Iron deficiency defined as depleted iron stores accompanied by unmet cellular iron requirements identifies patients at the highest risk of death after an episode of acute heart failure.

AIM: Acute heart failure (AHF) critically deranges haemodynamic and metabolic homoeostasis. Iron is a key micronutrient for homoeostasis maintenance. We hypothesized that iron deficiency (ID) defined as depleted iron stores accompanied by unmet cellular iron requirements would in this setting predict the poor outcome. METHODS AND RESULTS: Among 165 AHF patients (age 65 ± 12 years, 81% men, 31% de novo HF), for ID diagnosis we prospectively applied: low serum hepcidin reflecting depleted iron stores (<14.5 ng/mL, the 5th percentile in healthy peers), and high-serum soluble transferrin receptor (sTfR) reflecting unmet cellular iron requirements (≥1.59 mg/L, the 95th percentile in healthy peers). Concomitance of low hepcidin and high sTfR (the most profound ID) was found in 37%, isolated either high sTfR or low hepcidin was found in 29 and 9% of patients, and 25% of subjects demonstrated preserved iron status. Patients with low hepcidin and high sTfR had peripheral oedema, high NT-proBNP, high uric acid, low haemoglobin (P < 0.05), and 5% in-hospital mortality (0% in remaining patients). During the 12-month follow-up, 33 (20%) patients died. Those with low hepcidin and high sTfR had the highest 12-month mortality [(41% (95% CI: 29-53%)] when compared with those with isolated high sTfR [15% (5-25%)], isolated low hepcidin [7% (0-19%)] and preserved iron status (0%) (P < 0.001). Analogous mortality patterns were seen separately in anaemics and non-anaemics. CONCLUSION: Iron deficiency defined as depleted body iron stores and unmet cellular iron requirements is common in AHF, and identifies those with the poor outcome. Its correction may be an attractive therapeutic approach.

Value of oral glucose tolerance test in the acute phase of myocardial infarction.

BACKGROUND: Although European guidelines advise oral glucose tolerance test (OGTT) in patients with acute myocardial infarction (AMI) before or shortly after hospital discharge, data supporting this recommendation are inconclusive. We aimed to analyze whether disturbances in glucose metabolism diagnosed before hospital discharge in AMI patients represents a latent pre-existing condition or rather temporary finding. Additionally, we planned to investigate the value of pre-selected glycemic control parameters as predictors of long-term glucometabolic state. METHODS: We assessed admission glycemia, glycated hemoglobin, mean blood glucose concentration on days 1 and 2 in 200 patients with a first AMI but without overt disturbances of glucose metabolism. We also performed OGTT at discharge and 3 months after discharge. RESULTS: The prevalence of disturbances in glucose metabolism (as assessed by OGTT) at 3 months was significantly lower than at discharge (29% vs. 48%, p = 0.0001). Disturbances in glucose metabolism were not confirmed in 63% of patients with impaired glucose tolerance and in 36% of patients with diabetes mellitus diagnosed during the acute phase of AMI. Age >77 years, glucose ≥ 12.06 mmol/l at 120 minutes during OGTT before discharge and mean blood glucose level on day 2 >7.5 mmol/l were identified as independent predictors of disturbances in glucose metabolism at the 3-month follow-up. CONCLUSIONS: Disturbances in glucose metabolism observed in patients with a first AMI are predominantly transient. Elderly age, high plasma glucose concentration at 120 minutes during OGTT at discharge and elevated mean blood glucose level on day 2 were associated with sustained disturbances in glucose metabolism.

Coagulation and fibrinolysis variables in pregnant women with type 1 diabetes mellitus.

