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Purpose Dysfunction of the right ventricle (RV) is an important determinant of survival in patients with pulmonary arterial hypertension (PAH). The presence of late gadolinium enhancement (LGE) in cardiac magnetic resonance (CMR) at RV insertion points (RVIPs) has been found in majority of PAH patients and was associated with parameters of RV dysfunction. We hypothesize, that more detailed quantification of LGE may provide additional prognostic information. Material and methods Twenty-eight stable PAH patients (mean age 49.9 ​± ​15.9 years) and 12 healthy subjects (control group, 44.8 ​± ​13.5 years) were enrolled into the study. Septal LGE mass was quantified at the RVIPs and subsequently indexed by subject’s body surface area. Mean follow-up time of this study was 16.6 ​± ​7.5 months and the clinical end-point (CEP) was defined as death or clinical deterioration. Results Median LGE mass index (LGEMI) at the RVIPs was 2.75 ​g/m2 [1.41–4.85]. We observed statistically significant correlations between LGEMI and hemodynamic parameters obtained from right heart catheterization – mPAP (r ​= ​0.61, p ​= ​0.001); PVR (r ​= ​0.52, p ​= ​0.007) and from CMR – RVEF (r ​= ​−0.54, p ​= ​0.005); RV global longitudinal strain (r ​= ​0.42, p ​= ​0.03). Patients who had CEP (n ​= ​16) had a significantly higher LGEMI (4.49 [2.75–6.17] vs 1.67 [0.74–2.7], p ​= ​0.01); univariate Cox analysis confirmed prognostic value of LGEMI. Furthermore, PAH patients with LGEMI higher than median had worse prognosis in Kaplan-Meier analysis (log-rank test, p ​= ​0.0006). Conclusions The body surface indexed mass of LGE at RV septal insertion points are suggestive of RV hemodynamic dysfunction and could be a useful non-invasive marker of PAH prognosis.

Purpose Inflammatory mechanisms have been suggested to play a role in the heart failure with reduced ejection fraction (HF-REF) development, but the role of chemokines is largely unknown. Cardiac resynchronization therapy (CRT) may reverse the HF-REF course. We aimed to evaluate selected chemokines concentrations in HF-REF patients and their relationship with disease severity and clinical response to CRT. Materials and methods The study included 37 patients (64.1 ± 11.04 years, 6 females) with HF-REF subjected to CRT, controlled prior to implantation and after 6 months. The control population included 26 healthy volunteers (63.9 ± 8.1 years, 8 females). Serum chemokines concentrations were determined using multiplex method. Results HF-REF patients were characterized by the higher baseline MIF, NAP-2 and PF4 concentrations and lower Axl, BTC, IL-9, and IL-18 BPa concentrations comparing to controls. After 6 months of CRT only NAP-2 concentration decreased significantly in comparison to the baseline values. Conclusions HF-REF patients present altered chemokines profile compared to the control group. The CRT-related alleviation of HF-REF causes only slight changes in the chemokines concentrations especially in the platelet-associated ones. The precise chemokines role in the HF-REF pathogenesis and their prognostic value remains to be established.

Despite knowledge of classical coronary artery disease (CAD) risk factors, the morbidity and mortality associated with this disease remain high. Therefore, new factors that may affect the development of CAD, such as the gut microbiome, are extensively investigated. This study aimed to evaluate gut microbiome composition in CAD patients in relation to the control group. We examined 169 CAD patients and 166 people in the control group, without CAD, matched in terms of age and sex to the study group. Both populations underwent a detailed health assessment. The microbiome analysis was based on the V3–V4 region of the 16S rRNA gene (NGS method). Among 4074 identified taxonomic units in the whole population, 1070 differed between study groups. The most common bacterial types were Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria. Furthermore, a higher Firmicutes/Bacteroidetes ratio in the CAD group compared with the control was demonstrated. Firmicutes/Bacteroidetes ratio, independent of age, sex, CAD status, LDL cholesterol concentration, and statins treatment, was related to altered phosphatidylcholine concentrations obtained in targeted metabolomics. Altered alpha-biodiversity (Kruskal–Wallis test, p = 0.001) and beta-biodiversity (Bray–Curtis metric, p &lt, 0.001) in the CAD group were observed. Moreover, a predicted functional analysis revealed some taxonomic units, metabolic pathways, and proteins that might be characteristic of the CAD patients’ microbiome, such as increased expressions of 6-phospho-β-glucosidase and protein-N(pi)-phosphohistidine-sugar phosphotransferase and decreased expressions of DNA topoisomerase, oxaloacetate decarboxylase, and 6-beta-glucosidase. In summary, CAD is associated with altered gut microbiome composition and function.

Pulmonary embolism (PE) is one of the leading causes of cardiovascular mortality, therefore new parameters regarding risk stratification are sought after. In patients admitted for acute PE we investigated associations between the initial coagulation impairment, expressed by prothrombin time international normalised ratio (INR), and parameters reflecting PE severity. Furthermore, in-hospital, 30-day and long-term mortality were also evaluated. The analysis included 848 patients who were divided into two groups: with normal INR≤1.2, and elevated INR>1.2 (252 patients, 29.7%). The group with elevated INR presented higher incidence of tachycardia and lower systolic blood pressure, higher CRP, d-dimer, and NT-proBNP. This group presented higher estimated systolic pulmonary artery pressure (49 IQR39-62mmHg vs 43 IQR32-53mmHg, p

BackgroundIn pulmonary arterial hypertension (PAH) increased afterload leads to adaptive processes of the right ventricle (RV) that help to maintain arterio-ventricular coupling of RV and preserve cardiac output, but with time the adaptive mechanisms fail. In this study, we propose a multimodal approach which allows to estimate prognostic value of RV coupling parameters in PAH patients.MethodsTwenty-seven stable PAH patients (49.5 ± 15.5 years) and 12 controls underwent cardiovascular magnetic resonance (CMR). CMR feature tracking analysis was performed for RV global longitudinal strain assessment (RV GLS). RV-arterial coupling was evaluated by combination of RV GLS and three proposed surrogates of RV afterload—pulmonary artery systolic pressure (PASP), pulmonary vascular resistance (PVR) and pulmonary artery compliance (PAC). 18-FDG positron emission tomography (PET) analysis was used to assess RV glucose uptake presented as SUVRV/LV. Follow-up time of this study was 25 months and the clinical end-point was defined as death or clinical deterioration.ResultsCoupling parameters (RV GLS/PASP, RV GLS/PVR and RV GLS*PAC) significantly correlated with RV function and standardized uptake value (SUVRV/LV). Patients who experienced a clinical end-point (n = 18) had a significantly worse coupling parameters at the baseline visit. RV GLS/PASP had the highest area under curve in predicting a clinical end-point and patients with a value higher than (−)0.29%/mmHg had significantly worse prognosis. It was also a statistically significant predictor of clinical end-point in multivariate analysis (adjusted R2 = 0.68; p ConclusionsCoupling parameters are linked with RV hemodynamics and glucose metabolism in PAH. Combining CMR and hemodynamic measurements offers more comprehensive assessment of RV function required for prognostication of PAH patients.Trial Registration: NCT03688698, 09/26/2018, retrospectively registered; Protocol ID: 2017/25/N/NZ5/02689

