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Biomedical subjects

W Koenig

Publications and source records attributed to W Koenig.

At least 19 recordsLinked to original sources
PubMed2006

Soluble thrombomodulin as a predictor of type 2 diabetes: results from the MONICA/KORA Augsburg case-cohort study, 1984-1998.

AIMS/HYPOTHESIS: Previous studies have shown an inverse association between soluble thrombomodulin (sTM) and incident CHD, but there is a lack of data on the association between sTM and type 2 diabetes. Since CHD and type 2 diabetes share many risk factors, the aim of this study was to assess whether elevated sTM levels are associated with a lower incidence of type 2 diabetes. MATERIALS AND METHODS: A case-cohort study was performed in initially healthy middle-aged men and women based on data from the Monitoring of Trends and Determinants in Cardiovascular Disease/Cooperative Health Research in the Region of Augsburg (MONICA/KORA) studies conducted between 1984 and 1998. Levels of sTM were measured with an ELISA in serum samples from 138 men and 86 women who developed type 2 diabetes during follow-up (cases) and 534 men and 446 women who did not develop type 2 diabetes (non-cases). RESULTS: An inverse association was found between sTM and type 2 diabetes risk after multivariable adjustment for diabetes risk factors, including several other markers of inflammation and endothelial dysfunction. Markers of inflammation and endothelial dysfunction were particularly strong confounders of the observed association. In the fully adjusted model, a 1 SD increase in sTM was associated with a 27% decrease in the risk of type 2 diabetes (hazard ratio=0.73, 95% CI 0.58-0.91) in the total study population. We did not observe significant risk differences between men and women. CONCLUSIONS/INTERPRETATION: These data suggest that, in initially healthy middle-aged men and women, levels of sTM are inversely associated with the risk of type 2 diabetes.

Atherosclerosis↗
PubMed2006

Differential association of adiponectin with cardiovascular risk markers in men and women? The KORA survey 2000.

BACKGROUND: In men, high adiponectin concentrations were related to a lower risk of myocardial infarction, whereas no association with cardiovascular events was found in women. OBJECTIVE: To investigate sex differences in the associations of adiponectin with cardiovascular risk factors. DESIGN: Cross-sectional population-based KORA Survey 2000 in Southern Germany using the same study methods for cardiovascular risk factors as the former WHO MONICA project. PARTICIPANTS: A total of 697 men and 657 women, aged 55-74 years. Glucose tolerance status was assessed by oral glucose tolerance tests. RESULTS: Adiponectin (geometric mean, interquartile range; microg/ml) levels were significantly higher in women (11.1; 8.5-14.9) than in men (7.1; 5.2-9.6) (P<0.05). In univariate analyses, HDL-cholesterol and age were significantly positively correlated with adiponectin in both sexes. Negative correlations were observed with BMI, waist circumference, fasting and postchallenge glucose, insulin, HOMA-IR, HbA1c, triglycerides, uric acid and CRP (P<0.01). In sex-specific multivariate regression, age and HDL-cholesterol were independently positively, and fasting insulin and 2-h glucose were negatively related to adiponectin in both sexes. Uric acid was significantly inversely related to adiponectin in women only (sex interaction: P=0.02). Exploratory sex-specific factor analysis of adiponectin and the core components of the metabolic syndrome yielded four similar factors. Adiponectin loaded negatively on the 'lipids' factor in both sexes. CONCLUSION: The associations of adiponectin with cardiovascular risk factors showed a similar pattern in both sexes, except for uric acid. This small sex difference may not explain previous conflicting results on the association of adiponectin with cardiovascular events in men and women.

Adiponectin↗
PubMed2006

Fenofibrate reduces atherogenesis in ApoE*3Leiden mice: evidence for multiple antiatherogenic effects besides lowering plasma cholesterol.

