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Biomedical subjects

W Koenig

Publications and source records attributed to W Koenig.

At least 55 records · Page 3Linked to original sources
PubMed2000

Immunoradiometric assay of circulating C-reactive protein: age-related values in the adult general population.

BACKGROUND: : Increased values of C-reactive protein (CRP), the classical acute phase protein, within the range below 5 mg/L, previously considered to be within the reference interval, are strongly associated with increased risk of atherothrombotic events, and are clinically significant in osteoarthritis and neonatal infection. METHODS: : A robust new polyclonal-monoclonal solid- phase IRMA for CRP was developed, with a range of 0.05-10.0 mg/L. RESULTS: : Plasma CRP values in general adult populations from Augsburg, Germany (2291 males and 2203 females; ages, 25-74 years) and Glasgow, Scotland (604 males and 650 females; ages, 25-64 years) were very similar. The median CRP approximately doubled with age, from approximately 1 mg/L in the youngest decade to approximately 2 mg/L in the oldest, and tended to be higher in females. CONCLUSION: : This extensive data set, the largest such study of CRP, provides valuable reference information for future clinical and epidemiological investigations.

Adult↗
PubMed1999

Infection with Helicobacter pylori is not a major independent risk factor for stable coronary heart disease: lack of a role of cytotoxin-associated protein A-positive strains and absence of a systemic inflammatory response.

BACKGROUND: There is controversy about the association between Helicobacter pylori infection and manifestations of coronary heart disease (CHD), the potential role of the more virulent H pylori strains, and whether or not a positive serostatus is related to increased levels of markers of systemic inflammation. METHODS AND RESULTS: We assessed the prevalence of an infection with H pylori and in particular the anti-cytotoxin-associated protein A (CagA) antibody response of the more virulent strains expressing CagA in 312 patients with stable CHD and in 479 control subjects. Serological prevalence of H pylori infection (IgG titer) was significantly higher in patients than in control subjects after adjustment for age and sex (44.2% versus 31.3%, P<0.001). After adjustment for various covariates in multiple logistic regression, the odds ratio (OR) for CHD was 1.3 (95% CI, 0.9 to 1.9) given a positive IgG serostatus. The prevalence of CagA-positive strains was 27.9% in patients and 21.7% in control subjects (P=0.076 adjusted for age and sex). The OR for CHD in the fully adjusted model was 1.1 (95% CI, 0.7 to 1.7). None of the inflammatory markers (C-reactive protein, fibrinogen, plasma viscosity, or leukocytes) was significantly different according to serostatus. CONCLUSIONS: In this large case-control study, the association of H pylori infection with stable CHD was strongly reduced and was no longer statistically significant after controlling for potential confounders. We also found no independent association between the more virulent strains and CHD. In addition, a positive serostatus was not associated with a systemic inflammatory response. Thus, these data do not support the hypothesis that infection with H pylori might be a major risk factor for stable CHD.

Aged↗
PubMed1999

Increases in heart rate during an air pollution episode.

This paper assesses whether air pollution increases resting heart rates in 2,681 men and women aged 25-64 years who participated in the MONICA (monitoring of trends and determinants in cardiovascular disease) Augsburg cohort. Increases in heart rate were observed during the air pollution episode in January 1985 compared with non-episode days adjusted for cardiovascular risk factors and meteorologic parameters. Consistently, heart rates were also elevated at high concentrations of sulfur dioxide, total suspended particulates, or carbon monoxide. Acceleration in heart rates indicates an altered autonomic control of the heart in association with air pollution, which may contribute to the observed health effects in association with air pollution.

Adult↗
PubMed1999

C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992.