Introduction: Right ventricular (RV) function is a major determinant of survival in patients with pulmonary arterial hypertension (PAH). In our previous study, we confirmed that increased RV fluorodeoxyglucose (FDG) uptake in positron emission tomography (PET) (presented as higher ratio of FDG uptake of RV to LV) was associated with progressive RV dysfunction and preceded hemodynamic and clinical deterioration in PAH patients. Now, we obtained second PET/MRI assessments of the study group after 2-years of PAH-targeted treatment. Hypothesis: Altered cardiac glucose uptake in severe PAH patients may change after PAH specific treatment. Methods: Twenty-eight PAH patients (51.32±15.91 years) had simultaneous PET/MRI scans performed during baseline visit. Second PET/MRI assessments were done after 2 years in the group of twenty patients (four deaths, four patients did not agree to perform additional scans). Results: After follow-up period, we observed significant change of MRI-derived RV ejection fraction (45±10% to 51.2±12.7%, p=0.03), and improvement in hemodynamic parameters obtained from right heart catheterization e.g. mean pulmonary artery pressure, mPAP (48.5±17.2 to 41.8±17.1 mmHg, p=0.01) and pulmonary vascular resistance, PVR (8.7±5.3 to 7.0±4.2 WU, p=0.04). Follow-up SUVRV/SUVLV ratio was lower than baseline (0.84±0.57 vs 1.02±0.75, p=0.05) and significantly correlated with follow-up RV hemodynamic parameters confirming relationship between RV function and metabolic alterations. Interestingly, patients who had improvement in SUVRV/SUVLV (lower follow-up value than baseline, n=11) had significantly higher mPAP at baseline visit (58.9±18.7 vs 40.3±11.8 mmHg, p=0.02), suggesting that RV FDG accumulation in advanced PAH may decrease after the specific PAH-treatment in accordance with the degree of reduction in the pulmonary vascular resistance. Conclusions: Impaired RV function is associated with increased glucose uptake of RV myocytes estimated by FDG PET in PAH patients. Targeted treatment may improve RV function and thus affect previously altered cardiac glucose uptake.

ObjectiveRight ventricular (RV) function is a major determinant of survival in patients with pulmonary arterial hypertension (PAH). Metabolic alterations may precede haemodynamic and clinical deterioration. Increased RV fluorodeoxyglucose (FDG) uptake in positron emission tomography (PET) was recently associated with progressive RV dysfunction in MRI, but the prognostic value of their combination has not been established.MethodsTwenty-six clinically stable patients with PAH (49.9±15.2 years) and 12 healthy subjects (control group, 44.7±13.5 years) had simultaneous PET/MRI scans. FDG uptake was quantified as mean standardised uptake value (SUV) for both left ventricle (LV) and RV. Mean follow-up time of this study was 14.2±7.3 months and the clinical end point was defined as death or clinical deterioration.ResultsMedian SUVRV/SUVLV ratio was 1.02 (IQR 0.42–1.21) in PAH group and 0.16 (0.13–0.25) in controls, pRV/SUVLV significantly correlated with RV haemodynamic deterioration. In comparison to the stable ones, 12 patients who experienced clinical end point had significantly higher baseline SUVRV/SUVLV ratio (1.21 (IQR 0.87–1.95) vs 0.53 (0.24–1.08), p=0.01) and lower RV ejection fraction (RVEF) (37.9±5.2 vs 46.8±5.7, p=0.03). Cox regression revealed that SUVRV/SUVLV ratio was significantly associated with the time to clinical end point. Kaplan-Meier analysis showed that combination of RVEF from MRI and SUVRV/SUVLV assessment may help to predict prognosis.ConclusionsIncreased RV glucose uptake in PET and decreased RVEF identify patients with PAH with worse prognosis. Combining parameters from PET and MRI may help to identify patients at higher risk who potentially benefit from therapy escalation, but this hypothesis requires prospective validation.

Introduction . Strain and strain rate (SR) are techniques, which provide local information on myocardial deformation. The aim of the study was to assess the usefulness of strain and SR measurement in cardiac resynchronization therapy (CRT) response in chronic heart failure (CHF) patients. Materials and methods . The study included 35 CHF patients with QRS complex duration ≥ 120ms with LBBB morphology. Biochemical and clinical parameters were assessed before and after six months of CRT. TTE classical and tissue Doppler echocardiography parameters (longitudinal peak systolic strain — LPS and SR for basal segment of intraventricular septum and lateral wall) were evaluated. Results . Twenty-two patients (62.8%) benefited from CRT (the responders) and revealed improvement in septal and lateral LPS in the 6-month observation [-7.1 (-5.2– -11.1) vs -12.1 (-8.7– -14)%, p = 0.002; - 10.4 (-6.1– -17.6) vs - 13.8 (-8.9 – -17.8)%, p = 0.03; respectively]. Six months after CRT, the responders were characterised by higher increase in septal LPS comparing to the nonresponders (-4.6 ± 6.1 vs -2.4 ± 3.9%, p = 0.045). Septal LPS changes correlated positively with baseline cardiopulmonary exercise testing (CPET) parameters: peak oxygen uptake (r = 0.6, p = 0.004), peak carbon dioxide excretion (r = 0.62, p = 0.002) and negatively with VE/VCO2 slope (r = -0.5, p = 0.037). Conclusions . LV regional LPS appears to be a good parameter reflecting the improvement of clinical status in patients treated with CRT. The responders had better improvement of septal LPS, therefore positive response to this therapy may be related to the improvement of septal contractility.

Inflammatory processes and platelet activity play an important role in the pathophysiology of pulmonary arterial hypertension (PAH). Enhanced IL-6 signaling and higher concentration of stromal-derived factor alpha (SDF-1) have been previously shown to be linked with prognosis in PAH. We hypothesized that platelets of PAH patients have higher content of IL-6 and SDF-1 and thus are involved in disease progression.We enrolled into study 22 PAH patients and 18 healthy controls. Patients with PAH presented significantly higher plasma concentrations and platelet contents of IL-6, sIL-6R, and SDF-1 than healthy subjects (platelet content normalized to protein concentration: IL-6 (0.85*10–10 [0.29 – 1.37] vs. 0.45*10–10 [0.19–0.65], sIL-6R 1.54*10–7 [1.32–2.21] vs. 1.14*10–7 [1.01–1.28] and SDF-1 (2.72*10–7 [1.85–3.23] vs. 1.70*10–7 [1.43–2.60], all p

Thrombocytopenia (TP) following transcatheter aortic valve implantation (TAVI) procedure is a common phenomenon but the underlying mechanisms are neither well known nor described. Postinterventional severe TP is related to worse early and late outcome. Moreover, the statement of enhanced platelet and coagulation activation might justify even stronger antiplatelet and anticoagulation therapy following TAVI procedure. Thus, the examination of the pathomechanisms responsible for TP post TAVI seems to be crucial. Several hypotheses have been raised. TP can be caused by insufficient production or impaired platelet renewal. On the other hand, increased platelet activation, consumption and destruction might also be responsible for TP. These findings, mostly related to the procedure alone, need further investigation. Here, we summarize the potential multifactorial causes of post TAVI thrombocytopenia.

