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)

It was hypothesized that the presence of genetic polymorphisms that decrease activity of the detoxification enzymes glutathione-S-transferase (GST) and quinone oxido-reductase (NQO1) may contribute to heart disease and affect biomarkers of coronary health and oxidative stress. Sixty-seven patients with angiographically confirmed coronary heart disease (CHD) and 63 healthy controls were genotyped for polymorphisms in the GST isoforms Mu and Theta (GSTM and GSTT respectively) and NQO1. Participants' blood levels of homocysteine (Hcy), C-reactive protein (CRP), oxidized low density lipoprotein (LDL) and total antioxidant capacity (TAOX) were measured. TAOX levels were significantly lower in women than men (P < or = 0.001) and this finding was more marked in the control group (P < or = 0.001). Hcy levels were higher in CHD patients (P=0.003 vs. control) which was mostly attributed to female patients (P=0.034 case vs. control). GSTM polymorphisms were present with greater frequencies in CHD cases with the odds ratio (OR) for GSTM equal to 3.77 vs. control. CHD patients also have an increased incidence of both GSTM and GSTT null polymorphisms (OR=5.13). In contrast, NQO1 polymorphisms were protective in CHD patients (OR=0.18 vs. control), which when stratified for genotype was due to heterozygous individuals. Significantly higher C-reactive protein levels occurred in CHD patients with lower NQO1 activity (P=0.001), however, due to the large variations in CRP levels seen in CHD patients; the clinical importance of this difference is unclear. Smokers with the GSTM null polymorphism were more likely to have CHD than non-smokers expressing the GSTM null polymorphism (OR=3.54, P=0.079). We conclude that a lack of activity in the detoxification enzymes NQO1 and GSTM, and biomarker levels are strongly associated with coronary heart disease with sex as a mitigating factor.
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PMID:Polymorphisms in the NQO1, GSTT and GSTM genes are associated with coronary heart disease and biomarkers of oxidative stress. 1895 Jul 33

The effects of thiazolidinediones on cardiac function are controversial in humans with type 2 diabetes (T2DM) and in animals. Given the high prevalence and prognostic relevance of diastolic myocardial dysfunction in T2DM, we tested the hypothesis that by reducing oxidative stress rosiglitazone, but not glimepiride, may improve diastolic function. This randomised cross-over study investigated 12 metformin-treated T2DM patients without cardiovascular disease before and after 16 weeks of additional therapy with rosiglitazone (8 mg daily) or glimepiride (3 mg daily). Systolic and diastolic myocardial velocity (E') were assessed with tissue Doppler. In spite of similar non-significant lowering of glycosylated haemoglobin (HbA1C), rosiglitazone, but not glimepiride, significantly improved E' (p=0.04), reduced malondialdehyde (p=0.028), lowered high-sensitivity C-reactive protein (hsCRP) (p=0.019), and increased adiponectin (p=0.002). For rosiglitazone, multivariate regression analysis revealed malondialdehyde reduction as an independent determinant of treatment-induced improvement in E'. The rosiglitazone-induced improvements of diastolic function and oxidative stress may be of prognostic relevance in choosing therapy for T2DM patients without overt heart disease.
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PMID:Rosiglitazone, but not glimepiride, improves myocardial diastolic function in association with reduction in oxidative stress in type 2 diabetic patients without overt heart disease. 1895 42

Chronic disease has been strongly correlated with inflammation resulting from the body's release of inflammatory cytokines as a result of injury or infection. Specific interventions promoting weight loss, exercise, or intake of antioxidants have been used by several investigators in an effort to decrease inflammatory cytokines. C-reactive protein (CRP) is produced by the liver and its role in the development of inflammation has been well established. However, the strong association between CRP and risk for heart disease is a more recent discovery. During the inflammation process, the transcriptional activity of nuclear factor kappaB leads to the increased production of inflammatory cytokines associated with atherosclerosis, including tumor necrosis factor-alpha (TNFalpha). Increased concentrations of TNFalpha have been reported in obese patients; thus, weight loss is considered a key intervention to reduce the concentrations of this cytokine. In contrast to CRP and TNFalpha, adiponectin increases during weight loss and insulin sensitivity. Additionally, lower concentrations of this cytokine have been reported in cardiovascular disease and type-2 diabetes. Recent epidemiological studies and clinical interventions have reported contradictory findings related to dietary or exercise interventions and the resulting alterations in plasma cytokines. Part of the discrepancies may be due to the population studied, the time of the treatment, and the lack of weight loss in some studies. Although it is clear from the literature that these cytokines play a major role in the development of chronic disease, the best strategy to favorably alter the inflammatory response is still debatable.
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PMID:Modulation of C-reactive protein, tumor necrosis factor-alpha, and adiponectin by diet, exercise, and weight loss. 1902 47

