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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dynamic changes in the reduction-oxidation (redox) state of the tissue lead to the pathophysiological condition. Reduced homocysteine causes dysfunctions in endothelium. The proliferation of smooth muscle cells may lead to occlusive vascular disease, ischemia, and heart failure, but whether fibrosis and hypertension are a consequence of smooth muscle proliferation is unclear. Redox changes during hyper-homocyst(e)inemia may be one of the causes of premature atherosclerotic heart disease. To examine the effect of homocystine on human vascular smooth muscle cells (HVSMC), we isolated HVSMC from idiopathic dilated cardiomyopathic hearts. Coronaries in these hearts were apparently normal. HVSMC numbers in culture were measured by hemocytometer in the presence and absence of homocystine. Results show that homocystine induced cellular proliferation. This proliferation was reversed by the addition of the antioxidant N-acetylcysteine (NAC). Homocystine induces collagen expression in a dose- and time-dependent manner, as measured by Northern blot (mRNA) analysis. The 50% inhibitory concentration of 5 microM for collagen was estimated. The induction of collagen was reversed by the addition of NAC and reduced glutathione. To localize the receptor for homocystine on HVSMC, we synthesized fluorescamine-labeled homocystine conjugate. Incubation of labeled homocystine with HVSMC demonstrated membrane and cytosol localization of homocystine binding. The receptor-ligand binding was disrupted by NAC. Based on sodium dodecyl sulfate-polyacrylamide gel electrophoresis fluorography, we observed a 40- to 25-kDa homocystine redox receptor in HVSMC. Our results suggested that the redox homocysteine induces HVSMC proliferation by binding to the redox receptor and may exacerbate atherosclerotic lesion formation by inducing collagen expression.
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PMID:Homocysteine redox receptor and regulation of extracellular matrix components in vascular cells. 948 29

Several studies have reported the prevalence of medical conditions or investigated the relationships between the oral health status and general health conditions in the elderly. However, the relationship between medical conditions and oral health among the elderly is not well-described. Previous studies have not clearly identified a consistent association between medical conditions and oral health, specifically edentulism and tooth loss. The purpose of this study was to investigate the relationships between medical conditions and oral health, as assessed by edentulism and missing teeth, in an institutionalized elderly population. A systematic sample (n = 175), stratified by age and sex, was drawn from nursing home patients treated by the University of low' as Geriatric Mobile Unit (GMU) team. Data were extracted from GMU dental records, regarding history of medical conditions, medications, dental history, dentate status, and tooth-by-tooth conditions. Mean numbers of missing teeth were significantly higher among those who had a history of atherosclerotic vascular disease, heart failure, ischemic heart disease, and joint disease. Subjects who had a history of atherosclerotic vascular disease, heart failure, ischemic heart disease, and joint disease were more likely to be edentulous than subjects who did not have a history of those diseases. The biological basis for these relationships between dentate status and systemic medical conditions is unclear and warrants further study.
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PMID:Medical conditions associated with missing teeth and edentulism in the institutionalized elderly. 968 Sep 23

Many risk factors operate in both coronary heart disease and stroke, especially ischaemic stroke--age, sex, social class, blood pressure, pre-existing vascular disease (angina, myocardial infarction, cardiac failure, diabetes and peripheral vascular disease, transient ischaemic attack and stroke), atrial fibrillation and fibrinogen, smoking, alcohol and height. Total cholesterol has also recently been recruited to this list. The various mechanisms involved in stroke and its subtypes and the epidemiological problems in evaluating aetiological factors in stroke make the comparison with coronary heart disease more difficult. The recent discrepancy between much of the epidemiology and the clinical trials evaluating the role of lipids in stroke has spurred the systematic review (meta-analysis) of major prospective observational studies. These will provide a clearer assessment about the quantitative comparison of some of the more important risk factors for stroke and coronary heart disease in the near future.
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PMID:Are risk factors for stroke and coronary disease the same? 973 88

