INTRODUCTION Transcatheter aortic valve implantation (TAVI) and minimally invasive aortic valve replacement (minithoracotomy and ministernotomy) have become a valuable alternative to conventional surgical treatment of severe aortic stenosis (AS) in high-risk patients. OBJECTIVESThe aim of the study was to evaluate long-term results and complications in patients with symptomatic AS treated with TAVI, surgical aortic valve replacement (SAVR), minithoracotomy, or ministernotomy. PATIENTS AND METHODSA total of 173 patients with symptomatic AS were enrolled to the study between the years 2011 and 2013. Propensity scores were calculated for TAVI and each surgical method separately. Differences in clinical outcomes between patients treated with TAVI and those treated with surgical methods were adjusted for propensity scores using a logistic regression analysis and presented as adjusted odds ratios with 95% confidence intrervals.RESULTS A median follow-up was 583.5 days (interquartile range, 298-736 days). Before aortic valve replacement (AVR), no significant differences in ejection fraction (EF) were observed between the groups. At 1 week after AVR, mean EF values were significantly higher in patients after TAVI in comparison with the other groups (TAVI, 50.2% ±13.1%; minithoracotomy, 44.1% ±13.4%; ministernotomy, 37.8% ±12.8%; SAVR, 40.3% ±12.5%; P = 0.001). There were no differences in the longest available follow-up mortality between the analyzed groups (P = 0.8). To our best knowledge, this is the first study comparing minithoracotomy, ministernotomy, and SAVR with TAVI in terms of long-term outcomes such as the longest available follow-up mortality, left ventricular (LV) function, complications after the procedure, and conduction disturbances and arrhythmias after the procedure.CONCULSIONS Patients undergoing TAVI show more beneficial long-term outcomes in comparison with patients undergoing minithoracotomy, ministernotomy, and SAVR and do not differ in terms of the longest available follow-up mortality. TAVI seems to have a more favorable effect on LV function and an increase in EF in comparison with the surgical methods.

The term “microbiome” defines the collective genome of all commensal, symbiotic, and pathogenic microbes living in the human body. The composition of microbiota in the gut and skin is influenced by many factors such as the stage of life, nutrition, lifestyle, and gender. In the past few years, several scientific papers have demonstrated an implication of microbiota in many immune-mediated diseases, for example, diabetes, ulcerative colitis, and multiple sclerosis. The alterations in the proportion of gut microbiota have emerged as potential immunomodulators with the capacity to induce physiologic as well as pathologic immune responses against the human body, causing inflammation and destruction of tissues or organs. The microbiota influences the differentiation of adaptive immune cells not only in the gut but also in the skin. Alopecia areata (AA) is a dermatologic disorder which causes hair loss in most cases resistant to treatment. There are some clinical and experimental evidences indicating that AA is the demonstration of autoimmune attack against hair follicles. The factors that may implicate such an autoimmunity in AA still remain unknown. Despite more and more evidences demonstrate that human microbiome plays a key role in human health and diseases, to the best of our knowledge, no study has been conducted to analyze an implication of microbiome in the pathogenesis of AA. Undoubtedly, there is a need to performing a study which might explain the involvement of gut and skin microbiota in the unclear pathogenesis of AA and lead to alternative treatment options for numerous patients suffering from current treatment limitations.

Introduction:The aim of the study was to evaluate clinical and biochemical differences between patients with low-renin and high-renin primary arterial hypertension (AH), mainly in reference to serum lipids, and to identify factors determining lipid concentrations.Materials and methods:In untreated patients with AH stage 1 we measured plasma renin activity (PRA) and subdivided the group into low-renin (PRA < 0.65 ng/mL/h) and high-renin (PRA ⩾ 0.65 ng/mL/h) AH. We compared office and 24-h ambulatory blood pressure, serum aldosterone, lipids and selected biochemical parameters between subgroups. Factors determining lipid concentration in both subgroups were assessed in regression analysis.Results:Patients with high-renin hypertension (N = 58) were characterized by higher heart rate (p = 0.04), lower serum sodium (p < 0.01) and aldosterone-to-renin ratio (p < 0.01), and significantly higher serum aldosterone (p = 0.03), albumin (p < 0.01), total protein (p < 0.01), total cholesterol (p = 0.01) and low-density lipoprotein cholesterol (LDL-C) (p = 0.04) than low-renin subjects (N = 39). In univariate linear regression, only PRA in the low-renin group was in a positive relationship with LDL-C (R2 = 0.15, β = 1.53 and p = 0.013); this association remained significant after adjustment for age, sex, and serum albumin and aldosterone concentrations.Conclusions:Higher serum levels of total and LDL-C characterized high-renin subjects, but the association between LDL-C level and PRA existed only in low-renin primary AH.