OBJECTIVE: To demonstrate, quantify, and mechanistically dissect antiatherosclerotic effects of fenofibrate besides lowering plasma cholesterol per se. METHODS AND RESULTS: ApoE*3Leiden transgenic mice received either a high-cholesterol diet (HC) or HC containing fenofibrate (HC+FF) resulting in 52% plasma cholesterol-lowering. In a separate low-cholesterol diet (LC) control group, plasma cholesterol was adjusted to the level achieved in the HC+FF group. Low plasma cholesterol alone (assessed in LC) resulted in reduced atherosclerosis (lesion area, number and severity) and moderately decreased plasma serum amyloid-A (SAA) concentrations. Compared with LC, fenofibrate additively reduced lesion area, number and severity, and the total aortic plaque load. This additional effect in HC+FF was paralleled by an extra reduction of aortic inflammation (macrophage content; monocyte adhesion; intercellular adhesion molecule-1 [ICAM-1], soluble vascular cell adhesion molecule-1, granulocyte-macrophage colony-stimulating factor (GM-CSF), MCP-1, and NF-kappaB expression), systemic inflammation (plasma SAA and fibrinogen levels), and by an upregulation of plasma apoE levels. Also, enhanced expression of ABC-A1 and SR-B1 in aortic macrophages may contribute to the antiatherosclerotic effect of fenofibrate by promoting cholesterol efflux. CONCLUSIONS: Fenofibrate reduces atherosclerosis more than can be explained by lowering total plasma cholesterol per se. Impaired recruitment of monocytes/macrophages, reduced vascular and systemic inflammation, and stimulation of cholesterol efflux may all contribute to these beneficial effect of fenofibrate.

Animals↗
PubMed2006

Chemokines as risk factors for type 2 diabetes: results from the MONICA/KORA Augsburg study, 1984-2002.

AIMS/HYPOTHESIS: The chemokines monocyte chemoattractant protein-1 (MCP-1), IL-8 and interferon-gamma-inducible protein-10 (IP-10) are released by adipocytes and appear to be involved in atherosclerosis. We hypothesised that these chemokines may be risk factors for the development of type 2 diabetes. SUBJECTS AND METHODS: Using a case-cohort design based on data from the population-based Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA)/Kooperative Gesundheitsforschung in der Region Augsburg/Cooperative Health Research in the Region of Augsburg (KORA Augsburg) study, chemokine levels at baseline were analysed in 526 individuals with and 1,695 individuals without incident type 2 diabetes. The mean follow-up time was 10.8 years. RESULTS: MCP-1 was associated with type 2 diabetes, largely independently of classic risk factors, whereas various clinical and metabolic parameters as well as lifestyle factors were major confounders of the association of IL-8 and IP-10 with type 2 diabetes. Further adjustment for C-reactive protein (CRP) and IL-6 had no impact on the observed associations. The hazard ratio (HR) for subjects with systemic concentrations of all three chemokines (MCP-1, IL-8 and IP-10) above the respective median compared with those with all chemokines below or equal to the median was 1.79 (95% CI 1.18-2.72) and was comparable with the HR for elevated CRP and IL-6 together (adjusted for age, sex, survey, BMI, systolic blood pressure, total cholesterol:HDL cholesterol ratio, physical activity, alcohol intake, smoking and parental history of diabetes). CONCLUSIONS/INTERPRETATION: Elevated concentrations of MCP-1, IL-8 and IP-10 are associated with incident type 2 diabetes. Whereas the association of IL-8 and IP-10 with diabetes was attenuated by multivariable adjustment, high MCP-1 levels contributed to diabetes risk independently of previously described clinical, metabolic and immunological risk factors.

Blood Pressure↗
PubMed2005

Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis.

