1,721,083 research outputs found
Diagnostic interviews in acute treatment of patients after myocardial infarction in the new German states - A qualitative study on subjective theories of illness influenced by changes at home, at the workplace and in society
No full textDiagnostic interviews in acute treatment of patients after myocardial infarction in the new German states - A qualitative study on subjective theories of illness influenced by changes at home, at the workplace and in society
No full textInterleukin-1 and related proteins in cardiovascular disease in adults and children
No full textInterleukin-1 (IL-1) is a key mediator in the cytokine network, controlling important functions in the immune system, during development, infection, inflammation, cell-differentiation, tissue remodelling, and even cell death. The agonistic isoforms of IL-1 (i.e., IL-1 alpha and IL-beta), the IL-1 receptor antagonists, the receptors and receptor-associated proteins, as well as the recently identified IL-18 and its receptor belong to the IL-1 family of proteins. Activation of the IL-1 beta and IL-18 precursors is performed enzymatically by caspase-1, previously termed IL-1 beta -converting enzyme (ICE). This molecule is the founding member of the caspase family of enzymes, which are involved in maturation of cytokines and in initiation and execution of apoptotic processes. It has been suggested that cytokines and apoptosis are involved in pathogenesis of cardiovascular diseases such as atherosclerosis, chronic heart failure, myocarditis, cardiomyopathy, or stroke. Since IL-1, like TNF, is a central mediator in the cytokine network, it may act as a potent activator of cardiovascular cells. We know that cells of the vessel wall and the heart can produce IL-1 and respond to this mediator by production of other cytokines or regulation of other cardiovascular cell functions. Thus, this report summarizes general information about the molecules of the IL-1 family of proteins, including the caspases, as well as data regarding these proteins in relation to the vessel wall and the heart and their role in cardiovascular disease in adults and children. The summarized information indicates a role of these molecules in regulation of local inflammatory responses during cardiovascular disease
Direct costs of severe sepsis in three German intensive care units based on retrospective electronic patient record analysis of resource use
No full textObjective: To determine the direct costs of severe sepsis patients in German intensive care units (ICUs). Design: Retrospective electronic data analysis. Setting: Three adult intensive care units (surgical/medical) in three university hospitals in Germany. Patients: 385 patients identified by standard definitions as suffering from severe sepsis. Measurements and results: A bottom-up approach was used to determine the direct ICU cost on actual resource use (medication, laboratory tests, microbiological analysis, disposables, and clinical procedures) for patients with severe sepsis. To determine the total direct costs, center-specific personnel and basic bed ("hotel") costs were added to total resources consumed. Average hospital mortality of severely septic patients was 42.6%. Mean ICU length of stay (LOS) was 16.6 days. Survivors stayed on average 4 days longer than nonsurvivors. The mean direct ICU costs of care were 23,297 +/- 18,631 euros per patient and 1,318 euros per day. In comparison, average daily charges being paid for an ICU patient by the health care system in Germany are 851 euros (based on official statistics). Nonsurvivors were more expensive than survivors in total direct costs (25,446 vs. 21,984 euros) and in per day direct cost (1,649 vs. 1, 162 euros). Medication makes up the largest part of the direct costs, followed by expenses for personnel. Conclusions: Patients with severe sepsis have a high ICU mortality rate and long ICU LOS and are substantially expensive to treat. Nonsurviving septic patients are more costly than survivors despite shorter ICU LOS. This is due to higher medication costs indicating increased efforts to keep patients alive
Endogenous nitric oxide and soluble tumor necrosis factor receptor levels are enhanced in infants with congenital heart disease
No full textObjective. This study was designed to investigate cytokine and nitric oxide levels in pediatric patients suffering from chronic heart failure and to investigate effects of beta -blocker treatment on these levels. Patients: Fifteen infants with heart failure resulting from left-to-right shunts with pulmonary overcirculation were compared with 11 infants with cyanotic heart defects with reduced pulmonary blood flow. Four of these patients were finally treated with the beta -blocker propranolol. Measurements. Endogenous nitric oxide production was determined by measuring total plasma nitrite/nitrate (Griess method), and levels of soluble tumor necrosis factor receptors type 1 and type 2 (TNF-R1 and TNF-R2, respectively) were measured by commercially available enzyme-linked immunosorbent assay. Main Results. In infants with left-to-right shunts, soluble tumor necrosis factor receptor levels were significantly elevated as compared with infants with cyanosis (TNF-R1: 1.7 +/- 0.5 vs. 0.8 +/- 0.3 ng/mL; p = .0003; TNF-R2: 8.1 +/- 4.0 vs. 5.1 +/- 3.2 ng/mL; p = .049). In addition, we found a significant correlation between nitrate/nitrite levels and TNF-R1 (r = .70; p = .0001) or TNF-R2 (r = .62; p = .0013), respectively. Furthermore, the tumor necrosis factor receptor levels in four children after beta -blocker treatment were lower as compared with levels before beta -blocker treatment. Conclusions: Immune mechanisms, such as cytokine or nitric oxide production, may be involved in pathogenesis of heart failure in children, and may contribute to the beneficial effects of beta -blocker treatment observed in these patients
Cytokines in chronic heart failure: possible interaction in the neurohormonal and the cytokine system at the cAMP level?