Pentraxin 3 (PTX3) is an acute phase protein that, likely to C-reactive protein (CRP), belongs to pentraxin superfamily. PTX3 is produced as a response to inflammatory mediators by several types of cells directly associated with atherosclerosis such as endothelial cells or macrophages. Thus PTX3 appears to be a specific indicator of localized inflammatory process. PTX3 reflects inflammatory status in cardiovascular diseases such as subclinical atherosclerosis, coronary artery disease, acute coronary syndromes (ACS) and heart failure. Association of PTX3 with cardiovascular risk factors suggests that it can be a promising marker of subclinical and symptomatic atherosclerosis. Previous research suggests that PTX3 may be a useful diagnostic marker of ACS. Furthermore, in patients after ACS or with heart failure it appears an independent prognostic factor.

Pulmonary hypertension (PH) diagnosis requires invasive assessment by right heart catheterization (RHC), but screening and monitoring are performed using non-invasive methods: echocardiography and cardiopulmonary exercise testing (CPET). The aim of the study was to assess correlations between the parameters obtained in non-invasive testing and RHC in patients with PH of different etiologies.The study included 53 medical records of PH patients (32 women) aged 29-81 years. We analyzed correlations between RHC (systolic pulmonary artery pressure (sPAP), diastolic pulmonary artery pressure (dPAP), pulmonary vascular resistance (PVR), cardiac output (CO)) and echocardiographic (tricuspid annular plane systolic excursion (TAPSE), sPAP) and CPET parameters (end-tidal oxygen and carbon dioxide pressures (PetOEchocardiographic estimation correlated well with RHC measurement of sPAP (r=0.65, P0.001). TAPSE correlated with PVR assessed with thermodilution method (r=-0.5, P=0.005), dPAP (r=-0.53, P=0.002) and CO (r=0.53, P=0.002). PVR assessed with thermodilution and Fick methods showed positive correlation with PetOSimple cardiac function indicators obtained by commonly used non-invasive methods allow only approximate estimation of the main hemodynamic RHC-derived parameters: sPAP, CO and PVR. Obtained results suggest the relationship between RV dysfunction and ventilation abnormalities in PH patients.

BACKGROUND Atrial fibrillation (AF) is the most common arrhythmia occurring in 2% of the population. It is known that AF increases morbidity and limits quality of life. The CHA2 DS2 VASc score (congestive heart failure/left ventricular dysfunction, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular disease, age 65-74 and sex category (female)) is widely used to assess thrombotic complications. The CHA2 DS2 VASc score was not used until now in predicting the effectiveness of electrical cardioversion. AIM To assess the value of CHA2 DS2 VASc score in predicting unsuccessful electrical cardioversion. METHODS We analysed 258 consecutive patients with persistent AF who underwent electrical cardioversion between January 2012 and April 2016 in a Cardiology University Centre in Poland. RESULTS Out of 3500 hospitalised patients with AF, 258 (mean age 64 ± 11 years, 64% men) underwent electrical cardioversion. The CHA2 DS2 VASc score in analysed population (258 patients) was 2.5 ± 1.7 (range 0-8), and the HAS-BLED (hypertension, abnormal liver or renal function, stroke, bleeding, labile international normalised ratio, elderly, drugs or alcohol) was 1 ± 0.9 (range 0-4). Electrical cardioversion was unsuccessful in 12%. Factors associated with unsuccessful cardioversion were age (P = 0.0005), history of ischaemic stroke (P = 0.04), male gender (P = 0.01) and CHA2 DS2 VASc score (P = 0.002). The CHA2 DS2 VASc score in patients who had unsuccessful cardioversion was higher compared to patients who had successful cardioversion - 3.5 versus 2.4 (P = 0.001). In the logistic regression model, if the CHA2 DS2 VASc score increases by 1, the odds of unsuccessful cardioversion increase by 39% (odds ratio (OR) 1.39; confidence interval (CI): 1.12-1.71; P = 0.002). The odds of unsuccessful cardioversion are three times higher in patients with a CHA2 DS2 VASc score ≥ 2 than in patients with a CHA2 DS2 VASc score of 0 or 1 (OR 3.06; CI: 1.03-9.09; P = 0.044). CONCLUSION The CHA2 DS2 VASc score routinely used in thromboembolic risk assessment may be a simple, easy and reliable scoring system that can be used to predict unsuccessful electrical cardioversion.

Background The concept of coupling mainly refers to the relationship between ventricular contractility and afterload. Together, strictly related parameters may provide a more accurate estimation of the RV performance status. Indexing RV function, assessed by CMR feature tracking analysis, with a pulmonary artery systolic pressure (PASP) obtained from right heart catheterization (RHC) allows estimation of ventricular-arterial coupling and could help in prognostic stratification of pulmonary arterial hypertension (PAH) patients. Aim To verify the prognostic value of multimodal approach to estimate RV ventricular-arterial coupling in PAH patients. Methods Twenty-six stable PAH patients (mean age 49.92±15.94 years) and twelve healthy subjects (control group, 44.75±13.51 years) were enrolled into the study. CMR feature tracking analysis of the RV was performed for generation of RV global longitudinal strain (RV GLS); RV ejection fraction was also obtained by CMR. Right heart catheterization was carried out only in the PAH group with a standard technique.RV- arterial coupling was evaluated by the ratio of RV GLS/PASP. Mean follow-up time of this study was 16.6±7.5 months and the clinical end-point (CEP) was defined as death or clinical deterioration. Results In study group, RV GLS significantly correlated with hemodynamic parameters from RHC – mean pulmonary artery pressure, mPAP (r=0.53, p=0.04) and pulmonary vascular resistance, PVR (r=0.57, p=0.002). Mean RV GLS/PASP ratio in PAH group was (−)0.24±0.15%/mmHg. Patients who reached CEP (n=15) had a significantly higher RV GLS and RV GLS/PASP ratio (−13.3±7.9% vs −20.4±6.2%, p=0.01 and −0.15±0.09%/mmHg vs −0.36±0.19%/mmHg, p=0.005, respectively). However, ROC analysis revealed higher area under curve (AUC) of RV GLS/PASP in predicting CEP than of RV GLS alone (0.82 (95% CI 0.64–1) vs 0.77 (95% CI 0.58–0.96), p Figure 1 Conclusions Combining CMR and hemodynamic measurements via catheterization offers the potential for more comprehensive assessment of pulmonary vascular load and right heart function, as required for evaluation of the hemodynamic state in patients with PAH. Acknowledgement/Funding This work was supported by National Center for Science in Poland [“Preludium” grant 2017/25/N/NZ5/02689 to R.K.]