Introduction The aim of this study was to assess the relations between plasma renin activity (PRA), serum aldosterone concentration (ALDO) and selected asymptomatic organ damage (AOD) indices in mild primary arterial hypertension (AH). Material and methods We measured PRA, ALDO, and selected AOD indices (carotid-femoral pulse wave velocity (cfPWV), central aortic pulse pressure (cPP), estimated glomerular filtration rate (eGFR)) in 122 patients with untreated AH. Results Patients with high PRA (≥ 0.65 ng/ml/h) were characterized by lower plasma sodium and aldosterone to renin ratio (ARR), higher ALDO, but a similar level of AOD indices compared to patients with low PRA. cfPWV ( p = 0.04) and cPP ( p = 0.019) increased with ARR, while eGFR decreased with ALDO ( p = 0.008). Only eGFR was independently correlated with ALDO. In subjects with simultaneously high PRA and ARR values, we found significantly higher cfPWV ( p = 0.02) and cPP ( p = 0.04) and lower eGFR ( p = 0.02) than in those with high PRA but low ARR values. Conclusions Assessment of the influence of the renin-angiotensin-aldosterone system (RAAS) on AOD should include the relationship between renin and aldosterone. The PRA itself has no predictive value for AOD. More advanced arterial stiffness and renal impairment are associated with increased PRA and ARR. The RAAS activity might be useful in AOD prediction and hypertension severity assessment.

Background: Atherosclerosis is as a systemic inflammatory disease associated with the activation of many mediators, including matrix metalloproteinases (MMPs), and may be amplified by abnormal high serum uric acid (UA) concentration (hyperuricemia, HU). The aim of the study was to determine the relationship between serum UA concentration and activity of MMPs and their correlation with the hypertension-mediated organ damage (HMOD) intensity. Methods: One hundred and nine patients untreated with antihypertensive, hypolipemic or uratelowering drugs with diagnosed stage 1-2 essential hypertension were included in this study. In all participants blood pressure (BP) was measured, carotid-femoral pulse wave velocity (PWV), intima-media thickness (IMT), echocardiography and blood tests including UA, lipids and serum concentrations of MMPs (1, 2, 3, 9) were observed. The participants were divided into hyper-and normuricemic groups. Results: Uric acid concentration in the whole study group positively correlated with some HMOD parameters (IMT, PWV, left ventricular mass index, left atrial dimension). Among the studied metalloproteinases only MMP-3 activity positively correlated with serum UA concentration independently of age, body mass index and serum lipids (R2 = 0.11, p = 0.048). Multivariate regression analysis showed positive association between IMT and BP, UA concentration and MMP-3 activity, independently of waist circumference and serum lipids (R2 = 0.328, p < 0.002). Patients with HU were characterized by higher activity of MMP-3 than those without (19.41 [14.45; 21.74] vs. 13.98 [9.52; 18.97] ng/mL, p = 0.016). Conclusions: The present results may support the thesis that UA and the increased by UA activity of MMPs may take part in the development of HMOD, especially IMT.

In this retrospective study of patients with myocardial infarction treated with percutaneous coronary intervention primarily admitted to the Emergency Department we confirmed that acid-base balance parameters obtained from peripheral venous blood sample and assessed in point-of-care test (POCT) analyzers may be a reliable tool for early risk stratification.Elevated lactate level is associated with worse clinical condition and it can be suspected that lactic acidosis is a consequence of more severe derangement (i.e.: in patients with out-ofhospital cardiac arrest). In contrast, base excess may be considered as a marker of significant importance even in subtle degrees of acidosis, because it predicts both mortality in short-and long-term observation in the whole study group as well as in-hospital mortality in patients without out-of-hospital cardiac arrest.

