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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dutch GP's (General Practitioners) take care of people living in homes for the elderly. The population of these homes is selected on the basis of poor functioning on ADL (activities of daily living). We expected to find a group of elderly people within these homes that need more complex primary care. We describe the characteristics of care for an institutionalized elderly population and compare these to the care provided to their independently living peers. The design of this study is a matched case-control study in a Dutch General Practice in the study period 1/1/1998 to 1/7/2004. Our main results show that the rate of cognitive problems is two times, the prevalence of depression even three times higher in older people living in a home for the elderly than in those who live independently. Locomotory problems are a frequent problem in homes for the elderly. Rates of chronic pulmonary problems, atherosclerosis-related diseases and urinary tract infection are higher, whereas no significant differences for CVA, diabetes and cancer were found. Institutionalized older patients use more different types of medication. GP's do not have more contacts with people living in a home for the elderly than with older people living independently. We conclude that people living in homes for the elderly have complex problems, and need special attention for their specific vulnerability. Differences in care are not primarily explained by chronic disease but by problems with mobility, confusion, depression and cognition.
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PMID:[Primary care in homes for the elderly]. 1863 98

Peripherally produced corticotrophin-releasing hormone (CRH) is a strong proinflammatory factor involved in many inflammatory diseases. However, to date, there is no evidence about the action of CRH on atherosclerosis, a chronic disease characterized by inflammatory reactions. In this study we observed the effect of CRH on atherosclerosis in low-density lipoprotein receptor-deficient (LDLr-/-) mice. Twelve-week-old, male LDLr-/- mice were subcutaneously injected with CRH (10microg/kg) or vehicle once a day for 8 weeks. The results indicated aortic atherosclerotic lesions were larger (P<0.01) in CRH-treated mice than those in untreated mice. CRH significantly up-regulated the expression of both protein and mRNA for vascular cell adhesion molecule-1 (VCAM-1), together with a markedly increased activation of nuclear factor kappa B (NF-kappaB) in aortas. In addition, the blood lipid levels were not influenced by CRH subcutaneous injection. The significant proatherogenic effect of CRH in LDLr-/- mice was largely attenuated by selective CRH receptor 1 (CRHR1) antagonist NBI27914 but not by specific CRH receptor 2 (CRHR2) antagonist antisauvagine-30 (anti-Svg-30). Meanwhile, both the enhanced expression of VCAM-1 and increased activation of NF-kappaB induced by CRH in aortas of LDLr-/- mice were also largely suppressed by NBI27914, whereas these inhibitory effects were not observed in anti-Svg-30 group. Taken together, these findings indicated that CRH may accelerate atherosclerosis progression in LDLr-/- mice via CRHR1. The enhanced VCAM-1 expression which probably resulted from increased activation of NF-kappaB induced by CRH, may be one of the important molecular mechanisms by which CRH accelerates atherosclerosis. This study provides a new insight into the effect of CRH on atherosclerosis and suggests a potential target for the prevention and treatment of atherosclerosis.
Atherosclerosis 2009 Apr
PMID:Enhanced expression of vascular cell adhesion molecule-1 by corticotrophin-releasing hormone contributes to progression of atherosclerosis in LDL receptor-deficient mice. 1864 Jun 79

Cardiovascular disease remains the most common cause of death in the developed world and is predicted by the World Health Organization to kill approximately 20 million people worldwide each year until at least 2015. In light of these figures, work on producing superior tools for clinical use in the cardiovascular field is intensive. As proteins are the primary effectors of cellular function, a significant majority of this work focuses on the role of proteins in the cardiovascular system in physiological and pathological states in order to outline both mechanisms and markers of disease. One of the most effective ways to investigate these on a global basis is through proteomic analysis, which allows for broad spectrum screening of cellular protein or peptide complements during cardiovascular pathogenesis. Furthermore, specific technologies are now available to screen animal model or human blood samples for novel, improved markers of chronic disease states, such as atherosclerosis or for earlier indicators of acute myocardial stress, including ischemia/reperfusion injury and heart failure. This review summarizes current literature on the key aspects of proteomics and peptidomics related to clinical cardiovascular science.
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PMID:The role of proteomics in clinical cardiovascular biomarker discovery. 1866 14