Introduction: Increased expression of interleukin-6 (IL-6) has been described in left ventricular dysfunction in the course of chronic heart failure. Cardiac resynchronization therapy (CRT) is a unique treatment method that may reverse the course of chronic heart failure (CHF) with reduced ejection fraction (HF-REF). We aimed to evaluate the IL-6 system, including soluble IL-6 receptor (sIL-6R) and soluble glycoprotein 130 (sgp130), in HF-REF patients, with particular emphasis on CRT effects. Material and methods: The study enrolled 88 stable HF-REF patients (63.6 ±11.1 years, 12 females, EF < 35%) and 35 comorbidity-matched controls (63.5 ±9.8 years, 7 females). Forty-five HF-REF patients underwent CRT device implantation and were followed up after 6 months. Serum concentrations of IL-6, sIL-6R and sgp130 were determined using ELISA kits. Results : The HF-REF patients had higher IL-6 (median: 2.6, IQR: 1.6–3.8 vs. 2.1, IQR: 1.4–3.1 pg/ml, p = 0.03) and lower sIL-6R concentrations compared to controls (median: 51, IQR: 36–64 vs. 53. IQR 44–76 ng/ml, p = 0.008). There was no significant difference between sgp130 concentrations. In the HF-REF group IL-6 correlated negatively with EF (r = –0.5, p = 0.001) and positively with BNP (r = 0.5, p = 0.008) and CRP concentrations (r = 0.4, p = 0.02). Patients who presented a positive response after CRT showed a smaller change of sIL-6R concentration compared to nonresponders (ΔsIL-6R: –0.2 ±7.1 vs. 7 ±14 ng/ml; p = 0.04). Conclusions : HF-REF patients present higher IL-6 and lower sIL-6R levels. IL-6 concentration reflects their clinical status. CRT-related improvement of patients’ functional status is associated with a smaller change of sIL-6R concentration in time.

The relationship and clinical implications of atrial fibrillation (AF) in acute pulmonary embolism (PE) are poorly investigated. We aimed to analyze clinical characteristics and prognosis in PE patients with paroxysmal AF episode. Methods. From the 391 patients with PE 31 subjects with paroxysmal AF were selected. This group was compared with patients with PE and sinus rhythm (SR) and 32 patients with PE and permanent AF. Results. Paroxysmal AF patients were the oldest. Concomitant DVT varies between groups: paroxysmal AF 32.3%, SR 49.5%, and permanent AF 28.1% (p=0.02). The stroke history frequency was 4.6% SR, 12.9% paroxysmal AF, and 21.9% permanent AF (p<0.001). Paroxysmal AF comparing to permanent AF and SR individuals had higher estimated SPAP (56 versus 48 versus 47 mmHg, p=0.01) and shorter ACT (58 versus 65 versus 70 ms, p=0.04). Patients with AF were more often classified into high-risk group according to revised Geneva score and sPESI than SR patients. In-hospital mortality was lower in SR (5%) and paroxysmal AF (6.5%) compared to permanent AF group (25%) (p<0.001). Conclusions. Patients with PE-associated paroxysmal AF constitute a separate population. More severe impairment of the parameters reflecting RV afterload may indicate relation between PE severity and paroxysmal AF episode. Paroxysmal AF has no impact on short-term mortality.

Background: There is not much data on matrix metalloproteinase neutrophil gelatinase-associated lipocalin (MMP-NGAL) complex in patients with atrial fibrillation (AF). Aim: The aim of the study was to assess the value of MMP-NGAL complex in predicting AF recurrence after electrical cardioversion. Methods: The serum levels of NGAL, cystatin C, interleukin-6, high-sensitivity C-reactive protein, copeptin, MMP-NGAL complex, matrix metalloproteinase 2, tissue inhibitor of metalloproteinase 1, Von Willebrand factor, B-type natriuretic peptide and the urinary level of NGAL were evaluated before cardioversion. Results: A total of 83 patients with persistent AF were enrolled in the study. Left atrial diameter (LA) ≥4.5 cm was significantly associated with AF recurrence at follow-up (p = 0.009). In selected 39 obese patients, MMP-NGAL complex was associated with AF recurrence (p = 0.03). If the concentration of MMP-NGAL complex increased by 1 ng/ml, the odds of AF recurrence increased by 4% (OR 1.04; CI: 1.00-1.08; p = 0.03). MMP-NGAL complex did not correlate with AF recurrence in patients with a first episode of AF, in patients ≥65 years of age and in patients with a LA ≥4.5 cm or with chronic kidney disease. Conclusions: It is known that the greater the BMI at baseline, the higher the likelihood of progression from paroxysmal to permanent AF. However, European Society of Cardiology (ESC) guidelines do not consider obese patients a population with a low likelihood of success of cardioversion. That is why we need a sensitive marker to predict sinus rhythm maintenance in such a population. We found that MMP-NGAL complex may predict AF recurrence after successful cardioversion in obese patients.

Background Takotsubo cardiomyopathy (TTC) is characterised by transient contractility disturbances of the apex of the left ventricle. Methods We enrolled 101 patients from the northern-eastern part of Poland in the years 2008–2012 who were hospitalised for TCC. The control group consisted of female patients diagnosed with anterior myocardial infarction with ST-segment elevation (anterior STEMI) (n = 101). Results 89 % of the study group were women. Patients with TTC had diabetes (12.6 % vs 29.7 %; p = 0.002) and hyperlipidaemia (36.8 % vs 64.4 %; p = 0.0001) significantly less frequently, and better kidney function assessed by estimated glomerular filtration rate versus patients with anterior STEMI (74.52 % vs 64.30 %; p = 0.004). In the TTC group there were more patients with chronic obstructive pulmonary disease (11.6 % vs 1.0 %; p = 0.002) and thyroid disturbances, especially hyperthyroidism (23.4 % vs 11.0 %; p = 0.021). In patients with TTC sudden cardiac arrest, pulmonary oedema and cardiogenic shock were observed less frequently than in the control group (14.7 % vs 30.7 %; p = 0.0078). Hospitalisations in TTC patients were less frequently complicated by pneumonia (20.0 % vs 35.6 %; p = 0.0148) and urinary infection (4.2 % vs 21.8 %; p = 0.0003). Cardiac rupture occurred in 3 patients with TTC and in 1 with anterior STEMI. In-hospital mortality was significantly lower in the group with TTC. Also, mortality at 30 days, 3 months, 1 year and 2.5 years was significantly lower in patients with TTC than in patients with MI (p = 0.035; p = 0.0226; p = 0.0075; p = 0.009). Conclusions Previously considered to be a benign syndrome, TTC should be reconsidered as a clinical condition at risk for serious complications such as cardiac arrest, cardiogenic shock, pulmonary oedema and cardiac rupture leading to death and causing substantial early hazard. The prognosis in TTC is significantly better than in patients with anterior STEMI.

