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Biomedical subjects

W Koenig

Publications and source records attributed to W Koenig.

At least 19 recordsLinked to original sources
PubMed2002

[Sex specific trends of sudden cardiac death and acute myocardial infarction: results of the population-based KORA/MONICA-Augsburg register 1985 to 1998].

BACKGROUND AND AIM: Myocardial infarction (MI) is the main single cause of death in adult populations. For the MONICA Augsburg population, MI-morbidity, mortality, and 28-day case fatality and their determinants were assessed by gender, and suggestions for an intensified acute care program were presented. PATIENTS AND METHODS: From 1985 to 1998, 13 499 25- to 74-year-old MI cases (9537 men, 3962 women) were registered; 7873 cases (5300 men, 2573 women) died within 28 days. Cardiac deaths were identified by regional health departments; causes of death were validated by the last treating physician and the coroner (response > 90 %). Hospitalized patients were interviewed about history and circumstances of the acute event; treatment data were abstracted from hospital charts. The prehospital phase, the first and the 2nd to 28thday after hospitalization were analyzed separately. RESULTS: MI-morbidity per 100 000 population declined from 560 to 397 MI cases in men and from 161 to 145 in women; mortality decreased from 317 to 232 in men and from 101 to 96 in women. The decline in men was due to decreasing incident and recurrent MI whereas in women it was only due to a reduction of recurrent MI. One third died before hospitalization, mainly at home. Case fatality (CF) on the first day in hospital increased. In 24 hour survivors, evidence based treatment increased considerably, and was accompanied by decreasing 28-day-CF from 13.0 % to 8.4 % in men, and from 12.5 % to 10.7 % in women. CONCLUSION: Aggressive risk factor management and education of patients with cardiovascular risk factors concerning acute symptoms and the use of the emergency system will consequently improve pre-hospital and 28-day survival of the population.

Adult↗
PubMed2002

Impaired glucose tolerance is associated with increased serum concentrations of interleukin 6 and co-regulated acute-phase proteins but not TNF-alpha or its receptors.

AIMS/HYPOTHESIS: A population-based sample was studied to define immune abnormalities in individuals at risk of Type II (non-insulin-dependent) diabetes mellitus because of impaired glucose tolerance. METHODS: A total of 1653 individuals aged 55 to 74 years participated in a population based survey in Southern Germany (KORA Survey 2000). Those without a history of diabetes were subjected to an OGTT. Randomly selected subjects with IGT ( n=80) were compared with non-diabetic control subjects ( n=77) and patients with Type II diabetes ( n=152) of the same population-based sample after matching for age and sex. Immune parameters were analysed in serum with rigidly evaluated ELISA. RESULTS: Serum pro-inflammatory cytokine interleukin 6 (IL-6) concentrations were higher in subjects with IGT and Type II diabetes than in the control subjects (median 1.8 and 2.5 vs 0.8 pg/ml, p<0.0001). Soluble IL-6 receptors potentiate IL-6 bioactivity and their concentrations were mildly increased in Type II diabetes ( p<0.05). These immune changes seem relevant because IL-6 dependent acute-phase proteins C-reactive protein, serum amyloid A protein and fibrinogen were also increased in IGT and Type II diabetes. Circulating concentrations of TNF-alpha and its two receptors sTNF-R60 and sTNF-R80 were not increased in IGT subjects compared with the control subjects. CONCLUSION/INTERPRETATION: Our study shows systemic up-regulation of selected inflammatory mediators in patients with Type II diabetes and IGT. The pattern observed is non-random and fits with an IL-6 associated rather than TNF-alpha associated response.

Acute-Phase Proteins↗
PubMed2002

[Suspected acute coronary syndrome in patients without ST-elevation. Exclusion of infarction, early clinical estimation and non-coronary diagnoses].