BACKGROUND: Inflammatory reactions in coronary plaques play an important role in the pathogenesis of acute atherothrombotic events; inflammation elsewhere is also associated with both atherogenesis generally and its thrombotic complications. Recent studies indicate that systemic markers of inflammation can identify subjects at high risk of coronary events. METHODS AND RESULTS: We used a sensitive immunoradiometric assay to examine the association of serum C-reactive protein (CRP) with the incidence of first major coronary heart disease (CHD) event in 936 men 45 to 64 years of age. The subjects, who were sampled at random from the general population, participated in the first MONICA Augsburg survey (1984 to 1985) and were followed for 8 years. There was a positive and statistically significant unadjusted relationship, which was linear on the log-hazards scale, between CRP values and the incidence of CHD events (n=53). The hazard rate ratio (HRR) of CHD events associated with a 1-SD increase in log-CRP level was 1.67 (95% CI, 1.29 to 2. 17). After adjustment for age, the HRR was 1.60 (95% CI, 1.23 to 2. 08). Adjusting further for smoking behavior, the only variable selected from a variety of potential confounders by a forward stepping process with a 5% change in the relative risk of CRP as the selection criterion, yielded an HRR of 1.50 (95% CI, 1.14 to 1.97). CONCLUSIONS: These results confirm the prognostic relevance of CRP, a sensitive systemic marker of inflammation, to the risk of CHD in a large, randomly selected cohort of initially healthy middle-aged men. They suggest that low-grade inflammation is involved in pathogenesis of atherosclerosis, especially its thrombo-occlusive complications.

Biomarkers↗
PubMed1999

Fibrinogen and coronary risk.

The notion that fibrinogen is strongly, consistently, and independently related to coronary risk has been widely accepted. The evidence is based on numerous prospective epidemiological studies and clinical observations. However, the reasons why fibrinogen is elevated in coronary disease and in atherosclerosis are only incompletely understood. All cells involved in the atherogenetic process are able to produce cytokines which induce an acute phase reaction. The potential pathophysiologic mechanisms by which elevated fibrinogen levels mediate coronary risk are manifold: It forms the substrate for thrombin and represents the final step in the coagulation cascade; it is essential for platelet aggregation; it modulates endothelial function; it promotes smooth muscle cell proliferation and migration; it interacts with the binding of plasminogen with its receptor; and finally it represents a major acute phase protein. Whether or not fibrinogen is causally involved in atherothrombogenesis still remains to be determined, and even though other unsolved issues await conclusive answers, fibrinogen has emerged as an important additional marker of coronary risk.

Biomarkers↗
PubMed1999

Chronic infection with Helicobacter pylori does not provoke major systemic inflammation in healthy adults: results from a large population-based study.

It has been suggested that chronic infection with Helicobacter pylori (H. pylori), in particular infection with virulent strains producing the cytotoxin-associated protein CagA, may increase the risk of coronary heart disease by generation of a persistent low-grade inflammatory stimulus. We assessed the relation between serological markers of H. pylori infection and various markers of systemic inflammation in a population-based sample of 1834 men and women aged 18-88. A total of 39.3% of the sample had a positive IgG response, and among these a slight majority was CagA positive. Infection with H. pylori was unrelated to C-reactive protein and the leukocyte count, regardless of CagA status. There was an inverse relation between H. pylori infection and serum albumin. The adjusted OR (95% CI) of an albumin level in the bottom versus the top third were 2.2 (1.5-3.1) and 2.0 (1.4-3.1) for infection with CagA-positive and CagA-negative H. pylori strains, respectively. These results do not support the hypothesis that chronic infection with virulent H. pylori strains provokes major systemic inflammation. The mechanisms underlying the inverse association between H. pylori infection and serum albumin and the clinical relevance of this finding require further research.

Adolescent↗
PubMed1999

Cytomegalovirus infection and coronary heart disease: results of a german case-control study.

This case-control study investigated whether previous infection with cytomegalovirus (CMV) was associated with coronary heart disease (CHD). In total, 312 patients of German nationality aged 40-68 years who had a coronary stenosis of >50% of the luminal diameter were recruited for study. Controls (n=479) were voluntary blood donors. CMV serology was performed to determine presence of specific CMV antibodies (IgG, IgM, IgA ELA test; Medac, Hamburg, Germany). Rheologic and inflammatory markers were determined. The prevalence of specific IgG antibodies against CMV was 54.5% in cases and 49.9% in controls (P=.116). The odds ratio for CHD was 1.21 (95% confidence interval, 0.84-1.75) given a positive serostatus of specific IgG antibodies after adjustment for covariates. With the exception of C-reactive protein in controls, none of the rheologic or inflammatory markers was associated with CMV serostatus. Thus, serologic evidence of previous infection with CMV was not a major risk factor for CHD in this population.

Adult↗
PubMed1998

Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators.