We present a case of 85-year-old patient diagnosed with ST-segment elevation myocardial infarction of anterior wall due to coronary embolism secondary to persistent atrial fibrillation. The patient was performed coronary angiography and aspiration thrombectomy. Due to lack of atherosclerotic lesions, there was no need of stent implantation. On echocardiography we found left atrium appendage thrombus. After she was given dual antiplatelet therapy and rivaroxaban, gastrointestinal bleeding was observed. After that incident rivaroxaban was discontinued, which has led to the right axillary artery embolism. Afterwords she was given therapy only with oral anticoagulant and qualified to left atrium appendage closure.

Atrial fibrillation (AF) frequently occurs in patients with chronic kidney disease (CKD), and the rate reaches even 30% in patients with end-stage renal disease (ESRD). Patients with AF and CKD have a significantly higher risk of thrombotic complications, particularly ischemic stroke, and at the same time, a higher bleeding risk (proportionally to the grade of renal failure). In addition, AF and CKD share a number of comorbidities and risk factors, which results in increased mortality rates. Moreover, disturbances in hemostasis are common complications of kidney disease. Their occurrence and severity correlate with worsening renal function, including ESRD. At present, the incidence of bleeding is declining, while thrombotic complications have become the predominant cause of mortality. Prophylactic antithrombotic treatment reduces the rate of stroke and other thrombotic complications. Vitamin K antagonists (VKAs) have long been used in anticoagulant therapy, and more recently, non-vitamin K oral anticoagulants (NOACs) have been introduced, which are direct thrombin inhibitors. NOACs are a valuable anticoagulant option in this group of patients as long as a summary of product characteristics is followed. They are at least as effective as warfarin, while being safer, especially when it comes to intracranial hemorrhage. Renal function should be evaluated before initiation of NOACs and reevaluated when clinically indicated. Importantly, disturbances in hemostasis in patients with CKD and ESRD may lead to unexpected complications, such as extensive bleeding. If anticoagulation is administered to patients on dialysis, effects of an individual dialysis modality as well as interactions with other drugs given (eg, heparin) should be considered.

Inflammatory activation plays a pivotal role in chronic heart failure with reduced ejection fraction (HF-REF). A novel mediator from TNF family: soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) along its soluble decoy receptor CD163 (sCD163) recently has been investigated in other cardiovascular pathologies. We aimed to evaluate sTWEAK and sCD163 concentrations in HF-REF patients. The study enrolled 79 patients with stable HF-REF, EF35%. The control population without history of heart failure included two groups: 26 comorbidities matched patients and 27 healthy volunteers. sTWEAK and sCD163 serum concentrations were determined using ELISA kits. Univariate and multivariate analysis was performed to assess variables affecting concentration of sTWEAK and sCD163. HF-REF patients were characterized by higher sTWEAK (median 374 IQR: 321-429 vs 201 IQR: 145-412pg/ml, P=0.005), sCD163 (median 744 IQR: 570-1068 vs 584 IQR: 483-665pg/ml, P=0.03) concentrations and sTWEAK/sCD163 ratio (median 0.53 IQR: 0.32-0.7 vs 0.3 IQR: 0.22-0.37, P=0.001) comparing to healthy volunteers. Comparing to comorbidities matched controls, HF-REF patients had lower sTWEAK levels (median 374 IQR: 321-429 vs 524 IQR: 384-652pg/ml; P=0.002), while sCD163 and sTWEAK/sCD163 ratio didn't differ. Concentration of sTWEAK in HF-REF was affected by white blood cell count and aspirin intake, while sCD163 by exercise capacity, LV diastolic volume, CRP and presence of arterial hypertension.HF-REF patients present increased sTWEAK and sCD163 levels as well as sTWEAK/sCD163 ratio when compared to healthy subjects, however CHF itself appears to be associated with down-regulation of sTWEAK.

Objective The role of Galectin-3(Gal-3) in atherosclerosis progression has not been definitely acknowledged. The aim of the study was to establish the following: whether Gal-3 may act as an independent risk factor of coronary artery disease (CAD) occurrence and its advancement, if Gal-3 has potential relations with classical and new markers of cardiovascular risk (carotid intima-media thickness (cIMT), and whether Gal-3 may be a marker of mortality in the group of patients with myocardial infarction (MI) during mid-term follow-up. Patients and Methods The study group was composed of 233 patients with MI and 100 patients with a stable CAD. Selected risk factors were assessed, Gal-3 concentrations and cIMT were measured. The control group was composed of 100 healthy individuals. Results In the study group (MI and CAD patients) Gal-3 concentration was significantly higher than in the controls – median 7.9 ng/ml (p = 0.0001) and 10.7 ng/ml (p = 0.00001) vs. 5.5 ng/ml, respectively. Patients with 3-vessel disease had higher levels of Gal-3 than patients with 1-or 2-vessel disease (9.2 ng/ml vs 7.4 ng/ml, p = 0.003). In the group of MI patients who died during the follow-up (average period – 2.8 years), we found a significantly higher concentration of Gal-3 (20.0 ng/ml vs 8.0 ng/ml, p = 0.0005) and cIMT values (common carotid artery(CCA): 1.4 ± 0.4 mm vs. 1.0 ± 0.3 mm, p = 0.03; carotid bulb(CB): 2.3 ± 0.5 mm vs. 1.9 ± 0.4 mm, p = 0.009). In the model of multivariate logistic regression analysis, the variables influencing the mortality after MI during follow-up were: age > 65years, Gal-3 concentration > 8.7 ng/ml, IMT values and plaque occurrence in CB, previous MI and EF Conclusions Gal-3 is an independent risk factor of CAD occurrence, but cIMT values are better markers of CAD advancement. Both Gal-3 concentration > 8.7 ng/ml and IMT values in CB were an independent predictive indicators of increased risk of all-cause mortality in patients after MI during mid-term follow up.

Patients admitted to an intensive cardiac care unit (ICCU) are a heterogeneous population with a high mortality rate. The aim of our study was to investigate which clinical, biochemical, and echocardiographic parameters routinely assessed may affect long-term mortality in a non-selected ICCU population.A total of 392 patients hospitalized between 2008-2011 (mean age, 70 ± 13.8 years, 43% women) were consecutively and prospectively assessed with the following admission diagnoses: 168 with acute coronary syndromes (ACS), 122 with acute decompensated heart failure (ADHF), and 102 with other acute cardiac disorders. Patients were treated according to the current European Society of Cardiology (ESC) guidelines.During a mean 29.3 (± 18.9) months of observation, 152 (38.8%) patients died and 7.9% of the patients needed a red blood cell transfusion (RBC Tx). Patients who died were significantly older and had lower baseline levels of hemoglobin (Hb), serum iron concentration (SIC), total iron binding capacity (TIBC), cholesterol, and left ventricular ejection fraction (LVEF), as well as lower eGFR values, and higher white blood cell (WBC) counts and C-reactive protein (CRP) levels (P < 0.05). Predictors of death in multivariate regression analysis were age, Hb, LVEF, WBC, and CRP. The most powerful factor was hospitalization for non-ACS. The risk of long-term mortality increased with decreasing levels of Hb (P < 0.001), SIC (P = 0.001), TIBC (P = 0.009), and the need for RBC Tx (P < 0.001), as well as the diagnosis of ADHF (P < 0.001) and the absence of ACS (P = 0.007).In ICCU patients, age, Hb, parameters of iron status, and LVEF are strong predictors of long-term mortality. Among the ICCU population, patients with ACS diagnosis have better survival.