Glucagon-like peptide-1 (GLP-1) is an incretin secreted in response to nutrient ingestion. Understanding the incretin effect on diabetes pathophysiology has led to development of a new class of agents termed incretin mimetics. Exenatide is the first GLP-1 agonist approved to treat type 2 diabetes mellitus (T2DM). Clinical studies have demonstrated exenatide's efficacy in improving glycemic control, often coupled with weight loss. Studies are investigating the potential cardiovascular benefits of GLP-1 agonists. Blood pressure, cholesterol levels, C-reactive protein, and insulin resistance may improve in patients treated with exenatide. The direct effect of GLP-1 on cardiac myocytes and vascular smooth muscle has been an active area of investigation. Infusions of GLP-1 in animal models and human subjects with heart failure have demonstrated significantly improved cardia parameters. In patients with T2DM, GLP-1 infusion has been shown to improve endothelial function, irrespective of changes in insulin sensitivity. These pilot studies provide a foundation for developing therapies aimed at modulating incretin physiology for the additional benefit on the cardiovascular system in patients with T2DM and heart disease.
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PMID:The role of incretins in cardiovascular control. 1914 96

A reduced risk of fatal coronary artery disease has been associated with a high intake of (n-3) fatty acids (FA) and a direct cardioprotective effect by their incorporation into myocardial cells has been suggested. Based on these observations, the omega-3 index (eicosapentaenoic acid + docosahexaenoic acid in cell membranes of RBC expressed as percent of total FA) has been suggested as a new risk marker for cardiac death. In this study, our aim was to evaluate the omega-3 index as a prognostic risk marker following hospitalization with an acute coronary syndrome (ACS). The omega-3 index was measured at admission in 460 patients with an ACS as defined by Troponin-T (TnT) > or = 0.02 microg/L. During a 2-y follow-up, recurrent myocardial infarctions (MI) (defined as TnT > 0.05 microg/L with a typical MI presentation) and cardiac and all-cause mortality were registered. Cox regression analyses were used to relate the risk of new events to the quartiles of the omega-3 index at inclusion. After correction for age, sex, previous heart disease, hypertension, diabetes, smoking, high-sensitivity C-reactive protein, brain natriuretic peptide, creatinine, total cholesterol, HDL-cholesterol, triacylglycerol, homocysteine, BMI, and medication, there was no significant reduction in risk for all-cause mortality, cardiac death, or MI with increasing values of the index. In conclusion, we could not confirm the omega-3 index as a useful prognostic risk marker following an ACS.
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PMID:(n-3) Fatty acid content of red blood cells does not predict risk of future cardiovascular events following an acute coronary syndrome. 1915 16

A supramolecular assembly containing an isoguanosine pentaplex with both a "protein-binding" face and a "reporter" face has been generated. When phosphocholine is appended to the protein-binding face this supramolecular assembly binds multivalently to the pentameric human C-reactive protein, a biomolecule implicated in inflammation and heart disease.
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PMID:Multivalent protein binding and precipitation by self-assembling molecules on a DNA pentaplex scaffold. 1922 72

Chronic kidney disease and elevated serum C-reactive protein (CRP) have been suggested as clinical risk factors for cardiac attacks. The present study investigated postmortem blood urea nitrogen (BUN), creatinine (Cr) and CRP levels in the peripheral blood of sudden cardiac death cases. Adult autopsy cases of ischemic heart diseases (n=153, >20 years of age), including acute myocardial infarction (AMI, n=71), recurrent myocardial infarction (RMI, n=47), acute ischemic heart disease without infarction (AIHD, n=27) and chronic ischemic heart disease (CIHD, n=8), were examined and compared with chronic congestive heart disease (CHD, n=24), spontaneous cerebral hemorrhage (SCH, n=17) and mechanical asphyxiation (n=32). BUN was slightly higher for RMI and CHD, although Cr was slightly higher for SCH. CRP was higher for AMI than for AIHD. The correlation between BUN and Cr levels was significant for AMI, AIHD and CHD, but insignificant for RMI and CIHD. Heart weight was larger for all heart diseases and SCH than for asphyxiation, and was larger for RMI and CHD but lower for AIHD and CIHD among them. Body mass index (BMI) was slightly higher for AMI, RMI, AIHD and CHD, remaining within the reference interval in most cases, but was lower for CIHD. These findings suggest different risk factors or etiologies, including active atherosclerosis, latent renal failure, dehydration and cardiac hypertrophy, for sudden deaths due to these heart diseases.
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PMID:Potential risk factors for sudden cardiac death: an analysis of medicolegal autopsy cases. 1925 62

