Venous thromboembolism risk and prophylaxis in the acute hospital care setting--results of the ENDORSE study in Poland.

INTRODUCTION: Venous thromboembolism (VTE) is the most common preventable cause of in-hospital death. However, the risk of VTE and prophylaxis practices in Polish hospitals are not known. OBJECTIVES: The ENDORSE study in Poland was part of the global cross-sectional Epidemiologic International Day for the Evaluation of Patients at Risk for Venous Thromboembolism in the Acute Hospital Care Setting survey with the objective to assess the prevalence of VTE risk in acutely ill medical and surgical patients and to determine the proportion of at-risk patients who receive recommended prophylaxis. PATIENTS AND METHODS: In 10 non-academic Polish hospitals, a chart review was performed in all inpatients aged 40 or older admitted to medical wards, and in patients at the age of > or = 18 admitted to surgical wards. The VTE risk and recommended prophylaxis were assessed according to the 2004 American College of Chest Physicians (ACCP) guidelines. RESULTS: The study enrolled 2673 patients (1092 in surgical wards, 1581 in medical wards). Out of these, 1111 were judged to be at risk for VTE (597 surgical patients, 514 medical patients). Only 51.8% of all at-risk patients received ACCP-recommended VTE prophylaxis (54.7% of surgical patients, 32.5% of medical patients). CONCLUSIONS: In Polish hospitals more than 40% of patients hospitalized for acute illness are at risk of VTE, but only a small proportion of them receives appropriate prophylaxis. These results call for decisive actions to ensure that at-risk patients receive recommended VTE prophylaxis.

Anti-phospholipid antibodies and carotid-artery intima-media thickness in young survivors of myocardial infarction.

BACKGROUND: Not all coronary events occur in young individuals with traditional risk factors. In recent years some authors have observed increased prevalence of elevated anti-phospholipid (aPL) antibodies in young patients with myocardial infarction. Also, thickening of the combined arterial intima-media thickness (IMT) of superficial vessels has been identified as an independent risk factor for both stroke and heart attack. The objective of our study was to assess possible association between aPL antibodies and carotid IM thickening in young survivors of myocardial MATERIAL/METHODS: In a case control study we determined IgG and IgM antiphospholipid antibodies by enzyme-immunoassay, and IMT by ultrasonography in 50 male survivors of myocardial infarction under the age of 50, and compared them to 50 healthy controls. RESULTS: Elevated aPL antibody levels (IgG>10 GPL; IgM>20MPL) were detected in 12 of 50 patients (24%) with MI and in 3 of 50 controls (6%). The mean level of aPL antibodies was significantly higher in the patients than in the controls (IgG 9.15+/-3.53 vs 7.69+/-2.98 GMP, p=0.04 and IgM 18.46+/-7.61 vs 12.14+/-5.05 MPL, p<0.01). Patients with MI had a significantly greater IMT than healthy controls (0.9 mm vs 0.6 mm; p<0.01). There was a correlation between aPL and IM thickening (r=0.31; p=0.01). Among coronary risk factors only hypertension (r=0.28; p=0.01) and smoking (r=0.41; p=0.01) showed a relationship with IMT. CONCLUSIONS: The intima-media thickness of the carotid artery and elevated aPL antibodies are strongly associated with the risk of myocardial infarction in young patients.

Aspirin alters the cardioprotective effects of the factor XIII Val34Leu polymorphism.

BACKGROUND: The mechanism underlying decreased risk for myocardial infarction in carriers of the Leu34 polymorphism of the factor (F) XIII A-subunit is unclear. Given that acetylation of fibrinogen by aspirin can alter its clotting properties and the presence of fibrin stimulates thrombin-mediated activation of FXIII, we have tested the hypothesis that treatment with aspirin differentially modulates the influence of the FXIII Val34Leu polymorphism on its activation in vivo. METHODS AND RESULTS: The rates of the disappearance of FXIIIA chain and the appearance of its activated form (FXIIIAa) in sequential 30-second blood samples collected at the site of microvascular injury were compared in 14 healthy carriers of the Leu34 allele and 23 Val34 homozygotes both before and after a 7-day aspirin ingestion (75 mg/d), with the use of quantitative Western blotting. The presence of the Leu34 allele was associated with a significant increase in the maximum rate of FXIII activation by thrombin. Although the Leu34-positive and -negative subjects were similar with respect to aspirin-related impairment of thrombin generation, aspirin led to a more pronounced inhibition of the activation of FXIII in the Leu34 carriers as compared with the Val34 homozygotes. CONCLUSIONS: Inhibition of FXIII activation by aspirin is enhanced in the Leu34 carriers in vivo, suggesting that these subjects might benefit more than the Leu34-negative subjects from the reduction in risk for myocardial infarction with low-dose aspirin.