Background The role of IL-6 in pulmonary arterial hypertension (PAH) has been reported but the prevalence of soluble receptors for IL-6: sIL-6R and sgp130 and its potential role in PAH have not been studied. Our aim was to examine the IL-6 together with the soluble receptors and to assess its relationship with clinical status of PAH patients as well as to assess its potential prognostic significance. Methods Serum concentrations of IL-6, sIL-6R and sgp130 were quantified by ELISA in 26 patients with PAH and 27 healthy controls and related to functional and biochemical parameters and clinical outcome in PAH group. The PAH patients were followed up for 1 year, noting the end point of clinical deterioration (WHO class change, the need for escalation of therapy) or death. Results The PAH group was characterized by higher median serum IL-6 [2.38 (IQR 1.56–3.75) vs 0.87 (0.63–1.3) pg/ml, p = 0.000003] and sIL-6R concentrations [69.7 (IQR 60.4–84.4 vs 45.7 (34.6–70.3) ng/ml, p = 0.0036] compared to control subjects. Both groups did not differ in sgp130 concentrations. There were significant correlations in PAH group between IL-6 levels and uric acid, parameters of ventilatory efficiency in cardiopulmonary exercise testing: VE/VO 2 , VE/VCO 2 , VE/VCO 2 slope and peak PetCO 2 . sIL-6R levels inversely correlated with LDL cholesterol. After 1 year the clinical deterioration occurred in 11 patients, 15 remained stable. Patients in whom the clinical deterioration occurred showed significantly higher baseline concentrations of IL-6 [3.25 (IQR 2.46–5.4) pg/ml vs 1.68 (1.38–2.78) pg/ml, p = 0.004], but not sIL-6R. Median IL-6 ⩾ 2.3 pg/ml (91% sensitivity, 73% specificity) identified subjects with worse clinical course. In the univariate analysis, higher IL-6 level at baseline was associated with increased risk and earlier occurrence of clinical deterioration (HR 1.42, 95%CI 1.08–1.85, p = 0.015). Conclusions IL-6 trans-signaling is enhanced in PAH. Elevated concentration of sIL-6R suggests its potential unfavorable role in systemic amplification of IL-6 signaling in PAH. Levels of IL-6 are associated with clinical indicators of disease severity as well as indirectly with systemic metabolic alterations. IL-6 shows prognostic value regarding predicting clinical deterioration.

The aim of the study was to find whether patients carrying polymorphic allele of the rs10757278 polymorphism from 9p21 locus have changed risk of arrhythmia (atrial fibrillation, AF; sustained ventricular tachycardia or ventricular fibrillation, sVT/VF) during acute phase of myocardial infarction. Retrospective analysis of data collected prospectively from two independent centers was performed. The clinical data were pooled from two independent cardiac registries: (1) the Warsaw ACS genetic registry (STEMI and NSTEMI/UA patients hospitalized in the years 2008-2011; only STEMI patients were analyzed); (2) the Bialystok STEMI genetic registry (STEMI patients hospitalized in years 2001-2005, who survived the first 48 h from hospital admission). Data regarding sVT/VF and AF within first 24 h were analyzed. The patients were genotyped with rs10757278 polymorphism. 1083 patients were included in the analysis; 62 (5.7 %) patients had sVT/VF during acute phase and 78 (7.2 %) patients had AF, 46 (4.2 %) patients had new-onset AF. Minor allele frequency in all patients with AF was significantly different from those without AF (0.40 vs 0.51, p = 0.0096). When only new-onset AF was analyzed, the trend was the same, with significant protective effect in recessive model [OR 0.41 (95 % CI 0.17-0.97), p = 0.025]. The effect was independent of age and GRACE score. No relationship was found between sVT/VF and rs10757278. Patients with STEMI, who survived until hospitalization with polymorphic allele of 9p21 rs10757278 SNP have less AF during acute phase of STEMI. SNP rs10757278 is not linked with sVT/VF in acute phase of STEMI.

Introduction Although recommendations for the antithrombotic management of atrial fibrillation (AF) are based on strong evidence, the European guidelines are not fully implemented into practice. Objectives The objective of this study is to analyse antithrombotic treatment in AF in Poland after the publication of the European Society of Cardiology Guidelines in 2012. Patients and Methods We retrospectively studied 1556 patients with AF from the Reference Cardiology University Centre in Poland in 2012–2014. Results CHA2DS2VASc and HAS-BLED scores were 3.5 ± 1.7 and 2.4 ± 1.1. Anti-vitamin K agent were prescribed in 59%, with non-vitamin K antagonist oral anticoagulants in 12%, acetylsalicylic acid (ASA) alone in 18%. Older patients (p

The heterogeneous group of patients admitted to Intensive Cardiac Care Unit (ICCU) as well as nonspecific complaints associated with anemia might be the reason for underdiagnosing or minimization of this problem. Because of this heterogeneity, there are no clear guidelines to follow. It is known that anemia is impairing the outcome. Thus, it is crucial to keep alert in the diagnosis and treatment of anemia, especially in critically ill cardiac patients. The greatest groups of patients admitted to ICCU are those with acute coronary syndromes (ACS), acute decompensated heart failure (ADHF), severe arrhythmias as well as individuals after cardiac operations. However, patients suffering other critical cardiac illnesses quite often become anemic during hospitalization in ICCU. It is because anemia is typed in the clinical features of heavy diseases or may be the consequence of treatment. The current review focuses on the incidence, complex etiology and predictive role of anemia in a diverse group of ICCU patients. It discusses clinical aspects of anemia treatment in particular groups of critically ill cardiac patients because proper treatment increases chances for recovery and improves the outcome in this severe group of patients.

The inflammation underlying both atherosclerosis and acute coronary syndromes is strongly related to monocyte-related actions. However, different monocyte subsets can play differential roles in the formation and destabilization of atherosclerotic plaque as well as healing of damaged myocardial tissue. Monocytes are currently being divided into three functionally distinct subsets with different levels of CD14 (cluster of differentiation 14) and CD16 expression. Thus, there are classical CD14++CD16-, intermediate CD14++CD16+ and non-classical CD14+CD16++ monocytes. Here, we summarize the current knowledge on complex activities of different monocyte subsets in atherosclerosis and acute coronary syndromes. Moreover, we discuss which monocyte subsets can serve either as predictive biomarkers of cardiovascular risk or as potential targets used in atherosclerosis and its complications.

