A heparin-coated dialysis filter (AN69 ST) does not reduce clotting during hemodialysis when compared to a conventional polysulfone filter (F×8).

BACKGROUND: We investigated whether the heparin-coated AN69 ST hemodialysis (HD) filter induced less hypercoagulability during HD than a conventional polysulfone filter (F×8). METHODS: In a crossover design, 11 patients were treated alternately with AN69 ST and F×8 filters (45 sessions). All filters were primed with unfractionated heparin (UFH) and unadsorbed UFH was removed by saline flushing. Half the conventional dalteparin dose was given as a bolus dose at the start of HD. Clotting was evaluated hourly in the venous air trap. Prothrombin fragments 1 and 2 (PF1 + 2), antithrombin (AT), ß-TG and anti-FXa activity were repeatedly measured. RESULTS: One patient treated with enalapril had two repeated adverse reactions to the AN69 ST filter and was excluded from the study. Use of the AN69 ST filter did not decrease the mean clot score or PF1 + 2, but decreased ß-TG compared to the F×8 filter. CONCLUSION: The heparin-coated AN69 ST filter did not induce less coagulation when compared to the F×8 filter.

Association between tobacco smoke exposure and levels of C-reactive protein in the Oslo II Study.

It is well known that tobacco smoke exposure is related to the risk of developing cardiovascular diseases and events. One mechanism could be that tobacco smoke acts on the cardiovascular system by altering the autonomic function and/or inducing inflammatory responses. We used data from 3 744 men aged 67-77 years from the city of Oslo that participated in the health screening for the Oslo II Health Study in 2000, to explore associations between C-reactive protein and environmental exposures including exposure to tobacco smoke products. Levels of C-reactive protein were higher in current smokers (2.05 mg/l, IQR, 1.11-4.17 mg/l), compared to former-smokers (1.58 mg/l, IQR, 0.83-3.03 mg/l) and non-smokers (1.26 mg/l, IQR, 0.65-2.40 mg/l). The risk of elevated C-reactive protein increased with both numbers of current cigarettes smoked per day and numbers of pack-years of smoking, when other factors were adjusted for (P < 0.001). We found a positive dose-response relationship between amount of current cigarette smoking and elevated C-reactive protein levels. These findings support the idea that the induction or exacerbation of inflammation could be a mechanism by which smoking promotes atherosclerotic cardiovascular diseases.

Occult bleeding in three different antithrombotic regimes after myocardial infarction. A WARIS-II subgroup analysis.

INTRODUCTION: Warfarin, aspirin, and the combination of these, have all proven to be efficacious in preventing future events after myocardial infarction. The accompanying bleeding tendency is a concern. The aim of the present study was to compare the occurrence of occult bleeding and iron deficiency during these treatment modalities. METHODS: The 267 patients who had survived a myocardial infarction were randomly assigned in the Warfarin Aspirin Reinfarction Study to treatment with aspirin 160 mg/day, or warfarin (INR 2.8-4.2), or aspirin 75 mg/day plus warfarin (INR 2.0-2.5). The patients were screened for the occurrence of occult bleeding in faeces and urine after 3 months. Haemoglobin and iron metabolism parameters were measured at baseline, after 3 months, and at the end of the 4 years follow-up. RESULTS: The number of occult bleeding in faeces was 19 (7.1%) and in urine 29 (10.9%). There were no intergroup differences (p=0.45 and 0.39, respectively). In the occult bleeders, a second test showed 3 (1.1%) positive samples in faeces and 9 (3.4%) in urine. Further investigation revealed 2 cases of malignant disease. Haemoglobin and iron status variables were all within normal limits after 3 months and after 4 years in all treatment groups. CONCLUSIONS: Long-term treatment with aspirin, warfarin, or both, in the present doses and levels of anticoagulation did not lead to anemia or iron deficiency. The occurrence of occult bleeding in faeces and urine was a temporary phenomenon in most patients. Only macroscopic bleedings during these treatment modalities were of clinical importance, and screening for occult bleeding was of limit value.

A daily glass of red wine: does it affect markers of inflammation?

AIMS: Epidemiological studies have shown that moderate consumption of alcohol is associated with a decreased risk of developing cardiovascular disease, but the causal mechanisms are only partly understood. As inflammation is an important process in the progression of atherosclerosis, we hypothesized that the protective effect of red wine is partly mediated through a reduction in inflammation. METHODS: We conducted a randomized controlled crossover trial to study the effect of red wine on the levels of the inflammatory markers serum C-reactive protein (CRP) and plasma fibrinogen in healthy, non-smoking individuals. The subjects were randomized to drink one glass of red wine (150 ml, 15 g alcohol) every day ('wine period') or to undergo a period of total abstention from alcohol ('abstention period'). After 3 weeks they switched intervention group. Eighty-seven volunteers completed the study (mean age 50 years). RESULTS: Red wine did not reduce CRP levels and only marginally reduced fibrinogen levels compared with a similar period without alcohol. CONCLUSIONS: Consumption of 150 ml of red wine slightly reduced fibrinogen levels but did not reduce CRP levels.