Sphingolipids and their metabolic products are now known to have second-messenger functions in a variety of cellular signaling pathways. Lactosylceramide (LacCer), a glycosphingolipid (GSL) present in vascular cells such as endothelial cells, smooth muscle cells, macrophages, neutrophils, platelets, and monocytes, contributes to atherosclerosis. Large amounts of LacCer accumulate in fatty streaks, intimal plaque, and calcified intimal plaque, along with oxidized low density lipoproteins (Ox-LDLs), growth factors, and proinflammatory cytokines. A possible role for LacCer in vascular cell biology was suggested when this GSL was found to stimulate the proliferation in vitro of aortic smooth muscle cells (ASMCs). A further link of LacCer in atherosclerosis was uncovered by the finding that Ox-LDLs stimulated specifically the biosynthesis of LacCer. Ox-LDL-stimulated endogenous synthesis of LacCer by activation of UDP-Gal:GlcCer,beta1-4galtransferase (GalT-2) is an early step in this signaling pathway. In turn, LacCer serves as a lipid second messenger that orchestrates a signal transduction pathway, ultimately leading to cell proliferation. This signaling pathway includes LacCer-mediated activation of NADPH oxidase that produces superoxide. Such superoxide molecules stimulate the GTP loading of p21(ras). Subsequently, the kinase cascade (Raf-1, Mek2, and p44MAPK [mitogen-activated protein kinase]) is activated. The phosphorylated form of p44MAPK translocates from the cytoplasm to the nucleus and engages in c-fos expression, proliferating cell nuclear antigen (PCNA) such as cyclin activation, and cell proliferation takes place. Interestingly, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of GalT-2, can abrogate the Ox-LDL-mediated activation of GalT-2, the signal kinase cascade noted above, as well as cell proliferation. Additional studies have revealed that LacCer mediates the tumor necrosis factor-alpha (TNF-alpha)-induced nuclear factor-kappaB expression and intercellular adhesion molecule (ICAM-1) expression in vascular endothelial cells via the redox-dependent transcriptional pathway. LacCer also stimulates the expression of CD11/CD8, or Mac-1, on the surface of human neutrophils. Collectively, this phenomenon may contribute to the adhesion of neutrophils or monocytes to the endothelial cell surface and thus initiate the process of atherosclerosis. In addition, the LacCer-mediated proliferation of ASMCs may contribute to the progression of atherosclerosis. On the other hand, programmed cell death (apoptosis) by proinflammatory cytokines such as TNF-alpha, interleukin-1, and high concentrations of Ox-LDL occur via activation of a cell membrane-associated neutral sphingomyelinase (N-SMase). N-SMase hydrolyzes sphingomyelin into ceramide and phosphocholine. In turn, ceramide or a homologue serves as an important stress-signaling molecule. Interestingly, an antibody against N-SMase can abrogate Ox-LDL- and TNF-alpha-induced apoptosis and therefore may be useful for in vivo studies of apoptosis in experimental animals. Because plaque stability is an integral aspect of atherosclerosis management, activation of N-SMase and subsequent apoptosis may be vital events in the onset of plaque rupture, stroke, or heart failure. Interestingly, in human liver cells, N-SMase action mediates the TNF-alpha-induced maturation of the sterol regulatory-element binding protein. Moreover, a cell-permeable ceramide can reconstitute the phenomenon above in a sterol-independent fashion. Such findings may provide new avenues for therapy for patients with atherosclerosis. The findings described here indicate an important role for sphingolipids in vascular biology and provide an exciting opportunity for further research in vascular disease and atherosclerosis.
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PMID:Sphingolipids in atherosclerosis and vascular biology. 976 22

Malnutrition and hypoalbuminemia, which are prevalent in patients with end-stage renal disease (ESRD), are strong predictors of increased mortality. However, cardiovascular disease predominates among direct causes of death, whereas malnutrition appears to be of minor importance in this respect. Reports in the literature demonstrate that cardiac failure may cause malnutrition and that infection/inflammation may predispose to atherosclerosis as well as to catabolism and hypoalbuminemia. Proinflammatory cytokines, generated in response to cardiac failure, infection, and other inflammatory stimuli, appear to play a pivotal role by causing muscle wasting, hypoalbuminemia, and anorexia as well as reduced cardiac contractility and atherosclerotic vascular disease. We hypothesize that this scenario also applies to ESRD patients, in whom congestion, hypertension, cardiac failure, and ischemic cardiovascular disease are common. Malnutrition rarely may be the direct cause of death, except in elderly dialysis patients, but may contribute to a poor prognosis by aggravating pre-existing heart failure and increasing the susceptibility to infections.
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PMID:Malnutrition, cardiac disease, and mortality: an integrated point of view. 982 Apr 57

The prevalence of diabetes mellitus rises with age in men and women in the United States and in westernized regions, and the risk of vascular disease is typically increased twofold in diabetic men and threefold in diabetic women. Population-based data concerning the prevalence of diabetes mellitus and its impact on coronary heart disease (CHD) are reviewed. The vascular disease endpoints considered include death, angina pectoris, myocardial infarction (MI), cardiac failure, cardiac arrhythmias, and the experience of diabetics who have undergone angioplasty and revascularization. The impact of coronary risk factors in diabetics is considered for glycemic control, arterial pressure, microalbuminuria, and lipids. Recent guidelines and recommendations concerning lipids, glucose, and blood pressure for diabetics are discussed.
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PMID:Diabetes mellitus and coronary heart disease. 982 Apr 68