INTRODUCTION The CHA2DS2-VASc and R2CHA2DS2-VASc scoring systems were designed to stratify thromboembolic risk in patients with atrial fibrillation. The R2CHA2DS2-VASc score, compared with the CHA2DS2-VASc, was modified by adding reduced creatinine clearance. OBJECTIVES The aim of the study was to assess the long-term predictive value of these scores in patients with acute coronary syndrome (ACS) and to compare their utility with TIMI and GRACE scores in this patient group. PATIENTS AND METHODS We performed a pooled analysis of 5 independent populations with ACS with a long-term follow-up available. The primary endpoint was defined as all-cause mortality. The following risk scores were calculated: TIMI-STEMI or TIMI-NSTEMI, GRACE, CHA2DS2-VASc, and R2CHA2DS2-VASc RESULTS A total of 2557 patients were included in the final analysis with a median follow-up of about 5 years. The CHA2DS2-VASc and R2CHA2DS2 -VASc scores were significant predictors of total mortality in the pooled analysis. After correction for heart rate and systolic blood pressure on admission as well as previous myocardial infarction, the scores were still significantly predictive of mortality (hazard ratio [HR], 1.47; 95% confidence interval [CI], 1.39–1.54; P

Purpose Vascular cell adhesion molecule 1 (VCAM-1) plays a role in the adhesion and migration of leukocytes from blood to arterial intima and correlate with the development of atherosclerosis. The aim of the study was to establish whether soluble VCAM-1 (sVCAM-1) may act as an independent risk factor of coronary artery disease occurrence and whether it may reflect a degree of its advancement, if sVCAM-1 has a potential relation with intima-media thickness measurement (IMT), if sVCAM-1 may be useful as a predictor of further cardiovascular events. Material and methods The study group was composed of 78 patients who were consecutively hospitalized in 2010–2011 due to myocardial infarction (MI). Selected clinical and biochemical risk factors were assessed, sVCAM-1 concentrations and IMT were measured. Results Concentrations of sVCAM-1 were significantly higher in the study group as compared to the healthy controls. No significant dependence between sVCAM-1 concentration and the value of IMT in carotid arteries was found. There were no significantly statistical differences between the advancement of coronary artery changes and sVCAM-1 concentration. During the follow-up that lasted from 2 to 4 years (average period – 2.8 years), 4 patients died in the study group (5.1%). sVCAM-1 concentrations (but not IMT values) were significantly statistically higher in the group of patients who died (2248.5 ± 443.5 vs. 990.2 ± 433.6, p = 0.0003). Conclusions sVCAM-1 concentrations are useful indicators of the presence of atherosclerosis in coronary arteries, but not its advancement. sVCAM-1 (but not IMT) can be a predictive indicator of an increased risk of death during follow-up in patients after myocardial infarction.

Introduction rs9982601 (C>T) is a polymorphism of the noncoding region between the SLC5A3/MRPS6 and KCNE2 genes. It has been shown to be associated with early-onset myocardial infarction (MI) with T as a risk allele. Objectives The aim of our study was to investigate the association of the rs9982601 polymorphism with long-term overall mortality from MI and prevalence of MI in a Polish population. Patients and methods The study involved patients with MI treated invasively. Individuals who underwent paternity testing served as a population group. Genotyping was performed by the TaqMan method. The analyzed endpoint was the overall long-term mortality. Results The study group comprised 981 patients (mean age, 62.8 ±12.1 years; 259 women [26.4%]). The percentages of TT, CT, and CC genotypes were 3.1%, 25.6%, and 71.3%, respectively, in the whole group, and 2.4%, 16.8%, and 80.8% (P = 0.01) in the population group (n = 167). During follow-up (median, 1826 days), 157 patients died (16%). No significant differences were observed between the genotypes either in clinical characteristics or in mortality. However, in a subgroup of high-risk patients (GRACE risk score of 155 points or higher, n = 428), low-risk CC homozygotes had a significantly better survival rate compared with the other genotypes (hazard ratio, 0.64; 95% confidence interval, 0.43-0.96; P = 0.03). Conclusions We showed that the rs9982601 polymorphism of the region between SLC5A3/MRPS6 and KCNE2 genes is associated with long-term mortality in high-risk patients after MI. Additionally, our study supports the previous reports on the correlation of this polymorphism with the prevalence of MI.

Background : Pulmonary hypertension (PH) is a cardiovascular pathology leading to right-sided heart failure. A qualitative assessment of right ventricular (RV) function in echocardiography provides valuable information on a patient’s condition. The standard echocar- diographic parameter, assessed in PH patients, is RV free wall motion. Aim : To verify the utility of RV free wall motion assessment via echocardiography in PH patients. Methods : Data from 30 PH patients, regardless of aetiology (except for left heart disease), was retrospectively analyzed. Based on the RV free wall motion visual echocardiographic assessment the population was divided into: group 1- normokinetic; group 2- hypokinetic RV. All patients underwent a medical interview, physical examination, basic laboratory work-up, echocardiography, and right heart catheterization (RHC). Twenty-one patients underwent a cardiopulmonary exercise test (CPET). Results : The analysis revealed, that patients with RV free wall hypokinesis were characterized by impaired gas exchange parameters (higher values of ventilatory equivalents for oxygen and carbon dioxide, higher end-tidal oxygen pressures, lower end-tidal carbon dioxide pres- sures and higher minute ventilation – carbon dioxide production relation slope) and cardiovascular response to exercise (lower increase in O2 pulse during exercise) obtained in the CPET. RHC showed that patients with hypokinetic RV had higher diastolic and mean pul- monary artery pressures (dPAP, mPAP), lower cardiac index, and higher pulmonary vascular resistance. Conclusions : RV free wall motion abnormalities, assessed using echocardiography in PH patients, are found in those with more advanced disease. They are characterized by impaired ventilation in the CPET and more advanced haemodynamic abnormalities in RHC. The association between this parameter and prognosis requires validation in a larger population of patients. JRCD 2017; 3 (5): 161–167

Cardiac and extracardiac lipid metabolism is known to be significantly altered in the course of the heart failure with reduced ejection fraction (HF-REF), however the precise mechanisms are not fully elucidated. The aim of the study was to use of untargeted metabolomics to identify and validate changes in the blood metabolites profile, occurring as a result of HF-REF development. The analyses were performed first in the derivation set (36 chronic HF-REF patients and 19 controls without the disease) and repeated in validation cohort (31 chronic HF-REF patients and 20 controls). Independent analyses of both sets revealed statistically significant decline in intensities of phosphatidylcholine (PC): 34:4 and 36:5, lysophosphatidylcholine (lyso-PC): 14:0, 15:0, 18:0, 18:2, 20:3, lysophosphatidylethanolamine (lyso-PE): 18:1 and 18:2 in chronic HF-REF patients. More symptomatic patients and those with ischaemic etiology of HF-REF presented greater deficit in phospholipids (PLs) intensities. The decrease of identified PLs intensities (as compared to controls) correlated with decreased serum cholesterol level, impaired renal function, reduced exercise capacity, enhanced ventilatory response and metabolic parameters associated with altered fatty acids oxidation. In multiple regression analysis PLs deficit was significantly associated with age, carnitines serum intensity, renal function, uric acid, cholesterol level. In conclusion, HF-REF is associated with significant disturbances in phospholipids metabolism. Greater reduction in serum intensities of particular identified PLs is associated with older age, worse clinical condition, impaired oxidative muscle metabolism and enhanced catabolic status.