No full textIn recent years, the pathophysiological concept of chronic heart failure (CHF) has changed from an isolated hemodynamic view to a more complex concept involving neuroendocrine and inflammatory pathways. New therapeutic strategies, such as beta-blocker therapy, are based on these new concepts and provide clinical evidence for a clinical benefit in patients with CHF. The survival benefit of beta-blocker therapy in CHIT has been related to neurohumoral regulation. Thus, evidence evolved showing that following beta-blocker therapy cytokine levels in CHF patients are altered. We have shown that the levels of soluble TNF receptor type 2 correlated well with cAMP in leukocytes. Data from clinical studies in adult and infant CHF patients have demonstrated that beta-blocker therapy is accompanied by altered cytokine, cytokine antagonist, and/or soluble cytokine receptor levels. These alterations may result from a dysregulated interaction of beta-adrenergic pathways and the cytokine system, and are possibly related to cAMP-dependent regulation of the release or shedding of these mediators
Cytokines in chronic heart failure: possible interaction in the neurohormonal and the cytokine system at the cAMP level?
No full textIn recent years, the pathophysiological concept of chronic heart failure (CHF) has changed from an isolated hemodynamic view to a more complex concept involving neuroendocrine and inflammatory pathways. New therapeutic strategies, such as beta-blocker therapy, are based on these new concepts and provide clinical evidence for a clinical benefit in patients with CHF. The survival benefit of beta-blocker therapy in CHIT has been related to neurohumoral regulation. Thus, evidence evolved showing that following beta-blocker therapy cytokine levels in CHF patients are altered. We have shown that the levels of soluble TNF receptor type 2 correlated well with cAMP in leukocytes. Data from clinical studies in adult and infant CHF patients have demonstrated that beta-blocker therapy is accompanied by altered cytokine, cytokine antagonist, and/or soluble cytokine receptor levels. These alterations may result from a dysregulated interaction of beta-adrenergic pathways and the cytokine system, and are possibly related to cAMP-dependent regulation of the release or shedding of these mediators
Interleukin-1 and related proteins in cardiovascular disease in adults and children
No full textInterleukin-1 (IL-1) is a key mediator in the cytokine network, controlling important functions in the immune system, during development, infection, inflammation, cell-differentiation, tissue remodelling, and even cell death. The agonistic isoforms of IL-1 (i.e., IL-1 alpha and IL-beta), the IL-1 receptor antagonists, the receptors and receptor-associated proteins, as well as the recently identified IL-18 and its receptor belong to the IL-1 family of proteins. Activation of the IL-1 beta and IL-18 precursors is performed enzymatically by caspase-1, previously termed IL-1 beta -converting enzyme (ICE). This molecule is the founding member of the caspase family of enzymes, which are involved in maturation of cytokines and in initiation and execution of apoptotic processes. It has been suggested that cytokines and apoptosis are involved in pathogenesis of cardiovascular diseases such as atherosclerosis, chronic heart failure, myocarditis, cardiomyopathy, or stroke. Since IL-1, like TNF, is a central mediator in the cytokine network, it may act as a potent activator of cardiovascular cells. We know that cells of the vessel wall and the heart can produce IL-1 and respond to this mediator by production of other cytokines or regulation of other cardiovascular cell functions. Thus, this report summarizes general information about the molecules of the IL-1 family of proteins, including the caspases, as well as data regarding these proteins in relation to the vessel wall and the heart and their role in cardiovascular disease in adults and children. The summarized information indicates a role of these molecules in regulation of local inflammatory responses during cardiovascular disease
Competence and innovation in cardiovascular MRI: statement of the German Cardiac Society
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