Background: Atherosclerosis is as a systemic inflammatory disease associated with the activation of many mediators, including matrix metalloproteinases (MMPs), and may be amplified by abnormal high serum uric acid (UA) concentration (hyperuricemia, HU). The aim of the study was to determine the relationship between serum UA concentration and activity of MMPs and their correlation with the hypertension-mediated organ damage (HMOD) intensity. Methods: One hundred and nine patients untreated with antihypertensive, hypolipemic or uratelowering drugs with diagnosed stage 1-2 essential hypertension were included in this study. In all participants blood pressure (BP) was measured, carotid-femoral pulse wave velocity (PWV), intima-media thickness (IMT), echocardiography and blood tests including UA, lipids and serum concentrations of MMPs (1, 2, 3, 9) were observed. The participants were divided into hyper-and normuricemic groups. Results: Uric acid concentration in the whole study group positively correlated with some HMOD parameters (IMT, PWV, left ventricular mass index, left atrial dimension). Among the studied metalloproteinases only MMP-3 activity positively correlated with serum UA concentration independently of age, body mass index and serum lipids (R2 = 0.11, p = 0.048). Multivariate regression analysis showed positive association between IMT and BP, UA concentration and MMP-3 activity, independently of waist circumference and serum lipids (R2 = 0.328, p < 0.002). Patients with HU were characterized by higher activity of MMP-3 than those without (19.41 [14.45; 21.74] vs. 13.98 [9.52; 18.97] ng/mL, p = 0.016). Conclusions: The present results may support the thesis that UA and the increased by UA activity of MMPs may take part in the development of HMOD, especially IMT.

BackgroundAsymptomatic hyperuricemia (AHU) is de ned as elevated serum uric acid (UA) concentration without symptoms. This study aimed to determine the effects of AHU treatment with allopurinol on selected hypertension mediated organ damage (HMOD) indices in patients with uncomplicated essential arterial hypertension (AH). MethodsPatients aged 30-70 years with AHU and essential hypertension grade 1-2 with adequate blood pressure (BP) control, without previous urate lowering therapy (ULT) were divided into two groups: a) receiving allopurinol (ULT group) and b) age-and sex matched patients without ULT (control group). Both groups received UA-lowering diet. BP (o ce, 24 hour and central), echocardiographic parameters, pulse-wave velocity, carotid intima-media thickness (IMT) and lab tests (high-sensitivity C-reactive protein (hs-CRP) were measured at baseline and at 6 months follow-up. ResultsOut of 100 participants 87 completed the study (44 ULT patients and 43 controls). At 6 months follow-up, there was a signi cantly greater reduction in serum UA concentration in the ULT group than in the control group (464±68.8 µmol/l vs 314±55.6 µmol/l, p<0.0001). Patients receiving allopurinol had signi cant reductions in o ce systolic (137±11.8 mmHg vs 134±9.3 mmHg; p=0.025) and diastolic BP (83±9.9 mmHg vs 79±8.7 mmHg, p=0.017), central systolic BP (56±8.9 mmHg vs 51±12.9 mmHg, p=0.046), pulse pressure (43±10.4 mmHg vs 39±11.2 mmHg, p=0.017), IMT (0.773±0.121 mm vs 0.752±0.13 mm, p=0.044), left atrium volume index (40±13.5 ml/m 2 vs 38±12.3 ml/m 2 , p=0.044), and hs-CRP level (3.36±2.73 mg/l vs 2.74±1.91 mg/l, p=0.028) compared to controls. The decrease in UA concentration was signi cantly related to the reduction in IMT (R=0.37, p<0.001), central SBP (R=0.26, p=0.015) and hs-CRP concentration (R=0.30, p=0.004). Multivariate regression analysis revealed the independent relationship between reduction in IMT and UA lowering (R=0.3234, R2=0.0722, p<0.026). ConclusionsIn patients with AH and asymptomatic hyperuricemia treatment with allopurinol leads to further improvement in BP control and reduction in HMOD intensity, in particular IMT. The decrease in hs-CRP concentration associated with ULT may have a bene cial effect on patient long-term prognosis. BackgroundAsymptomatic hyperuricemia (AHU) is traditionally de ned as elevated serum uric acid (UA) concentration but in which neither symptoms of monosodium urate crystal deposition disease, such as gout, nor uric acid renal disease have occurred [1]. The prevalence of AHU has increased over several