CONTEXT: Plasma fibrinogen levels may be associated with the risk of coronary heart disease (CHD) and stroke. OBJECTIVE: To assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes based on individual participant data. DATA SOURCES: Relevant studies were identified by computer-assisted searches, hand searches of reference lists, and personal communication with relevant investigators. STUDY SELECTION: All identified prospective studies were included with information available on baseline fibrinogen levels and details of subsequent major vascular morbidity and/or cause-specific mortality during at least 1 year of follow-up. Studies were excluded if they recruited participants on the basis of having had a previous history of cardiovascular disease; participants with known preexisting CHD or stroke were excluded. DATA EXTRACTION: Individual records were provided on each of 154,211 participants in 31 prospective studies. During 1.38 million person-years of follow-up, there were 6944 first nonfatal myocardial infarctions or stroke events and 13,210 deaths. Cause-specific mortality was generally available. Analyses involved proportional hazards modeling with adjustment for confounding by known cardiovascular risk factors and for regression dilution bias. DATA SYNTHESIS: Within each age group considered (40-59, 60-69, and > or =70 years), there was an approximately log-linear association with usual fibrinogen level for the risk of any CHD, any stroke, other vascular (eg, non-CHD, nonstroke) mortality, and nonvascular mortality. There was no evidence of a threshold within the range of usual fibrinogen level studied at any age. The age- and sex- adjusted hazard ratio per 1-g/L increase in usual fibrinogen level for CHD was 2.42 (95% confidence interval [CI], 2.24-2.60); stroke, 2.06 (95% CI, 1.83-2.33); other vascular mortality, 2.76 (95% CI, 2.28-3.35); and nonvascular mortality, 2.03 (95% CI, 1.90-2.18). The hazard ratios for CHD and stroke were reduced to about 1.8 after further adjustment for measured values of several established vascular risk factors. In a subset of 7011 participants with available C-reactive protein values, the findings for CHD were essentially unchanged following additional adjustment for C-reactive protein. The associations of fibrinogen level with CHD or stroke did not differ substantially according to sex, smoking, blood pressure, blood lipid levels, or several features of study design. CONCLUSIONS: In this large individual participant meta-analysis, moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults. Assessment of any causal relevance of elevated fibrinogen levels to disease requires additional research.

Adult↗
PubMed2005

Helicobacter pylori seropositive subjects do not show a pronounced systemic inflammatory response even in the presence of the interleukin-1 receptor antagonist gene polymorphism.

The aim of this analysis was to evaluate the effects of the presence of the IL-1RA gene polymorphism and H. pylori infection on markers of a systemic inflammatory response taking into account virulence markers of this infection. Serum concentrations of interleukin (IL)-6, IL-8, and tumour-necrosis factor (TNF)-alpha of 479 occasional blood donors were not statistically significantly higher in subjects having antibodies against H. pylori, or more specifically against CagA and VacA, and being homozygous for the pro-inflammatory IL-1RN*2 allele compared to others after adjustment for covariates. The findings suggest that the possible pro-inflammatory effect of the IL-1RN*2 allele in combination with H. pylori infection is limited to the mucosal level.

Adult↗
PubMed2005

Systemic low-grade inflammation and risk of coronary heart disease: results from the MONICA/KORA Augsburg cohort studies.

Atherosclerosis is characterised by a non-specific local inflammatory process accompanied by a systemic response. A number of prospective studies in initially healthy subjects and in patients with manifest atherosclerosis have now convincingly demonstrated a strong and independent association between even slightly elevated concentrations of various systemic markers of inflammation (plasma viscosity, C-reactive protein [CRP], and other acute phase reactants) and a number of cardiovascular endpoints. Presently, CRP, the classical acute phase protein, seems to be the marker of choice for the clinical situation. Initial evidence suggests that measurement of CRP adds to global risk assessment based on the Framingham risk score. The recent AHA/CDC consensus report recommends the measurement of CRP in asymptomatic subjects at intermediate risk for future coronary events (10-year risk of 10-20 %) and in selected patients after an acute coronary syndrome. Whether CRP shall alter treatment strategies in subjects without clinically manifest atherosclerosis is presently being tested in a large randomised clinical trial. In addition, recent research has suggested that CRP may not only be a risk marker, but may be directly involved in the pathogenesis of atherothrombosis. However, there are other emerging biomarkers. Lipoprotein-associated phospholipase A (2) (Lp-PLA (2)), an enzyme produced by monocytes/macrophages, T-cells and mast cells was found to generate proinflammatory and proatherogenic molecules from oxidised LDL. We tested the association of these new biomarkers with traditional risk factors and their ability to predict incident coronary events, using the MONICA/KORA database.

Adult↗
PubMed2005

Inflammation and type 2 diabetes: results from KORA Augsburg.