Diagnostic value of a rapid test for B-type natriuretic peptide in patients presenting with acute dyspnoe: effect of age and gender.

BACKGROUND: B-type natriuretic peptide (BNP) measurements are useful for diagnosing congestive heart failure (CHF) in patients presenting to the Emergency Department with acute dyspnoe. Whether the diagnostic accuracy of BNP is affected by the age and gender of the patients remains unknown. AIMS: To evaluate the accuracy of BNP testing for diagnosing CHF in an unselected group of patients admitted to the emergency department of a Norwegian teaching hospital with a principal complaint of shortness of breath and to assess whether the diagnostic accuracy of the test differs according to age and gender. METHODS: BNP levels in plasma were determined by a point-of-care device upon arrival in 155 patients presenting with acute dyspnoe. The diagnostic 'gold' standard for CHF was adjudicated by two independent cardiologists who were blinded to the BNP data. RESULTS: By univariate logistic regression analysis, BNP was strongly related to a diagnosis of CHF. In a multivariate model BNP provided additional prognostic information to patient age and gender, radiographic evidence of pulmonary congestion and cardiomegaly, and the presence of pulmonary rales and jugular vein distention by physical examination. There was no significant interaction between age and BNP or between gender and BNP with regard to the accuracy of diagnosing CHF. The area under the receiver-operating characteristics-curve was 0.86 (95% confidence interval 0.78-0.93) in women and 0.90 (0.82-0.97) in men. The area under the curves were 0.82 (0.73-0.92) and 0.88 (0.80-0.97) for patients (both genders) aged > or = 76 and <76 years, respectively. CONCLUSION: Point-of-care BNP measurement in the emergency department discriminates well between patients with dyspnoe of cardiac and non-cardiac origin regardless of age and gender.

Influence of aspirin on inflammatory markers in patients after acute myocardial infarction.

The aim of this study was to assess the influence of aspirin on selected inflammatory markers in patients recovering from acute myocardial infarction (AMI). Patients participating in the Warfarin Aspirin Re-Infarction Study-II were randomized to either aspirin 160 mg/day or aspirin 75 mg/day + warfarin, or warfarin alone after AMI. After AMI, aspirin 160 mg/day was associated with significantly lower levels of high-sensitivity C-reactive protein and tumor necrosis factor-alpha than warfarin alone over 4 years. However, the same levels were not predictors for clinical end points.

A twin study of C-Reactive Protein compared to other risk factors for coronary heart disease.

Coronary heart disease (CHD) tends to cluster in families, and several established risk factors for the disease are to some extent inherited. Inflammation plays a key role in the development of atherosclerosis and CHD. A low-grade inflammation may be detected by highly sensitive C-Reactive Protein (CRP) determination, which is strongly associated to CHD. In order to uncover any role of genetics in low-grade inflammation, we measured CRP in healthy monozygotic twins. The within-pair correlation coefficient of CRP was 0.40, suggesting an important genetic contribution to the control of CRP level. CRP correlated significantly to other CHD risk factors like body mass index (BMI), systolic blood pressure, diastolic blood pressure, plasma fibrinogen, serum high-density lipoprotein cholesterol, plasma homocysteine, and serum triglycerides. Of these variables, BMI was most significantly associated to CRP in a linear multiple regression analysis. We conclude that CRP level (reflecting a low-grade inflammation) exhibits a moderate, but significant degree of heritability. The association between CRP and BMI, which has a larger degree of heritability, could partly explain the heritability of serum CRP level.

C-reactive protein predicts death in patients with previous premature myocardial infarction--a 10 year follow-up study.

Atherosclerosis is an inflammatory disease. C-reactive protein (CRP), a marker of inflammation, is associated with coronary heart disease (CHD). We measured CRP in a cohort of 247 patients (193 males and 54 females) who had had their first myocardial infarction (MI) at age < or = 55 (males) or < or = 60 (females). The cut-off values of the 25th, 50th and 75th centiles of CRP were 1.20, 2.37 and 4.20 mg/l. After 10 years, a total of 44 patients (17.8%) had died, 36 (81.8%) of cardiac causes. Unadjusted and adjusted (i.e. for age, ejection fraction (EF), serum total cholesterol (TC), fibrinogen, smoking and hypertension) relative risks (RRs) for total and cardiac mortality were generated. CRP was a strong predictor of death of all causes due to its strength as predictor of cardiac death. The RR of cardiac death was doubled with increasing CRP quartiles, and patients in the top quartile had six times as high risk of cardiac death as patients in the lowest quartile. The RRs were moderately attenuated after adjustment, but still significant. We conclude that CRP is a strong predictor of mortality in patients with premature MI. Thus, inflammation appears to be a critical prognostic factor in patients with previous premature MI.