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

A major limitation of past work on the social patterning of atherosclerosis has been the reliance on measures of neighborhood or individual-level socioeconomic position (SEP) assessed at a single point in time in adulthood. Risk of chronic disease is thought to accumulate throughout the life-course, so the use of a measure for a single point in time may result in inaccurate estimates of the social patterning of subclinical disease. Using data from the US Multi-Ethnic Study of Atherosclerosis (MESA), we examined the relation between childhood SEP [CSEP] (father or caretaker's education), adulthood SEP [ASEP] (a summary score of income, education, and wealth), and 20-year average exposure to neighborhood poverty [NSEP] (residential addresses geocoded and linked to census data) and the prevalence of subclinical atherosclerosis, as assessed by common carotid intimal-medial thickness (IMT) in mid to late adulthood. Participants were 45-84 years of age at baseline and were sampled from six study sites in the United States. After adjustment for age, CSEP and ASEP were both inversely and independently associated with IMT in men. All three indicators CSEP, ASEP, and NSEP were inversely and independently associated with IMT in women. Associations were somewhat reduced after adjustment for cardiovascular risk factors, suggesting that these factors may play a mediating role. There was evidence of heterogeneity in effects of NSEP by gender, and in the effects of ASEP and NSEP by race/ethnicity. Our results contribute to the growing body of work that shows that SEP at multiple points in the life-course, and at the individual and neighborhood level, contributes to the development of atherosclerosis.
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PMID:Life-course socioeconomic positions and subclinical atherosclerosis in the multi-ethnic study of atherosclerosis. 1908 60

Low levels of high-density lipoprotein cholesterol (HDL-C) represent a major cardiovascular risk factor, with a stronger relationship to coronary heart disease than that seen with elevated levels of low-density lipoprotein cholesterol (LDL-C). HDL-C has important antiatherogenic effects, including reverse cholesterol transport, inhibition of LDL-C oxidation, and antiplatelet and anti-inflammatory actions. Patients with low HDL-C are also at an amplified risk of coronary heart disease due to the common coexistence of other risk factors, including excess adiposity, metabolic syndrome, type 2 diabetes mellitus, hypertriglyceridemia, and the atherogenic dyslipidemia characterized by small dense LDL-C. First-line therapy of low HDL-C generally consists of nonpharmacologic measures such as improved fitness and weight loss. Current pharmaceutical options include statins, fibrates, and nicotinic acid. A host of novel approaches involving HDL-C and reverse cholesterol transport hold the promise of fundamentally changing the natural history of atherosclerosis, the most common and important chronic disease in humans.
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PMID:The importance of recognizing and treating low levels of high-density lipoprotein cholesterol: a new era in atherosclerosis management. 1912 82

The huge improvement in the therapeutic arsenal for HIV infection has led to HIV becoming a chronic disease. Like us, our patients are aging and their life expectancy is close to that of the general population. Consequently, we need safe, easily administered drugs with interactions that can be controlled and the least possible impact on highly prevalent comorbidities such as atherosclerosis or coinfection with hepatotropic viruses. Drugs should fit the patient's lifestyle without affecting quality of life and, above all, be free of effects leading to stigma, such as lipoatrophy, a major concern for most recently diagnosed patients. The choice of the two nucleoside analogue reverse transcriptase inhibitors used at the start of antiretroviral therapy should be based on careful evaluation of the abundant data accumulated on all these determining factors which are heralding a new era in the control of HIV infection. Thus, in this scenario, thymidine analogues have been relegated to alternative use. Fixeddose combinations of tenofovir and emtricitabine (TDF/FTC) or abacavir and lamivudine (ABC/3TC) are the backbone of choice when initiating antiretroviral therapy. Direct comparative data are still scarce but suggest similar virological efficacy, with highly preliminary data suggesting some disadvantages associated with the use of ABC/3TC. After excluding patients at risk of hypersensitivity to ABC, both combinations are well tolerated, but TDF/FTC is associated with a better lipid profile. Recent data from the Data Collection on Adverse Events of Anti-HIV drugs (DAD) study show an unexpected association of ABC with increased cardiovascular risk and thus more detailed studies are required.
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PMID:[Are all analogue combinations equal?]. 1919 37