Type 2 diabetes is associated with a systemic low-grade inflammation. First data provided by cross-sectional studies from as early as the 1960s demonstrated elevated systemic levels of glycoproteins and acute-phase reactants and increased leukocyte counts in type 2 diabetes patients. Subsequently, prospective studies showed that elevated concentrations of several acute-phase proteins and cytokines are predictive of later type 2 diabetes. Immune gene variants in man and in animal models were found to affect insulin resistance and diabetes incidence. Antidiabetic treatment by medication, diet or physical activity results in a significant decrease of systemic immune mediator concentrations. Immunological analyses of the KORA Survey S4 (1999/2001) allowed us to show that levels of circulating acute-phase proteins like CRP and of IL-6 are highly correlated and associated not only with overt type 2 diabetes, but already with impaired glucose tolerance (IGT) pointing out a role of these mediators in the pathogenesis of type 2 diabetes. On the contrary, TNFalpha was neither coregulated with CRP nor associated with diabetes status. Our study therefore shows that type 2 diabetes is accompanied by a non-random and differential upregulation of components of the innate immunity and suggests that this inflammatory condition is involved in the aetiology of the disease. Future work will extend the range of analysed immune mediators to chemokines and will also investigate the association of immune markers with indices of obesity to elucidate the relevance of this traditional risk factor for low-grade inflammation.

Acute-Phase Proteins↗
PubMed2005

Genetics of type 2 diabetes: impact of interleukin-6 gene variants.

The KORA studies serve as a powerful tool for the genetic analysis of complex diseases like type 2 diabetes or the metabolic syndrome. These studies include more than 2,000 prevalent and incident type 2 diabetes cases. DNA of these patients is available to be used in genetic studies. Up to now the analyses have focussed on genes coding for proteins being involved in the inflammatory response. Interleukin-6 (IL-6) as the key mediator of the acute phase reaction is of interest. Elevated protein concentrations of IL-6 in the blood have been shown to predict type 2 diabetes. We investigated the association of the IL-6 single nucleotide polymorphism (SNP) C-174G with type 2 diabetes in a case-control study of 704 elderly participants of the KORA Survey S4 (1999/2001). When BMI, HDL cholesterol, physical activity, hypertension, hormone replacement therapy and smoking were considered as covariables the SNP C-174G showed a trend for association with type 2 diabetes (- 174G: OR 1.20, 95 % CI 0.90 - 1.59, p = 0.21).

Adult↗
PubMed2005

Association of humoral immunity to human Hsp60 with the IL-6 gene polymorphism C-174G in patients with type 2 diabetes and controls.

The relationship between humoral immunity to hsp60 and type 2 diabetes along with other relevant metabolic, inflammatory and immunogenetic variables was studied in 76 non-diabetic and 74 diabetic persons aged 55-74 years selected from the population-based KORA Survey 2000. Antibodies to human hsp60 were measured in serum samples by ELISA. Hsp60 antibodies were detected in all but two individuals in a considerable range of titres (22-1,856 AU/ml). There was no significant association to age and sex, or to key clinical or metabolic parameters (BMI, WHR, HbA1c, total cholesterol, LDL cholesterol, HDL cholesterol, systolic and diastolic blood pressure, albumin, uric acid) or immunological parameters (CRP, IL-6, sIL-6R, TNFalpha, sTNFalpha R60, sTNFalpha R80). Analysis of antibody-positive individuals revealed an association between hsp60 antibodies and diabetes at borderline significance (p = 0.047), which was lost when the two antibody-negative individuals were included. Genetic analyses indicated that this association was significant in carriers of the C allele of the IL-6 promoter region polymorphism at nucleotide -174 (p = 0.02), but not in GG genotype carriers. We conclude that humoral immunity to human hsp60 may be enhanced in those diabetic patients carrying the -174C allele of the IL-6 gene. This finding may contribute to an understanding of the relationship between the -174C allele and increased risk of atherosclerosis.

Aged↗
PubMed2004

Overall alcohol intake, beer, wine, and systemic markers of inflammation in western Europe: results from three MONICA samples (Augsburg, Glasgow, Lille).

AIM: Anti-inflammatory effects of moderate alcohol consumption have been proposed to explain why moderate alcohol intake lowers coronary heart disease risk. We investigated the relationship between overall alcohol, beer or wine consumption and markers of systemic inflammation in three different geographical areas in Europe. METHODS AND RESULTS: Cross-sectional samples, each representative of the general population from Germany, Scotland, and France (MONICA Augsburg 1994/95, 2275 men and 2186 women, 25-74 years; Glasgow MONICA 1994/95, 561/616, 25-74 years, and MONICA Lille 1994/95, 581/574, 35-64 years) were studied. Alcohol intake was assessed by standardized interview. Adjusted means of C-reactive protein (CRP), fibrinogen, white blood cell (WBC) count, plasma viscosity (PV), and albumin were calculated among categories of alcohol intake, and separately for beer or wine consumption, by multiple linear regression. Self-reported moderate daily alcohol intake up to 40 g was associated with lower concentrations of CRP, fibrinogen, PV and WBC count, compared to non-drinking and heavy drinking, even after adjustment for various potential confounders. CONCLUSIONS: Moderate consumption of either wine or beer is associated with lower levels of systemic inflammatory markers in three different European areas, suggesting that ethanol itself might be largely responsible for the potential anti-inflammatory effects of these beverages.

