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1.  New oral anticoagulants – a practical guide 
Oral direct inhibitors of thrombin and activated factor Xa are approved as new anticoagulant drugs. In contrast to vitamin K antagonists (VKA) and heparins, the new agents have single targets in the coagulation cascade and more predictable pharmacokinetics, but they lack validated and available antidotes. Unlike VKA, they do not require routine monitoring of coagulation. However, the measurement of their pharmacologic effects might be of value in selected patients. They interfere with the routine coagulation tests, which should be interpreted with caution. Specific tests exist and can be used in case of emergencies. Adequate supportive care and temporary removal of all antithrombotic agents constitute the basis for management of serious bleeding complications. The administration of coagulation factors, such as fresh frozen plasma, prothrombin complex concentrates or recombinant activated FVII, can benefit in life-threatening bleeding or emergency surgery. Specific antidotes for non-vitamin K oral anticoagulants are in clinical development.
This review aims at answering in a brief and simplified manner some clinical questions.
PMCID: PMC4550032  PMID: 26336492
anticoagulation; rivaroxaban; dabigatran; apixaban
2.  The impact of chronic kidney disease on the annual prognosis in patients 80+ years old suffering from chronic heart failure 
It is well known that the function of kidneys is impaired with age.
The purpose of the study was to evaluate whether chronic kidney disease (CKD) is a predictor for 1-year follow-up mortality among hospitalized chronic heart failure (CHF) patients aged 80+.
Material and methods
The study included 141 consecutive patients aged 80-92 (mean: 82.4 years, 44.7% men). The prospective analysis contains 61 variables with glomerular filtration rate (GFR) and the occurrence of death at the 1-year follow-up. Patients were divided and analyzed depending on GFR.
Chronic kidney disease defined as estimated GFR < 60 ml/min/1.73 m2 was recorded in 93 patients (66%). A relationship with GFR < 60 was found for older age (p = 0.0001), lower body mass index – BMI (p = 0.003), more advanced NYHA class III (p = 0.007), higher concentrations of N-terminal probrain natriuretic peptide – NT-proBNP (p = 0.023), lower hemoglobin (p = 0.0004) and LVEF (p = 0.005), longer hospitalization (p = 0.005), more frequent ventricular blocks in ECG (p = 0.017) and rarely performed coronary angiography (p = 0.021). In turn, GFR < 30 ml/min/1.73 m2 was recorded in 14 patients (9.9%). Similar relationships as in GFR < 60 were found for GFR < 30 and additionally higher concentrations of high-sensitivity C-reactive protein (hsCRP) (p = 0.003), D-dimer (p = 0.002) and more frequent dyslipidemia (p = 0.004) and left main coronary artery disease (p = 0.007). Annual mortality for the total population was 14.2% (n = 20) and was higher (16.1%) if GFR was < 60 and even more (21.4%) in GFR < 30. However, the relationship between deaths and GFR was not statistically significant (for GFR < 60, p = 0.505 and GFR < 30, p = 0.547).
Annual mortality in the patients 80+ who suffered from CHF was high but not statistically significantly associated with CKD.
PMCID: PMC4283880  PMID: 26336438
elderly; heart failure; chronic kidney disease; prognosis
3.  Soluble ST2 protein in chronic heart failure is independent of traditional factors 
ST2 protein is the interleukin 33 (IL-33) receptor, whose serum level depends on the biomechanical strain of cardiac myocytes. The aim of this study was to analyse the relationship between soluble ST2 (sST2) level and traditional factors in patients with chronic heart failure.
Material and methods
Sixty-six patients (mean age 62 years, 75% males) in stable NYHA class I-III with left ventricular ejection fraction < 45% were included in the study. Clinical, biochemical, electrocardiographic, echocardiographic and angiographic data were analysed. Patients were divided into groups depending on sST2 median: > 0.28 ng/ml (n = 31) vs. ≤ 0.28 ng/ml (n = 35). sST2 was measured using a quantitative ELISA kit. In order to define factors associated with sST2 levels uni- and multivariate regression analysis was performed.
There was no relationship between sST2 levels and age (p = 0.67), body mass index (p = 0.19), hsTnT (p = 0.7) or other analysed parameters (all p > 0.05), except for N-terminal prohormone B-type natriuretic peptide (NT-proBNP). A significant positive correlation between sST2 and NT-proBNP was found (p = 0.013, R = 0.395). Multivariate analysis revealed that the stage of coronary artery disease and NT-proBNP were independent factors associated with sST2 concentration (p = 0.04). Intriguing is the fact that the fewer the sclerotic changes present in arteries, the higher was the sST2 level (β = –0.381, p = 0.04).
sST2 protein is independent of traditional factors which usually affect levels of NT-proBNP. In chronic heart failure, sST2 protein may be of greater importance in idiopathic dilated cardiomyopathy than in ischaemic aetiology, which seems to be associated with the molecular mechanism (biomechanical strain) related to sST2.
PMCID: PMC3598130  PMID: 23515651
ST2; chronic heart failure; biomarkers
4.  Genetic Polymorphisms and the Risk of Myocardial Infarction in Patients Under 45 Years of Age 
Biochemical Genetics  2012;51(3-4):230-242.
This study investigates the potential role of 17 chosen polymorphisms in 15 candidate genes and the risk of myocardial infarction in patients under 45 years of age. The study consists of 271 patients with myocardial infarction and 141 controls. The analysis of genetic polymorphisms was performed using the PCR–RFLP method. Of the chosen polymorphisms, two (Leu125Val PECAM1 and A1/A2 FVII) are related to myocardial infarction and two (C677T MTHFR and 5A/6A MMP3) to advanced stenosis in arterial vessels (> 75%). We also found that the frequency of some combinations among the analyzed genes and environmental factors varied between the patient and control groups.
PMCID: PMC3599159  PMID: 23274712
Myocardial infarction; Coronary artery disease; Atherothrombosis; Polymorphism
6.  Genetic variability and the risk of myocardial infarction in Poles under 45 years of age 
Myocardial infarction is caused by the obstruction of an artery in places of atherosclerosis plaque rupture. Endothelial cells during their activation express chemoattractant and adhesion molecules whereas infiltrating inflammatory cells produce enzymes, predisposing a lesion to rupture.
Material and methods
We investigated the correlation between polymorphisms in the human genes E-selectin (Ser128Arg), ICAM1 (K469E), OLR1 (K167N), MMP1 (1G/2G) and MMP3 (−1612 5A/6A) and the risk of MI in young Poles under 45 years. There was no significant difference in the frequency of single nucleotide polymorphism (SNP) of the studied genes E-selectin (Ser128Arg), ICAM1 (K469E), OLR1 (K167N) and MMP3 (−1612 5A/6A) between patients with MI and controls.
The analysis of the association of the 1G2G polymorphism with the risk of myocardial infarction indicated an odds ratio (OR) of 5.68 (95% confidence interval [95% CI] 2.60 to 12.36). Other factors associated with myocardial infarction were: smoking (OR 4.12; 95% CI 1.63–10.44), male sex (OR 16.02; 95% CI 5.90–43.46), hypercholesterolaemia (OR 2.74; 95% CI 1.29–5.83) and arterial hypertension (OR 4.56; 95% CI 1.66–14.47).
We found that only MMP1 1G/2G polymorphism is associated with myocardial infarction in the Polish population of individuals younger than 45 years. Clinical factors seemed to play a greater role in the analysed group.
PMCID: PMC3281334  PMID: 22371740
gene polymorphism; coronary artery disease; atherosclerosis

Results 1-6 (6)