BACKGROUND AND OBJECTIVE: Patients admitted to the hospital with suspected acute coronary syndrome (ACS) represent a collective at high risk. The NOWIS substudy aimed at evaluating 3 points: (1) Safe exclusion of myocardial infarction by history, symptoms, biochemical markers and the ECG, (2) value of the first diagnosis by the physician in the emergency room, and (3) prevalence and distribution of non-coronary leading diagnoses. PATIENTS AND METHODS: In 164 patients admitted with suspected ACS without ST-segment elevation (73 % men, median age 66 years) the cardiac markers myoglobin, troponin T and CK/CK-MB were assessed on admission and 4 h later. In 2 of the NOWIS centers, the diagnosis on admission, derived from the ECG, history and clinical symptoms, was compared with the leading diagnosis at discharge, based on coronary angiography and, if negative, on additional esophago-gastroscopy. RESULTS: (1) Myoglobin was the biochemical marker with the highest sensitivity 4 h after admission for acute myocardial infarction (classic) definition by CK-MB elevation) with 90.4 %, followed by troponin T with 84.6 %. Four h after admission, in 15.4 % of the infarction patients (prevalence 31.7 %) troponin T was normal. (2) The admission diagnosis instable angina pectoris was confirmed in 46.7 % (57 of 122), suspected acute infarction in 76.2 % (32 of 42). On the other hand, 90.4 % (57 of 63) of the patients with instable angina as leading diagnosis at discharge were correctly diagnosed on admission, but only 61.5 % (32 of 42) of the patients with infarction. (3) At discharge, 29.9 % (49 of 164) of the patients had a non-coronary leading diagnosis. Here, the most common were gastro-intestinal (55.1 %), costo-vertebral (18.4 %) and broncho-pulmonary (16.3 %). CONCLUSIONS: (1) Troponin and myoglobin are helpful in patients without ST-segment elevation; yet, 4 h after admission, a safe exclusion of myocardial infarction is not possible. (2) The clinical diagnosis on admission is important. However, it corresponds with the leading diagnosis at discharge, based on coronary angiography, in only 50 to 75 %. Patients admitted with suspected ACS should be monitored for 24 h in the hospital (chest pain units or coronary care units). (3) Nearly one third of the patients initially admitted with suspected ACS show a non-coronary leading diagnosis, thus underlining the value of further investigations and of an interdisciplinary approach.

Acute Disease↗
PubMed2002

Homocysteine and methylenetetrahydrofolate reductase genotype: association with risk of coronary heart disease and relation to inflammatory, hemostatic, and lipid parameters.

AIM: It has been suggested that homocysteine (tHcy) levels and methylenetetrahydrofolate reductase (MTHFR) genotype are primary risk factors for coronary heart disease (CHD). We performed a case-control study to investigate whether tHcy levels and MTHFR genotype (677 C-->T mutation and 1298 A-->C mutation) are associated with CHD under special consideration of the possibility for confounding. METHODS: German speaking patients aged 40-68 years who underwent coronary angiography at the University of Ulm between April 1996 and November 1997 and who had at least one coronary stenosis greater than 50% were included in the study. Controls were sampled from voluntary blood donors and were matched for sex and age. tHcy levels were measured by high performance liquid chromatography and MTHFR genotype by means of polymerase chain reaction. In addition, C-reactive protein, fibrinogen, plasma viscosity, leukocytes, HDL-cholesterol and Lp(a) were determined. RESULTS: Overall, 312 patients and 479 controls were enrolled in the study (response in patients 78%, in controls 84%). Mean tHcy value was 9.43 micromol/l in CHD patients and 8.91 micromol/l in controls (P=0.145). Prevalence of 677TT-polymorphism was 9.9% in patients and 10.4% in controls (P=0.295). Prevalence of 1298CC-polymorphism was 9.7% in patients and 13.8% in controls (P=0.346). There was a clear association of tHcy-values, but not of 677TT- or 1298CC-genotype with conventional CHD risk factors. After adjustment for these risk factors no increased risk for CHD could be associated with increased tHcy-values, with 677TT or 1298CC-genotype, or with their combination. Also no statistically significant relationships of these parameters to inflammatory, rheologic or hemostatic parameters or lipids were detectable. CONCLUSION: These results do not confirm an independent relationship of tHcy values and MTHFR genotype with risk of CHD in the population studied.

Adult↗
PubMed2002

Immunomodulation by perioperative administration of n-3 fatty acids.