Adult↗
PubMed2004

Severity and extent of osteoarthritis and low grade systemic inflammation as assessed by high sensitivity C reactive protein.

BACKGROUND: Although osteoarthritis (OA) is thought to derive from defective chondrocyte metabolism and thus inherently lack the large scale systemic response of rheumatoid arthritis, there is increasing interest in the acute phase proteins in OA. OBJECTIVE: To assess the association between high sensitivity C reactive protein (hsCRP) and severity and extent of OA in patients with advanced hip and knee OA. METHODS: Preoperative hsCRP was measured in frozen serum samples from 770 consecutive patients with hip or knee joint replacement due to advanced OA recruited between 1995 and 1996. Pain was measured by a visual analogue scale and the Western Ontario and McMaster Universities OA index (WOMAC). The extent of OA in different joints was assessed clinically and radiographically. RESULTS: The (geometric) mean hsCRP was 2.5 mg/l among all patients. Severity of pain was associated with mean hsCRP (adjusted elevation highest v lowest quintile = 35%, p = 0.01) after controlling for known or suspected predictors of hsCRP, including age, smoking, and body mass index. Neither the bilateral nor the generalised extent of OA, nor any of the dimensions of the WOMAC were associated with mean hsCRP levels. CONCLUSIONS: Severity of pain, but not extent of OA, was associated with hsCRP levels in this group of patients with advanced OA. Longitudinal studies with repeated assessments of hsCRP and pain are needed to assess the possible value of hsCRP for monitoring or predicting the clinical course of OA.

Acute Disease↗
PubMed2004

Significant association of the interleukin-6 gene polymorphisms C-174G and A-598G with type 2 diabetes.

Elevated blood concentrations of IL-6 have been shown to predict type 2 diabetes. Because the impact of IL-6 gene polymorphisms on diabetes status, parameters of the metabolic syndrome, and low-grade systemic inflammation has not been analyzed in a population-based study, we investigated the association of the IL-6 single nucleotide polymorphisms C-174G and A-598G on these parameters in 704 elderly participants of the Kooperative Gesundheitsforschung im Raum Augsburg/Cooperative Research in the Region of Augsburg (KORA) Survey 2000. Both -174G and -598G alleles were significantly associated with type 2 diabetes (-174G: odds ratio = 1.51, 95% confidence interval = 1.11-2.07, P = 0.0096; -598G: odds ratio = 1.56, 95% confidence interval = 1.13-2.15, P = 0.0069) but not with impaired glucose tolerance. In subgroup analyses, the association reached statistical significance in men and in leaner subjects (body mass index <or= 28.7 kg/m(2), i.e. study median) but not in women or more obese persons. Circulating IL-6 levels were not associated with the IL-6 polymorphisms, but significantly elevated levels of the chemokine monocyte chemoattractant protein-1/CC chemokine ligand 2 in carriers of the protective genotypes indicated an indirect effect of these single nucleotide polymorphisms on the innate immune system. Our findings confirm that immune gene polymorphisms can be considered as independent risk factors in the etiology of type 2 diabetes and suggest that their contribution may be indirect, by influencing the levels of other immune mediators like monocyte chemoattractant protein-1.

Adult↗
PubMed2003

[Moderate alcohol consumption and plasma concentration of sensitive markers of inflammation. Comment on an atheroprotective relationship].