Peroxisome proliferator-activated receptors (PPARs) are key players in lipid and glucose metabolism and are implicated in metabolic disorders predisposing to atherosclerosis, such as dyslipidaemia and diabetes. Whereas PPARgamma promotes lipid storage by regulating adipocyte differentiation, PPARalpha stimulates the beta-oxidative degradation of fatty acids. PPARalpha-deficient mice show a prolonged response to inflammatory stimuli, suggesting that PPARalpha is also a modulator of inflammation. Hypolipidaemic fibrate drugs are PPARalpha ligands that inhibit the progressive formation of atherosclerotic lesions, which involves chronic inflammatory processes, even in the absence of their atherogenic lipoprotein-lowering effect. Here we show that PPARalpha is expressed in human aortic smooth-muscle cells, which participate in plaque formation and post-angioplasty re-stenosis. In these smooth-muscle cells, we find that PPARalpha ligands, and not PPARgamma ligands, inhibit interleukin-1-induced production of interleukin-6 and prostaglandin and expression of cyclooxygenase-2. This inhibition of cyclooxygenase-2 induction occurs transcriptionally as a result of PPARalpha repression of NF-kappaB signalling. In hyperlipidaemic patients, fenofibrate treatment decreases the plasma concentrations of interleukin-6, fibrinogen and C-reactive protein. We conclude that activators of PPARalpha inhibit the inflammatory response of aortic smooth-muscle cells and decrease the concentration of plasma acute-phase proteins, indicating that PPARalpha in the vascular wall may influence the process of atherosclerosis and re-stenosis.

Acute-Phase Proteins↗
PubMed1998

Sex differences in selection of pacemakers: retrospective observational study.

OBJECTIVE: To evaluate the effect of patients' sex on selection of pacemakers. DESIGN: Retrospective univariate and multivariate analysis of a large database. SETTING: German central pacemaker register. SUBJECTS: Records collected at the register for 1992 and 1993 (n=31 913), covering 64% of all implantations in Germany. MAIN OUTCOME MEASURE: Probability of receiving a single chamber, dual chamber, or rate responsive pacemaker in relation to sex. RESULTS: Univariate analysis showed that women were more likely to receive single chamber pacemakers and less likely to receive dual chamber or rate responsive systems than men. After demographic and clinical variables were controlled for, women were still more likely to receive a single chamber system (atrial pacing: odds ratio 0.89, 95% confidence interval 0.74 to 1.07; ventricular pacing: 0.85, 0.80 to 0.92) and less likely to receive a dual chamber (1.20, 1.12 to 1.30) or a rate responsive system (1.26, 1.17 to 1.37) than men. CONCLUSIONS: The data suggest sex differences in the selection of a pacemaker system which cannot be explained by the underlying cardiac disorder. Further research is needed to evaluate why guidelines for implanting pacemakers are not better adhered to.

Aged↗
PubMed1998

[Epidemiology of coronary heart disease].

The incidence of acute myocardial infarction (AMI) shows large regional differences. This variability cannot be completely explained by differences in classical risk factors. 28-day case fatality of AMI remains unacceptably high with 50% on the average, although therapeutic possibilities have improved considerably. Time trends in mortality from ischaemic heart disease (IHD) show a decrease in most Western European countries and an increase in Eastern Europe. On a population level, the impact of medical care on the short-term and long-term prognosis of AMI is not completely understood. Despite considerable progress in primary and secondary prevention, the incidence and prevalence of IHD will increase in the future due to aging of the population.

Coronary Disease↗
PubMed1998

Effects of hormone replacement therapies on fibrinogen and plasma viscosity in postmenopausal women.

In women, cardiovascular morbidity and mortality sharply increase after the onset of menopause. There is substantial evidence that hormone replacement therapy (HRT) may decrease the risk of coronary heart disease (CHD); however, the mechanisms of this preventive effect are unclear. We investigated the association between HRT and plasma viscosity as well as fibrinogen levels in postmenopausal women of a population-based sample (n=300, age 52-65 years). A total of 94 women used HRT; of these, 50 took oestrogen monotherapy and 44 used oestrogen-progesterone combinations. HRT was associated with significantly lower fibrinogen concentrations (2.32 v 2.68 g/l, P<0.001) and decreased plasma viscosity (1.147 v 1.176 mPa/s, P=0.01). Multivariate analyses controlling simultaneously for the effects of age, smoking, body mass index, and use of diuretics confirmed decreased fibrinogen and plasma viscosity values in women using HRT. A trend towards lower plasma viscosity (1.139 v 1.160 mPa/s) and plasma fibrinogen (2.28 v 2.44 g/l) was observed in women on oestrogen-progesterone combinations as compared with oestrogen monotherapy users: however, after controlling for the above-mentioned variables these differences were not statistically significant. This study demonstrates decreased plasma viscosity in women on HRT. Improved rheology offers a mechanism by which HRT lowers the risk of CHD in postmenopausal women.