It has been increasingly reported that administration of n-3 fatty acids is beneficial in patients with inflammatory processes. This effect is most likely caused by different biological characteristics, including an immunomodulating effect of the products derived from n-3 fatty acids through eicosanoid metabolism. The aim of this study was to investigate the effect of perioperative administration of n-3 fatty acids on inflammatory and immune responses as well as on the postoperative course of patients with extended surgical interventions of the abdomen. In particular, the effect of n-3 fatty acids on interleukin-6 release and on granulocyte/monocyte function (HLA-DR expression) was studied. There was a downregulation of the inflammatory response, and, simultaneously, a smaller postoperative immune suppression in the n-3 fatty acid group. In addition, we observed shorter postoperative periods in the intensive care unit and on the regular medical wards as well as lower rates of severe infections. The results suggest that perioperative administration of n-3 fatty acids may have a favourable effect on outcome in patients with severe surgical interventions by lowering the magnitude of inflammatory response and by modulating the immune response.

Abdomen↗
PubMed2001

Different effects of antisense RelA p65 and NF-kappaB1 p50 oligonucleotides on the nuclear factor-kappaB mediated expression of ICAM-1 in human coronary endothelial and smooth muscle cells.

BACKGROUND: Activation of nuclear factor-kappaB (NF-kappaB) is one of the key events in early atherosclerosis and restenosis. We hypothesized that tumor necrosis factor-alpha (TNF-alpha) induced and NF-kappaB mediated expression of intercellular adhesion molecule-1 (ICAM-1) can be inhibited by antisense RelA p65 and NF-kappaB1 p50 oligonucleotides (RelA p65 and NF-kappaB1 p50). RESULTS: Smooth muscle cells (SMC) from human coronary plaque material (HCPSMC, plaque material of 52 patients), SMC from the human coronary media (HCMSMC), human endothelial cells (EC) from umbilical veins (HUVEC), and human coronary EC (HCAEC) were successfully isolated (HCPSMC, HUVEC), identified and cultured (HCPSMC, HCMSMC, HUVEC, HCAEC). 12 hrs prior to TNF-alpha stimulus (20 ng/mL, 6 hrs) RelA p65 and NF-kappaB1 p50 (1, 2, 4, 10, 20, and 30 microM) and controls were added for a period of 18 hrs. In HUVEC and HCAEC there was a dose dependent inhibition of ICAM-1 expression after adding of both RelA p65 and NF-kappaB1 p50. No inhibitory effect was seen after incubation of HCMSMC with RelA p65 and NF-kappaB1 p50. A moderate inhibition of ICAM-1 expression was found after simultaneous addition of RelA p65 and NF-kappaB1 p50 to HCPSMC, no inhibitory effect was detected after individual addition of RelA p65 and NF-kappaB1 p50. CONCLUSIONS: The data point out that differences exist in the NF-kappaB mediated expression of ICAM-1 between EC and SMC. Experimental antisense strategies directed against RelA p65 and NF-kappaB1 p50 in early atherosclerosis and restenosis are promising in HCAEC but will be confronted with redundant pathways in HCMSMC and HCPSMC.

Journal Article↗
PubMed2001

Aspirin (5 mmol/L) inhibits leukocyte attack and triggered reactive cell proliferation in a 3D human coronary in vitro model.

BACKGROUND: Leukocyte attack (LA) and the triggered reactive proliferation of smooth muscle cells (SMCs) are key events for the development of early atherosclerosis and restenosis. In the present study, we used a 3D human coronary in vitro model of LA (3DLA model) to examine the effect of high-dose aspirin on the adhesion and chemotaxis of leukocytes and the reactive proliferative response of SMCs. METHODS AND RESULTS: For dose-finding, the effect of aspirin (1, 2, 5, and 10 mmol/L) on the tumor necrosis factor-alpha-induced upregulation of intercellular adhesion molecule-1 was analyzed in monocultures of human coronary endothelial cells (HCAEC) and the SMCs of the human coronary media (HCMSMC). In cytoflow and Northern blot experiments, the expression of intercellular adhesion molecule-1 was slightly reduced after incubation with 5 mmol/L aspirin, and strong inhibition was found after incubation with 10 mmol/L. In 3DLA models, HCAECs and HCMSMCs were cultured on both sides of a porous filter. For LA, human monocytes or CD4(+) lymphocytes were seeded on the HCAEC side of the 3DLA unit. A dose of 5 mmol/L aspirin inhibited the adherence of monocytes or CD4(+) lymphocytes by 50% (P:<0.01) and the chemotaxis of monocytes by 90% (P:<0.01). The reactive proliferative response of cocultured HCMSMCs after LA, as measured by the uptake of bromodeoxyuridine, was significantly reduced by 83% after selective monocyte attack (P:<0.001) and by 42% after selective CD4(+) lymphocyte attack (P:<0.05). CONCLUSIONS: A local concentration of 5 mmol/L aspirin should be accepted as the lowest rational concentration for the beneficial in vitro effects of high-dose aspirin to be reproduced in clinical studies.