BACKGROUND AND OBJECTIVE: Changes in lipoproteins and hemostasis only incompletely explain the reduced cardiovascular mortality associated with light to moderate alcohol consumption. Since increasing evidence suggests that atherosclerosis can be considered to be a chronic inflammatory process, we sought to assess the association between daily alcohol consumption and levels of sensitive markers of inflammation. STUDY PARTICIPANTS AND METHODS: 478 voluntary blood donors (358 men, 120 women) aged 40 to 68 years were categorized into four groups according to their self-reported amount of daily alcohol consumption: 0 g/day, >0 - 20 g/day, >20 - 40 g/day, and > 40 g/day. Means of various sensitive markers of inflammation (C-reactive protein (CRP), serum amyloid A (SAA), interleukin-6 (IL-6), intercellular adhesion molecule-1, plasma viscosity und albumin) were calculated and compared by bivariate and multivariate analyses. RESULTS: More than 80 % of the study participants reported to consume alcohol, mainly beer. We found statistically significantly decreased levels of SAA, CRP, and plasma viscosity in subjects with light-to-moderate alcohol intake (>0 - 20 g/day and > 20 - 40 g/day, respectively), and a trend for increased levels of albumin in these subjects compared to non-drinkers. After multivariable adjustment for potential confounders (age, gender, body mass index, cigarette smoking, years of school education, and physical activity) a significant U-shaped association (p = 0.02) between levels of SAA and the amount of daily alcohol intake remained: there were 0.75 mg/l and 0.70 mg/l lower mean levels, respectively, of SAA in subjects with light-to-moderate alcohol intake compared to those of non-drinkers. Subjects with an alcohol intake of > 40 grams per day showed a statistically significant increase in levels of interleukin-6 (0.50 pg/ml) compared to non-drinkers. CONCLUSION: Potential anti-inflammatory properties of moderate alcohol consumption might represent an additional mechanism to explain its atheroprotective effect.

Adult↗
PubMed2003

[Effect of molsidomine on rheological parameters and the incidence of cardiovascular events].

BACKGROUND AND OBJECTIVE: In-vitro studies revealed that nitric oxide (NO) may affect rheological parameters. We studied the effect of highly-dosed NO-donor molsidomine on blood rheology and the impact of rheological parameters on the incidence of severe cardiovascular events. PATIENTS AND METHODS: In this randomized, placebo-controlled and double-blind trial 166 patients (60 +/- 10 years) with stable angina pectoris and coronary intervention received molsidomine 3 x 8 mg t. i. d. (controlled release tablets) or placebo for 6 months. Patients with inflammatory/neoplastic disorders or elevated values of C-reactive protein were excluded from analysis. A rheological profile (plasma viscosity, blood viscosity, aggregation and flexibility of erythrocytes, filtrability of leukocytes, fibrinogen levels) was done initially and after 6 months. Adverse cardiovascular events (death, myocardial infarction, stroke, coronary/peripheral revascularization) were recorded during 12 months. Furthermore, the impact of rheological parameters regarding the occurrence of severe cardiovascular events (death, myocardial infarction, stroke) was evaluated during a follow-up of median 38 months. RESULTS: The data of 137 patients (n = 71 placebo, n = 66 molsidomine) were analysed. The difference of rheological parameters between the two measurements did not vary between the two groups. Analysis of event-free survival with Kaplan-Meier technique revealed no difference between the two groups. Multivariate Cox regression analysis with adjustment for diabetes mellitus, smoking and therapy with statin showed a significant association of fibrinogen and plasma viscosity with the occurrence of severe cardiovascular events. CONCLUSION: Treatment with molsidomine 3 x 8 mg/day for 6 months does not improve blood rheology or reduce cardiovascular events. But elevated levels of fibrinogen and plasma viscosity were associated with the occurrence of severe cardiovascular events.

Blood Viscosity↗
PubMed2003

C-reactive protein and atherosclerosis. Is there a causal link?

C-reactive protein (CRP) is a powerful cardiovascular risk marker. Evidence suggests that this may be due to its direct proatherogenic properties. Because of different biological functions of CRP in different species, an appropriate animal model for the study of its role in atherogenesis is difficult to set up. Binding to low density lipoprotein (LDL), activation of the complement system and interaction with monocyte/macrophages are rigorously defined pathogenic properties of CRP which might contribute to an active role of the molecule in human atherogenesis. Furthermore, direct effects on arterial wall cells, i.e. endothelial cells and smooth muscle cells, have been reported. The molecular basis of CRP interaction with these cells, however, remains unclear. Should CRP indeed be actively involved in human atherogenesis, the molecule may become a target for therapy. Pharmaceutical companies develop CRP-inhibitors.

Animals↗
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↗