In vivo imaging analysis of the interaction between unusually large von Willebrand factor multimers and platelets on the surface of vascular wall.

To elucidate how unusually large von Willebrand factor (UL-VWF) multimers facilitate thrombus formation, their behavior was analyzed together with that of platelets in living mice deficient in the gene encoding the protease that cleaves UL-VWF, a disintegrin-like and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13-/-). By crossing ADAMTS13-/- mice with green fluorescent protein-expressing transgenic mice (GFP mice), GFP-ADAMTS13-/- mice were obtained. The dynamics of GFP-expressing platelets were monitored employing intravital confocal fluorescent microscopy. Administration of a vasopressin derivative, DDAVP, a secretagogue of VWF increased the number of platelets adhered to vascular endothelial cells (VECs) on mesentery at sites recognized by an anti-VWF antibody. Some of these platelets were interconnected and aligned as beads on a string. They reached their maximum length at 5 min and were longer in GFP-ADAMTS13-/- mice than in GFP mice (5.3 ± 4.3, N = 6 vs 2.9 ± 2.1 µm, N = 4) (mean±SE). Focal injury of VECs by topical application of FeCl(3) developed longer (25, 3-50 vs 10, 2-25 µm, P < 0.01) (mean, 10th-90th percentile) and more stable (1.3, 0.3-6.3 vs 0.3, 0.2-1.3 s, P < 0.01) connected platelets in GFP-ADAMTS13-/- mice than in GFP mice. This study revealed that ADAMTS13 cleaves platelet-bound UL-VWF multimers, both during their secretion from VECs and after their adherence to injured vascular walls in veins. UL-VWF multimers either being secreted from VECs or circulating in plasma of ADAMTS13-/- mice appeared to facilitate the accumulation of longer and more stable VWF strings with more associated platelets on injured vascular walls.

[SEN virus infection in maintenance hemodialysis patients]. / Zakazenie wirusem sen u pacjentów przewlekle hemodializowanych.

SEN virus (SENV) is a new, mostly parenterally transmitted, hepatotropic agent. The prevalence of SENV among patients undergoing maintenance hemodialysis (HD) in Poland, as well as risk factors for the infection are not established. Serum samples of 91 patients receiving maintenance HD in Bialystok were tested for the presence of strain H SENV (SENV-H) DNA by means of polymerase chain reaction. Fifty-one non-dialysis subjects, age- and sex-matched with the HD patients, mostly with chronic kidney diseases (96%), without hepatitis B (HBV) and C (HCV) or the history of blood transfusion and donation served as controls. SENV-H viremia was prevalent in 40% of HD patients and in 2% of control subjects (p < 0.0001). On multivariable logistic analysis, neither age (63.1 +/- 13.2 years), gender (49% females), dialysis vintage (29, 2-200, months), previous transfusions of packed red blood cells (84%) or fresh frozen plasma (4%), seropositivity for HBs antigen (13%), HCV antibodies (23%) or HCV RNA (17%) were independently associated with SENV-H prevalence in HD patients (chi2 for the model = 13.3, p = 0.103). No associations between SENV-H status and clinical or biochemical markers of liver disease, including serum aminotransferases levels were observed. In conclusion, SENV-H viremia is widespread among patients receiving maintenance HD in north-eastern Poland. Risk factors for its occurrence are equivocal; the infection may well be transmitted by parenteral and feco-oral routes. SEN virus is not directly responsible for liver damage in maintenance HD patients.

The significance of anaemia in patients with acute ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention.

BACKGROUND: The effects of pre-existing anaemia on the occurrence and course of an acute coronary syndrome has recently become a topic of extensive research. The data on the significance of anaemia in patients with ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI) are less abundant and the conclusions equivocal. AIM: To evaluate the incidence of anaemia and its impact on early outcomes in patients undergoing primary PCI for STEMI. METHODS: Based on a retrospective review of the medical records of hospitalised patients we selected a study group comprising 551 consecutive patients with STEMI, including 164 females, mean age 63.4 ± 12 years, undergoing primary PCI within the first 12 hours after the onset of chest pain. Anaemia was diagnosed according to the World Health Organisation criteria based on haemoglobin (Hb) values on admission (〈 12 g/dL for females, 〈 13 g/dL for males). RESULTS: Anaemia was diagnosed in 61 (11%) patients (in 13% of females and 10% of males). The anaemic patients were older (71 vs 63 years, p 〈 0.001), had a lower body mass (70 vs 80 kg, p 〈 0.003) and a higher TIMI risk score for STEMI (5 vs 3, p 〈 0.0001). Their laboratory results showed a greater renal impairment (GFR 66.8 vs 75.8 mL/min, p 〈 0.008) and higher C-reactive protein levels (24.8 vs 14.4 mg/L, p 〈 0.001). There were no significant differences in post-infarction myocardial damage as estimated on the basis of ejection fraction and the baseline and peak CK-MB levels. During treatment, in both groups, there was a significant decrease in Hb levels from 11.9 to 11.0 g/dL in the anaemic patients (p 〈 0.0004) and from 14.3 to 13.3 g/dL in the non-anaemic patients (p 〈 0.001). While GFR did not change significantly in the anaemic patients, there was a significant increase in the non-anaemic patients from 75.8 to 80.9 mL/min (p 〈 0.001). The in-hospital mortality was low with a total of 8 (1.3%) patients dying: 5 (8.2%) in the anaemic group and 3 (0.6%) in the non-anaemic group (p 〈 0.001). The anaemic patients were also characterised by a higher incidence of cardiovascular complications (33% vs 17%, p = 0.003). In the multivariate analysis, older age, systolic blood pressure on admission and elevated white blood count were independently associated with a higher risk of death and cardiovascular complications, whereas baseline Hb level was a significant prognostic factor only in the univariate analysis. CONCLUSIONS: Patients with anaemia who develop STEMI are, right from the admission, a separate, higher-risk population of patients with considerably increased risk of death and in-hospital cardiovascular complications. The unfavourable impact of anaemia on outcomes in patients with acute MI undergoing PCI is complex and cannot be explained by the increased extend of post-infarction myocardial damage. In patients with STEMI, anaemia on admission should be treated as an additional risk factor.