Since the recognition that L-arginine (LA) is the natural metabolic donor of nitric oxide, this amino acid has reached the medical spotlight. LA exerts favorable effects in the prevention and treatment of endothelial damage and the restoration of endothelial function in patients with cardiovascular risk factors (hypercholesterolemia, smoking, hypertension, diabetes and advanced age) or with several chronic cardiovascular disorders (coronary, peripheral and cerebral vascular disease, and mild-to-moderate heart failure). LA administration is likely to represent a potentially novel therapeutic strategy during angioplasty, coronary bypass grafting and cardiac transplantation. More conclusive research findings for the rediscovered role of this well-known substance merit close attention.
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PMID:L-Arginine: rediscovery in progress. 989 62

The ability of the Eagle criteria (age >70 years, angina, diabetes, Q wave on EKG, history of congestive heart failure) to predict adverse cardiac events following major vascular surgery has previously been demonstrated. However, the utility of these criteria for lower-extremity amputation is not well established. To determine the value of the Eagle criteria for predicting cardiac morbidity and operative mortality following major lower-extremity amputation, we reviewed 214 consecutive procedures performed at two institutions over a 3-year period. Mean age was 62.7 years and 85% of the patients were male. Diabetes was the most frequent Eagle criterion (74%). The mean number of Eagle criteria was 1.6. Fifty-six percent of the amputations were below the knee, 24% were above the knee, and 20% were guillotine. On multivariate regression analysis, the presence of two or more Eagle criteria (16% vs. 4%, p = 0.04) and decompensated heart failure (39% vs. 7%, p = 0.003) were predictive of adverse cardiac events. The only predictor of postoperative mortality was the presence of two or more Eagle criteria (15% vs. 4%, p = 0.004). Our evaluation of the results of this study led us to conclude that patients requiring major lower-extremity amputation for major vascular disease who have multiple Eagle criteria or decompensated congestive heart failure are at high risk for adverse cardiac events and postoperative death. These findings should be used to guide perioperative cardiac evaluation and therapy.
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PMID:Cardiac morbidity and operative mortality following lower-extremity amputation: the significance of multiple Eagle criteria. 1007 63

Accelerated allograft vasculopathy significantly limits the survival of heart transplant recipients. The prevalence of allograft coronary artery disease is as high as 18% by 1 year and 50% by 5 years following heart transplant. Heart failure and sudden cardiac death are the two most common clinical presentations. In heart transplant recipients with severe, discrete focal allograft vascular disease, percutaneous balloon angioplasty is a viable palliative option. However, its application is limited by a significant restenosis rate and progression of allograft disease in nontreated segments. Diffuse disease with tapering of vessels may be approached by debulking devices. Emerging revascularization modalities for focal stenoses and some of the diffuse tapering vessels include coronary stents, rotational atherectomy, various wavelength lasers, and, to a lesser extent, directional atherectomy. Conceivably, stents will reduce restenosis rates related to focal, discrete plaques; yet it is unknown whether they will be efficacious in short- and long-term treatment of diffusely diseased segments affected by allograft disease. Accurate assessment of clinical outcomes and long-term evaluation is imperative prior to acceptance of these devices as fundamental interventional tools for treatment of allograft coronary artery disease.
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PMID:Percutaneous revascularization modalities in heart transplant recipients. 1034 51

A 49 year old man developed intractable heart failure three years after undergoing heart transplantation. Coronary angiography showed no evidence of graft vascular disease. An initial cardiac biopsy identified one episode of rejection which responded to augmented immunosuppressive treatment. The patient became inotrope dependent and has now survived at home for 22 months using an ambulatory delivery system for intravenous adrenaline (epinephrine), without significant complications. There has been a noticeable improvement in symptoms and left ventricular systolic performance, both clinically and as seen through echocardiographic and radiographic examination. This improvement was substantiated by the results of cardiac catheterisation, which showed a return to normal left ventricular filling pressure and cardiac output. The case is noteworthy because this treatment has allowed a patient who otherwise would have been hospital bound to return to the community. With the current shortage of organs, he would have been unlikely to receive a second transplant. The clinical features and outcome, and social, medicolegal, and financial issues are discussed.
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PMID:Home inotrope treatment for intractable heart failure following heart transplantation. 1040 48


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