BACKGROUND: Many studies have reported changes in the hemostatic system in patients with type 1 diabetes in whom coagulation processes predominate over fibrinolytic activity. The aim of this study was to assess some of the hemostatic variables during pregnancy women with in type 1 diabetes. MATERIAL/METHODS: The current study included 31 pregnant diabetic women and 24 healthy pregnant women. At 12, 24, and 36 weeks of gestation, we determined blood concentrations of the following: platelet count, fibrinogen, tissue plasminogen activator antigen, and plasminogen activator inhibitor-1. RESULTS: When we compared pregnant diabetic women in the third trimester with those in the first trimester, we observed a statistically significant decrease in the platelet count (172.0+/-9.0 vs 200.6+/-9.8 G/L, P<0.05) and a statistically significant increase in the levels of fibrinogen (3.5+/-0.2 vs 2.9+/-0.2 g/L, P<0.05), tissue plasminogen activator antigen (14.9+/-2.2 vs 4.7+/-0.6 ng/mL, P<0.001), and plasminogen activator inhibitor-1 (17.2+/-2.8 vs 4.0+/-1.0 IU/mL, P<0.001). Similar fibrinogen, tissue plasminogen activator: A, and plasminogen activator inhibitor-1 changes were observed in pregnant women (3.8+/-0.3 vs 2.9+/-0.2 g/L, P<0.05; 7.7+/-0.9 vs 5.2+/-0.3 ng/mL, P<0.05; and 17.6+/-2.1 vs 5.1+/-1.1 IU/mL, P<0.05, respectively). Tissue plasminogen activator antigen was the only variable to significantly increase during the third trimester in pregnant diabetic women with microangiopathy compared with women without microangiopathy (21.0+/-3.2 vs 8.4+/-1.7 ng/mL, P<0.01). CONCLUSIONS: (1) In patients with type 1 diabetes without microangiopathy and with good metabolic control, fibrinogen and tissue plasminogen activator antigen concentrations and changes in the activity of plasminogen activator inhibitor-1 are similar to those found in patients with a normal pregnancy; (2) the marked decrease in platelet count in patients with type 1 diabetes during pregnancy may be an additional source of plasminogen activator inhibitor-1; and (3) during pregnancy, diabetic microangiopathy leads to a greater increase of tissue plasminogen activator antigen concentration as a marker of endothelial cell injury.

The role of intrinsic fibrinolytic system activation in pathogenesis of hemostasis disturbances in hemodialyzed patients with chronic renal failure.

In the hemodialysis patient, hemostasis changes may occur. The contribution of fibrinolysis in pathogenesis of these disorders is unclear. The aim of the study was to estimate intrinsic fibrinolysis pathway in patients treated with hemodialysis (HD) because of chronic renal failure caused by chronic glomerulonephritis. The study was performed with 43 patients; the control group consisted of 51 healthy volunteers chosen by sex and age. The following parameters were determined: concentration of the urokinase plasminogen activator antigen (uPA:Ag), plasmin--antiplasmin complexes (PAP), fibrin and fibrinogen degradation products (FDP), activity of prekallikrein (PK) and C1-inhibitor (C1-INH) and also euglobulin clot lysis time (ELT). The above parameters were assessed in the patients before and after HD and were compared with the control group. In the HD patients, in comparison with the control group, prolonged statistically ELT [153 (125;215) vs. 105 (75;142) min.; p<0.001], with increase of PAP (508.6 +/- 274.7 vs. 184.7 +/- 69.4 microg/L; p<0.001) and FDP concentrations [5 (5;15) vs. 2.5 (0;0.3) microg/mL; p<0.05] before the procedure were determined. It suggests increased plasmin production and fibrin digestion despite determination of decreased general fibrinolytic activity. The C1-INH activity before HD was also significantly increased as compared with the control group [157 (136;171) vs. 107 (100;124)%; p<0.001], and its significant decreased after the HD is 157.7 +/- 23.9 vs. 122.3 +/- 20.3%; p<0.001, as it seems to be a nondirect proof of intrinsic pathway contribution in fibrinolysis activation in the HD patients. The remaining examined parameters did not change significantly after the dialysis procedure.