Aspirin↗
PubMed2001

Effect of alcohol consumption on systemic markers of inflammation.

BACKGROUND: Epidemiological studies suggest that light to moderate alcohol intake is associated with lower all-cause mortality than abstention or heavy alcohol intake, primarily through reduced risk of coronary heart disease. The underlying mechanisms are incompletely understood. METHODS: We investigated the association between alcohol consumption (assessed by a 7-day food record) and concentrations of C-reactive protein (CRP), alpha1-globulins, alpha2-globulins, albumin, and transferrin, and leucocyte count in a sample of 2006 men and women aged 18-88 years participating in a national health survey carried out in former West Germany in 1987-88. Analyses were based on 781 men and 995 women with complete data. FINDINGS: Among men, alcohol consumption showed a U-shaped association with mean values of CRP (p for linear term 0.65, for quadratic term 0.048), alpha1-globulins (p=0.20, 0.0006), alpha2-globulins (p=0.82, 0.31), and leucocyte count (p=0.51, 0.26) even after adjustment for age, smoking, body-mass index, HDL and LDL cholesterol, history of hypertension, education, and income. There were inverted U-shaped associations between the negative acute-phase reactants albumin (p=0.41, 0.006) and transferrin (p=0.14, 0.28) and alcohol intake. In women, the associations were less strong for CRP (p=0.35, 0.31), leucocyte count (p=0.28, 0.15), and transferrin (p=0.86, 0.83). Concentrations of alpha1-globulins and alpha2-globulins were inversely related to alcohol consumption, and albumin showed a positive association with increasing alcohol intake in women. INTERPRETATION: Non-drinkers and heavy drinkers had higher CRP concentrations than moderate drinkers. In view of the robust association between markers of inflammation, especially CRP, and risk of coronary heart disease, an anti-inflammatory action of alcohol could contribute to the link between moderate consumption and lower cardiovascular mortality.

Acute-Phase Proteins↗
PubMed2001

Role of novel markers of inflammation in patients with stable coronary heart disease.

The role of novel markers of inflammation in patients with coronary heart disease (CHD) is still unclear. We conducted a case-control study to assess the association between various markers of inflammation and the presence and severity of chronic stable CHD. We included 312 clinically stable patients with angiographically documented CHD, aged 40 to 68 years. Voluntary blood donors (n = 479) matched for age and gender served as controls. High-sensitivity C-reactive protein, serum amyloid A, plasminogen activator inhibitor-1 activity, von Willebrand factor, fibrinogen, plasma viscosity, albumin, and neutrophils were determined. The severity of CHD was evaluated by 3 coronary scoring systems: the clinical 1- to 3-vessel disease score, the American Heart Association extension score (1 to 15 segments), and the Gensini score. All markers of inflammation were highly significantly elevated (all p <0.005) in patients with stable CHD compared with controls. After multivariable adjustment by means of logistic regression analysis, the association between CHD and fibrinogen, plasma viscosity, von Willebrand factor, and plasminogen activator inhibitor-1 activity remained substantial, whereas it decreased in high-sensitivity C-reactive protein, serum amyloid A, and neutrophils. The combination of > or = 2 markers of inflammation was associated with a strongly increased risk of CHD. No association between markers of inflammation and any of the coronary scores applied was found. These results document an independent association between most of the markers of inflammation and chronic CHD, even in clinically stable patients. The combination of several of these biochemical markers, i.e., the determination of an "inflammatory risk profile," may be useful to further stratify cardiovascular risk.

Adult↗
PubMed2001

Helicobacter pylori heat shock protein 60 and risk of coronary heart disease: a case control study with focus on markers of systemic inflammation and lipids.