The aim of this study was to assess the impact of conjugated linoleic acids (CLAs), vitamin E, and combination of these nutrients on serum lipid profiles and blood pressure (BP) in patients with active rheumatoid arthritis (RA). In a randomized, double-blind, placebo-controlled trial, 87 patients with active RA were divided into four groups receiving one of the following daily supplements for three months: Group C: CLAs 2.5 g equivalent to 2 g mixture of cis 9-trans 11 and trans 10-cis12 CLAs in a rate of 50/50; Group E: vitamin E: 400 mg; Group CE: CLAs and vitamin E at above doses: Group P: placebo. After supplementation, SBP levels decreased significantly in the group C in comparison with groups E and P and mean arterial pressure reduced significantly in groups C and CE. There weren't significant differences in the levels of prostaglandin E2 (PGE2), triglycerides, cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), LDL/HDL, cholesterol/HDL, fasting blood sugar, C-reactive protein (CRP), arylestrase activity, platelet count and body mass index between groups. CRP dropped nonsignificantly in groups P, C, E and CE (19%, 24%, 55%, and 39%, respectively). Erythrocytes sedimentation rate levels decreased in groups C, E and CE (P < or = 0.05, P < or = 0.05, P < or = 0.001, respectively). It is concluded that supplementation of CLAs decreased BP and vitamin E decreased CRP. Therefore co-supplementation of CLAs and vitamin E might be profitable for heart disease prevention in RA patients.
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PMID:Effect of conjugated linoleic acid, vitamin E and their combination on lipid profiles and blood pressure of Iranian adults with active rheumatoid arthritis. 1933 55

Inflammatory processes are implicated in a number of diseases for which there are known socioeconomic status (SES) disparities, including heart disease and diabetes. Growing evidence also suggests SES gradients in levels of peripheral blood markers of inflammation. However, we know little about potential gender and racial/ethnic differences in associations between SES and inflammation, despite the fact that the burden of inflammation-related diseases varies by gender and race. The present study examines SES (education and income) gradients in levels of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6), in a biethnic (White and Black) sample of men and women (n=3549, aged 37-55 years) in the USA from the CARDIA Study. Health status, behavioral and psychosocial variables that may underlie SES differences in inflammatory biomarker levels were also examined. Age-adjusted CRP and IL-6 levels were inversely associated with education level in each race/gender group except Black males. Income gradients were also observed in each race/gender group for IL-6 and in White females and males for CRP. In general, differences in CRP and IL-6 levels between low and high SES groups were reduced in magnitude and significance with the addition of health status, behavioral, and psychosocial variables, although the impact of the addition of model covariates varied across race/gender groups and different SES-inflammation models. Overall, findings indicate SES gradients in levels of inflammation burden in middle-aged White and Black males and females.
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PMID:Association of socioeconomic status with inflammation markers in black and white men and women in the Coronary Artery Risk Development in Young Adults (CARDIA) study. 1952 46

This article provides a detailed review of the association of major depression with coronary heart disease (CHD), examines the biological variables underpinning the linkage and discusses the clinical implications for treatment. When considering the co-morbidity between major depressive disorder (MDD) and CHD it is important to differentiate between (i) the prevalence and impact of MDD in those with existing CHD and (ii) MDD as a risk factor for the development of CHD. Whether the same biological mechanisms are at play in these two instances remains unknown. Depression is common in patients with CHD. Importantly, depression in these patients increases mortality. There is also consistent evidence that MDD is a risk factor for the development of CHD. The relative risk of developing CHD is proportional to the severity of depression and is independent of smoking, obesity, hypercholesterolaemia, diabetes mellitus and hypertension. There is a clear need to identify the underlying neurochemical mechanisms responsible for MDD and their linkage to the heart and vascular system. Of particular interest are activation of stress pathways, including both the sympathetic nervous system and hypothalamic-pituitary-adrenal axis, and inflammatory-mediated atherogenesis. Elevated sympathetic activity, reduced heart rate variability and increased plasma cortisol levels have been documented in patients with MDD. In addition to direct effects on the heart and vasculature, activation of stress pathways may also be associated with increased release of inflammatory cytokines such as interleukin-6 and tumour necrosis factor-alpha. Elevated levels of C-reactive protein are commonly observed in patients with MDD. The majority of investigations examining treatment of depression following myocardial infarction have focused on safety and efficacy; there is little evidence to indicate that treating depression in these patients improves survival. Given that strategies for preventive therapy remain incompletely formulated, future research should focus on generating a better understanding of the neurobiology of MDD and heart disease as a basis for rational and effective therapy.
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PMID:Cardiovascular abnormalities in patients with major depressive disorder: autonomic mechanisms and implications for treatment. 1955 86


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