We have recently demonstrated elevated plasma levels of an endogenous nitric oxide synthase inhibitor, asymmetric dimethyl-L-arginine (ADMA), and its association with carotid atherosclerosis in rheumatoid arthritis (RA). Both an elevated risk of myocardial infarction and increased levels of anticitrullinated protein antibodies (ACPAs), specific for RA, had been shown to precede the onset of clinical RA symptoms. Therefore, our aim was to verify the hypothesis that ADMA accumulation might accompany raised ACPAs titers in RA of short duration (< or = 3 years). Twenty patients (16 women, 4 men; mean age, 45 +/- 12 years; mean disease duration, 2.3 +/- 0.5 years) with active RA despite chronic disease-modifying antirheumatic medication, free of cardiovascular disease or atherosclerotic risk factors, were studied. Plasma levels of ADMA and its stereoisomer, symmetric dimethyl-L-arginine (SDMA), were assayed by liquid chromatography/tandem mass spectrometry. The ACPAs were measured by a second-generation enzyme-linked immunosorbent assay. In addition to routine biochemical assays, plasma concentrations of tumor necrosis factor alpha, monocyte chemoattractant protein-1, and vascular cell adhesion molecule-1 soluble form were analyzed with respective enzyme-linked immunosorbent assays. A significant positive correlation between levels of ACPAs and ADMA (r = .60, P = .005), but not SDMA (r = -.02, P = .9), was found. Neither ADMA nor SDMA was correlated to any of the clinical or biochemical parameters reflecting disease activity and inflammatory activation. Thus, excessive ADMA accumulation accompanies elevated ACPAs levels in patients with RA of short duration free of cardiovascular disease or risk factors.
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PMID:Plasma asymmetric dimethylarginine is related to anticitrullinated protein antibodies in rheumatoid arthritis of short duration. 1921 45

Type 1 diabetes (T1D) is a common disease of childhood with a current prevalence of almost 2 cases per 1000 adolescents, according to the third National Health and Nutrition Examination Survey. Modern insulin treatment has resulted in improved quality of life for children with this chronic disorder. However, T1D continues to carry a long-term burden of increased microvascular and macrovascular complications and mortality risk. Compared to the nondiabetic population, patients with T1D are more likely to have >or=1 cardiovascular risk factor and often at an earlier age. Since the prevalence of cardiovascular risk factors increases with age in young persons with T1D, there is a clear need for early screening and counseling to prevent their occurrence and manage long-term health ramifications. The purpose of this review is to describe how traditional risk factors for cardiovascular disease such as an abnormal lipid profile, hypertension, obesity, and insulin resistance contribute to the accelerated atherosclerosis seen in young persons with T1D. A summary is given of the guidelines and recommendations published for clinical care for these patients.
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PMID:Prevalence and significance of cardiometabolic risk factors in children with type 1 diabetes. 1924 17

Chlamydia pneumoniae, an intracellular bacterial pathogen, is known as a leading cause of human respiratory tract infections worldwide. Over the last decade, several reports in the literature have suggested that infection with C. pneumoniae may contribute to the pathogenesis of atherosclerosis. In order to play a causative role in chronic disease, C. pneumoniae would need to persist within infected tissue for extended periods of time, thereby stimulating a chronic inflammatory response. C. pneumoniae has been shown to disseminate systemically from the lungs through infected peripheral blood mononuclear cells and to localize in arteries where it may infect endothelial cells, vascular smooth muscle cells, monocytes/macrophages and promote inflammatory atherogenous process. The involvement of C. pneumoniae in atherosclerosis was investigated by seroepidemiological and pathological studies, in vivo and in vitro studies, and in clinical antibiotic treatment trials. This review will provide an update on the role of C. pneumoniae in atherosclerosis focusing on the recent insights and suggesting areas for future research.
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PMID:Chlamydia pneumoniae and atherosclerosis: current state and future prospectives. 1930 47


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