AIM: it has been suggested that antibodies against heat shock proteins seem to be involved in the pathogenesis of coronary heart disease (CHD). We conducted a case-control study to investigate whether antibodies against Helicobacter pylori heat shock protein 60 (hsp60) are associated with CHD, and focused specifically on markers of systemic inflammation and lipids. METHODS: all patients of German nationality aged 40-68 years who underwent coronary angiography at the University of Ulm between October 1996 and November 1997 and who had at least one coronary stenosis greater than 50% were included in the study. Controls were sampled from voluntary blood donors and were matched for sex and age. H. pylori hsp60 was assessed by Western blot (H. pylori Westernblot, AID Co., Strassberg, Germany). In addition, C-reactive protein, fibrinogen, plasma viscosity, leukocytes, HDL-cholesterol and Lp(a) were determined. RESULTS: overall, 312 patients and 479 controls were enrolled in the study (response in patients 78%, in controls 84%). Whereas 25.0 and 22.4% of the cases showed a hsp60 extinction of 100 or 20-99% (according to the reference blot), respectively, only 21.3 and 14.8% of the controls did so (P=0.004). The age and sex adjusted odds ratio (OR) for CHD was 1.53 (95% confidence interval (CI) 1.14-2.06) given an extinction of 20-100% compared with an extinction of 0-19%. The OR for CHD decreased to 1.28 (95% CI 0.90-1.81) after further adjustment for other covariates. With exception of HDL-cholesterol (lowest in subjects with the highest hsp60 extinction) none of the investigated inflammatory markers was associated with the hsp60 distribution. CONCLUSION: a high H. pylori hsp60 extinction seems not to be an independent risk factor for CHD in this population.

Adult↗
PubMed2001

Exercise and thrombosis.

Long-term moderate or strenuous physical activity is associated with a considerable reduction in cardiovascular morbidity and mortality in primary and secondary prevention. Various mechanisms, including changes in lipids, lifestyle habits, and other positive physiologic effects, have been suggested to mediate these beneficial effects. In addition, the hemostatic and fibrinolytic systems appear to play an important role. Fibrinogen has been convincingly shown to be an independent cardiovascular risk factor. Other hemostatic and fibrinolytic parameters that are predictive of coronary events include factor VII, platelet hyperreactivity, plasminogen-activator inhibitor 1 (PAI-1), and tissue-plasminogen activator. The effects of exercise on fibrinogen have been intensively studied. Several randomized controlled trials, various other intervention studies and a large number of population-based cross-sectional studies all found an inverse relationship between measures of sport activity or leisure activity and plasma fibrinogen. The magnitude of the effect reported might be associated with a sizeable reduction in major coronary events. Relatively few data are available on the effects of endurance exercise on markers of the fibrinolytic system, with inconsistent results. Acute exercise leads to a transient activation of the coagulation system, which is accompanied by an increase in the fibrinolytic capacity in healthy subjects. Patients with ischemic heart disease, who cannot increase their fibrinolytic potential, however, may be at considerable risk for acute ischemic events if they are exposed to unaccustomed strenuous physical exertion.

Blood Coagulation Factors↗
PubMed2001

Particulate air pollution is associated with an acute phase response in men; results from the MONICA-Augsburg Study.

AIMS: Episodes of increased air pollution are associated with increases in hospital admissions for cardiovascular disease. Even modest acute phase responses are associated with increased risk of coronary heart disease. The study investigates whether induction of an acute phase response by exposure to air pollution may contribute to cardiovascular pathology. METHODS AND RESULTS: A prospective cohort study based on a survey in 1984/85 with a 3-year follow-up was conducted in 631 randomly selected men aged 45 to 64 years free of cardiovascular disease at entry 1984/85. Serum C-reactive protein concentrations were determined by a high sensitivity immunoradiometric assay. C-reactive protein concentration was increased in association with the 1985 air pollution episode. In multivariate analyses, elevated concentrations were independently associated with concentrations of total suspended particles and the sulphur dioxide episode. At ambient concentrations of pollution, as noted during the 1985 air pollution episode, the odds of observing C-reactive protein concentrations above 5.7 mg. l(-1)(>90th percentile) tripled, and increases of 26 microg. m(-3)total suspended particles (mean of 5 days) raised the odds of C-reactive protein levels 50% above the 90th percentile. CONCLUSIONS: Exposure to current levels of particulate matter in the atmosphere elicits an acute phase response in randomly selected healthy middle-aged men, which may contribute to the increased cardiovascular risk caused by air pollution.