Aged↗
PubMed1998

Comparison of the proximal flow convergence method and the jet area method for the assessment of the severity of tricuspid regurgitation.

AIMS: To compare the value of the proximal flow convergence method and the jet area method for the determination of the severity of tricuspid regurgitation. METHODS AND RESULTS: The proximal isovelocity surface area radius and the jet area/length were measured in 71 consecutive patients with angiographically graded (grade 0/I-III) tricuspid regurgitation. Rank correlation coefficients with the angiographic grade were 0.71 (P < 0.001) for the proximal isovelocity surface area radius (aliasing border of 28 cm.s-1), 0.66 (P < 0.001) for the jet area, and 0.63 (P < 0.001) for the jet length. The proximal isovelocity surface area radius was significantly correlated with the jet area/length (correlation coefficients 0.82/0.77, P < 0.001). Correct differentiation between mild to moderate (grade I-II) and severe (grade III) tricuspid regurgitation was achieved in 62 of 71 patients (87%) by means of the proximal isovelocity surface area radius, in 61 of 71 (86%) by the jet area, and in 62 of 71 (87%) by the jet length. Grade III tricuspid regurgitation was not identified in five of 21 patients (24%) by means of the proximal isovelocity surface area radius, in six of 21 (29%) by the jet area, and in seven of 21 (33%) by the jet length. CONCLUSION: The flow convergence method and the jet area method are of similar value for the determination of the severity of tricuspid regurgitation. Both methods differentiated mild to moderate from severe tricuspid regurgitation in most patients. However, underestimation of severe tricuspid regurgitation in 20-30% of the cases represents a serious limitation of both methods.

Adult↗
PubMed1998

Expression of intercellular adhesion molecule-1 in human coronary endothelial and smooth muscle cells after stimulation with tumor necrosis factor-alpha.

BACKGROUND: The intercellular adhesion molecule-1 (ICAM-1) is one of several human cell adhesion molecules that play a critical role in the early stages of postangioplasty restenosis. In this study, the in-vitro expression of ICAM-1 in human coronary endothelial cells and human coronary smooth muscle cells (SMC) after stimulation with tumor necrosis factor-alpha (TNF-alpha) was investigated. METHODS AND RESULTS: SMC were isolated from the media of normal human coronary arteries (n = 26) up to 10 h post mortem (HCMSMC) and from human atherosclerotic coronary arteries (HCPSMC) that were extracted by thrombendarterectomy (n = 25). Endothelial cells of human coronary arteries (HCAEC) were purchased from Clonetics (Cell System, Remagen, Germany), and endothelial cells from human umbilical cord veins (HUVEC) were isolated after vaginal delivery. For investigations of the effect of TNF-alpha (2.5, 5, 10, and 20 ng/ml) on the proliferative activity of HUVEC, HCAEC, HCPSMC, and HCMSMC, serum-free media was used. After 24 h cell number and cell size distribution were measured in a cell analyzer system. The proliferation of HCPSMC and HCMSMC was increased by TNF-alpha; however, significant differences compared with controls were not reached. The proliferation of HUVEC and HCAEC was significantly reduced by TNF-alpha. For investigations of the effect of TNF-alpha (2.5, 5, 10, and 20 ng/ml) on the surface expression of ICAM-1, monoclonal anti-ICAM-1 antibodies (84H10) were used. The expression of ICAM-1 was analyzed using an immunofluorescence microscope. For flow cytometry analysis, 5 x 10(3) cells (100% gated) were analyzed using a fluorescence-activated cell sorter. In control cultures with no stimulation, the expression of ICAM-1 was positive in HCAEC, HCPSMC, HCMSMC, and HUVEC. TNF-alpha stimulated the expression of ICAM-1 in a time- and dose-dependent manner. After maximal stimulation with TNF-alpha (20 ng/ml for 24 h), the expression of ICAM-1 was stronger in HCMSMC than in HCPSMC. CONCLUSIONS: These results suggest that the cytokine TNF-alpha regulates the expression of ICAM-1 in both human coronary endothelial cells and SMC, and could therefore play an important role in the pathophysiology of inflammatory and immune processes in restenosis after angioplasty.

Cell Division↗