wider spectrum of tissues. In the cardiovascular field, the beneficial effect of estrogen replacement therapy in postmenopausal women which reduces the incidence of cardiovascular disease by some 40% and the lower incidence of cardiovascular disease in premenopausal women have mostly been explained by the beneficial action of estrogens on the lipid profile (increase in HDL and decrease in LDL cholesterol). Recently, functional estrogen receptors have also been shown in vascular smooth muscle cells and in the endothelium. Our own group has characterized the presence of estrogen receptors in the myocardium and in cardiac fibroblasts. We have also shown that these receptors are transcriptionally active because they are able to drive a minigene composed of a triple estrogen responsive DNA regulatory element (promoter) coupled to the firefly luciferase gene which serves as a reporter by way of its ability to drive a light-emitting reaction. We are in the process of characterizing the target genes for estrogen in the myocardium. A specific series of immediate-early genes is induced by estradiol (the major premenopausal estrogen) and we have also characterized a number of tissue-specific genes whose expression is driven by estrogens in the myocardium. The ultimate goal of these investigations is to explore the use of estrogens in the treatment of cardiac hypertrophy (and failure) by way of their properties to counteract (at least some of) the pathological switches in gene expression in these disease entities.
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PMID:Modulation of cardiac hypertrophy by estrogens. 943 14

The purpose of this double-blind study was to investigate the influence of adding a quercetin-containing supplement to the diet on plasma quercetin status, serum/platelet fatty acid levels and risk factors for heart disease. Healthy men and women with cholesterol levels of 4.0-7.2 mmol/L, consumed four capsules daily of either a quercetin-containing supplement (1.0 g quercetin/d) or rice flour placebo for 28 d. Quercetin intakes were approximately 50-fold greater than the dietary intakes associated with lower coronary heart disease mortality on the basis of epidemiologic studies. Subjects consuming quercetin-containing capsules had plasma quercetin concentrations approximately 23-fold higher than those of subjects consuming the control capsules. Quercetin supplementation did not modify serum total, LDL or HDL cholesterol or triglyceride levels. There were also no alterations of other cardiovascular disease or thrombogenic risk factors, including platelet aggregation, platelet thromboxane B2 production, blood pressure or resting heart rate. Furthermore, there was no effect on the levels of (n-6) or (n-3) polyunsaturated fatty acids in serum or platelet phospholipids. In conclusion, supplementation with quercetin-containing capsules markedly enhanced the plasma quercetin concentration but had no effect on other cardiovascular or thrombogenic risk factors.
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PMID:Supplementation with quercetin markedly increases plasma quercetin concentration without effect on selected risk factors for heart disease in healthy subjects. 948 69

Syndromes of risk factor disturbance may contribute to the development of coronary heart disease and non-insulin-dependent diabetes mellitus, but their definition and quantification remain problematic. Using factor analysis, constellations of risk factor variables that could indicate distinct syndromes of metabolic disturbance were explored in the baseline data of the first follow-up cohort of 742 men from the Heart Disease and Diabetes Risk Indicators in a Screened Cohort (HDDRISC) study. The primary analysis considered 16 intercorrelated variables measured in more than 90% of cohort participants. A missing-values estimation routine was used to ensure inclusion of all participants in the analysis. Subanalyses were undertaken, including a repeat of the primary analysis on the 522 individuals who had received measurement of HDL cholesterol, an oblique rather than orthogonal factor rotation procedure performed on primary and HDL subset analyses, a repeat of these two primary and HDL subset analyses using only those participants with complete measurements, and a repeat of these six analyses including only the seven variables conventionally associated with the metabolic syndrome. The principal factor that emerged in all analyses undertaken comprised oral glucose tolerance test insulin and glucose response, serum uric acid, and body mass index. Fasting serum triglyceride concentration was included in this factor in 11 of the 12 analyses undertaken, fasting plasma insulin in 8, fasting plasma glucose in 5, and mean arterial pressure in 3. HDL cholesterol factored in isolation from insulin in all analyses undertaken. These findings provide strong support for a core metabolic cluster, which is unlikely to include blood pressure and does not include HDL. The factor scores relating to this cluster will provide a means of assessing its quantitative importance in prospective analysis of the development of CHD and diabetes in this cohort.
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PMID:Factors of the metabolic syndrome: baseline interrelationships in the first follow-up cohort of the HDDRISC Study (HDDRISC-1). Heart Disease and Diabetes Risk Indicators in a Screened Cohort. 948 85

Cardiovascular disease is the leading cause of death among older American women. Estrogen replacement therapy (ERT) appears to reduce the risk of heart disease. For nearly five decades, the Type A behavior pattern (TABP) has been implicated in the cardiac morbidity and mortality of both men and women, but no studies have examined the use of replacement estrogen or whether its association with heart disease risk factors is different in Type A versus Type B women. We examined the effects of ERT and TABP on heart disease risk factors in a large population-based sample. Subjects were 1070 postmenopausal women, aged 50-89 years, who had been participants in the Rancho Bernardo Study. At a clinic visit made during 1984-1987, TABP was assessed with the Bortner Rating Scale, and heart disease risk factors (total cholesterol, high-density and low-density lipoprotein (HDL and LDL), triglycerides, fasting and postchallenge insulin and glucose, and blood pressure) were measured. Based on a median split (median = 154.0) of scores on the Bortner Rating Scale, 52% of these women were classified as Type A. Type A women were significantly younger than Rating women (mean = 68.4 versus 71.0 years, respectively). After adjustment for age, significantly more Type A than Type B women were on ERT (35% versus 24.7%, p = 0.001). Analyses stratified by TABP indicated that within the Type A group, current users of ERT had higher levels of HDL cholesterol (p) = 0.001) and lower levels of LDL cholesterol (p < 0.01), fasting plasma glucose (p < 0.001), and fasting insulin (p < 0.01). Among Type B women, current users of ERT had higher levels of HDL cholesterol (p = 0.07) and triglycerides (p < 0.01), lower levels of LDL cholesterol (p < 0.01), and lower systolic blood pressure (p < 0.05) but no significant differences in either fasting or postchallenge levels of either plasma glucose or serum insulin (each p < 0.01). Results of this study suggest that ERT may be associated with significant differences in the heart disease risk factor profile in Type A versus Type B women, and these differences may favor Type A women.
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PMID:Type A behavior pattern, heart disease risk factors, and estrogen replacement therapy in postmenopausal women: the Rancho Bernardo Study. 951 Nov 32


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