Adult↗
PubMed2001

Characteristics of differences in Helicobacter pylori serology and 13C-urea breath-testing in an asymptomatic sample of blood donors.

Numerous tests, both invasive and non-invasive, are available for the diagnosis of Helicobacter pylori infection. The aim of this study was to evaluate the extent and determinants of differences in serology and 13C-urea breath test (13C-UBT) in diagnosing H. pylori. Four-hundred-and-seventy-four asymptomatic blood donors aged 40 to 68 years (mean age 55.8 years) and of German nationality were recruited between October 1996 and November 1997. H. pylori infection was measured with 13C-UBT and with a commercial IgG-ELISA test (Medac; Hamburg, Germany). A standardized questionnaire was applied to identify factors which could explain discrepant results of 13C-UBT and serology. Prevalence of infection was similar according to both tests (33.1% for 13C-UBT and 30.8% for serology). From the 146 subjects with a positive serology, 121 (82.7%) had a positive 13C-UBT. Previous treatment of H. pylori infection was the strongest predictor of a negative 13C-UBT given positive IgG serology (odds ratio (OR)= 12.87, 95% CI=4.10-40.36). Coffee consumption of more than 3 cups/day was also associated with an increased odds of a negative 13C-UBT given positive serology (OR = 3.12, 95% CI=1.16-8.43). No significant determinants of positive 13C-UBT given negative serology could be identified. These findings suggest a delayed fall in serum antibodies following eradication of the infection to be a major source of differences in H. pylori diagnosis using non invasive 13C-UBT and serology.

Antibodies, Bacterial↗
PubMed2001

Alcohol as a gastric disinfectant? The complex relationship between alcohol consumption and current Helicobacter pylori infection.

Alcoholic beverages have antimicrobial effects against Helicobacter pylori in vitro. To elucidate the relation between alcohol consumption and current infection with H. pylori in vivo, we carried out a pooled analysis of three recent studies from Southern Germany, comprising 1410 adults age 15 to 69. Detailed information on consumption of various alcoholic beverages was collected through standardized questionnaires. Helicobacter pylori infection was measured by 15C-urea breath test. Overall, prevalence of current H. pylori infection was lower among subjects who consumed alcohol (34.9%) than among nondrinkers (38.0%). The adjusted odds ratio was 0.79, with a 95% confidence interval of 0.58-1.08. Furthermore, alcohol consumption showed a strong inverse relation to the result of the 13C-urea breath test, a semiquantitative measure of the bacterial load, among infected subjects. The inverse association between alcohol consumption and H. pylori infection was not monotonic, however. Odds of infection were lowest at moderate levels of alcohol consumption and increased at higher levels of alcohol consumption, regardless of the type of alcoholic beverages consumed. These results support the hypothesis that moderate alcohol consumption may favor suppression and eventual elimination of H. pylori infection. At higher levels of alcohol consumption, the antimicrobial effects of alcoholic beverages may be opposed by adverse systemic effects of drinking, such as adverse effects on the immune defense.

Adolescent↗
PubMed2001

Coronary heart disease risk reduction in a predominantly beer-drinking population.

Moderate alcohol consumption protects against coronary heart disease, but there is ongoing debate about whether the effects and the underlying mechanisms differ by type of alcoholic beverage. In our case-control study from Germany, we assessed and compared the effect of alcohol consumption from various sources on risk of coronary heart disease and its underlying mechanisms. The sample included 312 patients with clinically stable, angiographically confirmed coronary heart disease and 479 healthy controls. After control for potential confounding factors, the odds ratio for coronary heart disease was 0.55 (95% confidence interval = 0.37--0.83) for drinkers compared with nondrinkers. Risk reduction was particularly strong among the majority of study participants who reported drinking predominantly or exclusively beer. Alcohol consumption from various sources was consistently associated with a more favorable profile of lipids and hemostatic factors. Nevertheless, a strong inverse association persisted between beer drinking and coronary heart disease even after control for these "intermediate variables." Our results support suggestions that the protective effect of moderate alcohol consumption against coronary heart disease is mediated in part by beneficial effects of ethanol on lipids and hemostatic factors. Additional mechanisms may account for the strong protective effect of moderate beer consumption.

Adult↗