To determine the time point at which thrombocytopenia after TAVI procedure is an indicator of the worst prognosis, with special consideration of perioperative platelet and coagulation activation as its potential causes.Thirty two patients (mean age 78.5±7.9years, 62% females) qualified for TAVI procedure were prospectively evaluated. Platelet counts were assessed at baseline and for the next three postoperative (POD) days. Platelet activation was evaluated by P-selectin (PS, serum, ELISA) and platelet factor 4 (PF-4, CTAD plasma), and blood coagulation activation by prothrombin fragments 1+2 (F1+2, plasma, ELISA). Composite end point (CEP) including death and the need of cardiovascular rehospitalization was assessed after a mean of 14.1±6.7months.During the follow up period half of the patients reached CEP. Thrombocytopenia was more profound and frequent in patients with CEP as compared to those without (p0.05). No differences regarding either the biomarkers of platelet (PS, PF-4) or coagulation (F1+F2) activation between the groups with and without CEP were found. Patients with moderate-to-severe thrombocytopenia at baseline had worse prognosis (log-rank test, p=0.0003). Based on the receiver operating characteristic curve analysis, the differences between platelet count on each postoperative day and the baseline count did not have any predictive value in CEP occurrence.Patients with thrombocytopenia following TAVI procedure have poor prognosis, however, the changes on the particular days are not more important than initial platelet count. Further studies are needed to evaluate platelet and blood coagulation activation as potential causes of thrombocytopenia and impaired prognosis related to it.

Introduction Inflammation plays a significant role in the pathogenesis of pulmonary arterial hypertension (PAH). Soluble receptor activator of nuclear factor-ĸB ligand (sRANKL) and osteoprotegerin (OPG) are tumor necrosis factor α family members of immunomodulatory activity. Objectives The aim of the study was to evaluate sRANKL and OPG concentrations in patients with PAH as potential factors contributing to the development of the disease. Patients and methods We studied 26 patients with PAH, 31 volunteers, and 24 stable patients with chronic systolic left ventricular heart failure (LVHF) without pulmonary hypertension. The PAH group was followed up for 6 months for clinical deterioration or death. Results sRANKL levels were higher in the PAH group compared with controls and the LVHF group (5.6 [interquartile range, 3.9-7.9) vs. 2.0 [0.9-4.4] pmol/l; P = 0.0001, and 2.4 [1.3-4.2] pmol/l; P = 0.001, respectively). OPG levels were higher in PAH patients compared with controls (4.07 ±1.9 vs. 3.27 ±0.95 pmol/l; P = 0.048). We found significant correlations between sRANKL levels and parameters of ventilatory efficiency during exercise in the PAH group. OPG levels correlated with brain natriuretic peptide levels and with invasive hemodynamic parameters. Patients with clinical deterioration during 6-month follow-up (n = 9) showed higher baseline OPG levels compared with stable patients (n = 17, 5.09 ±2.6 vs. 3.52 ±1.19 pmol/l; P = 0.043). In the univariate analysis, the elevated OPG concentration at baseline was associated with an increased risk and earlier occurrence of clinical deterioration (hazard ratio, 1.43; 95% confidence interval, 1.06-1.9; P = 0.017). Conclusions Concentrations of sRANKL and OPG are elevated in patients with PAH and are associated with indicators of disease severity and prognosis. sRANKL is a better discriminant between PAH and LVHF than OPG. The baseline OPG concentration is significantly associated with adverse outcomes in patients with PAH.

Purpose Cardiogenic shock (CS) is a severe complication of acute coronary syndromes (ACS). Intra-aortic balloon pump (IABP) is considered important mechanical therapy for acute CS. We aimed to analyze the natural history and possible prognostic factors in patients with CS complicating ACS. Patients/methods All 126 patients (mean age 65.8 ± 12.5 years), who were hospitalized in single center due to an episode of CS in the course of ACS, had IABP and were scheduled for coronary angiography. The assessed end-point was 5-year death from any cause. Results Median left ventricle ejection fraction (LVEF) 28% (interquartile range (IQR) 23–35%), 39 patients (31%) were female, in 91 (72%) the initial diagnosis was ST-elevation myocardial infarction (STEMI). Mean time on the IABP was 3.8 ± 3 days. During index hospitalization there were 56 deaths (44%). Other 27 patients (out of 70 discharged – 38.5%) died during 5-year follow-up. In univariate logistic regression, the significant effect on long term mortality had age, female gender, reduced ejection fraction below 31% and hypotension on admission. The out of hospital survival was also determined by age, gender and hypotension, while LVEF lost its predictive value The multivariate survival analysis both in whole group and in patients discharged from hospital was independently affected by age and hypotension on the admission. Conclusions The mortality of patients with CS despite treatment with IABP remains very high, especially during the in-hospital period and early after discharge. Among assessed parameters age and hypotension on the admission are the most important predictors of adverse long term prognosis.

Paraoxonase 1 (PON1) is an enzyme responsible for the antioxidant properties of high density lipoprotein (HDL). The activity of PON1 is decreased in patients with coronary artery disease, myocardial infarction or chronic kidney disease. rs662 and rs854560 are single nucleotide polymorphisms (SNPs) associated with PON1 activity and 10-year cardiovascular mortality of patients with stable coronary artery disease. We investigated the association of rs662 and rs854560 SNPs of the PON1 gene with 5-year mortality in patients with ST-elevation myocardial infarction (STEMI) treated invasively. We analyzed the data of consecutive patients with STEMI treated with primary PCI. Genotyping was performed with the TaqMan method. The analyzed end-point was total 5-year mortality. Additional subgroup analysis was performed for survival of patients depending on their eGFR. The study group comprised 634 patients (mean age 62.3 ± 11.85 years; 25.2 % of women, n = 160; PCI successful in 92.3 %, n = 585). No clinically relevant differences in baseline characteristics were found between the genotypes. No association between either genotype and 5-year mortality was found: p = 0.4 for the rs662 SNP, p = 0.73 for the rs854560 one (log-rank test). However, in a subgroup of patients with eGFR below median value (78.6 ml/min/1.73m2) the rs854560 AA homozygotes had a significantly lower probability of survival (p = 0.047, log-rank test). The AA genotype of the rs854560 SNPs of the PON1 gene is associated with increased mortality in patients after myocardial infarction in the subpopulation of patients with lowered eGFR. This phenomenon may be explained by potentially lower PON1 activity in kidney disease.

Access-site vascular complications in patients undergoing transradial coronary procedures are rare but may have relevant clinical consequences. The aim of the study was to evaluate: (1) radial artery’s (RA) patency immediately after the procedure and in long-term observation, (2) factors influencing the frequency of radial artery’s occlusion (RAO) after percutaneous coronary intervention (PCI) procedures performed via transradial access in the group of 220 patients with acute coronary syndromes (ACS). RA ultrasound was performed 48–72 h after the procedure and in those who were diagnosed with RAO-again after 6–12 months. According to the ultrasonographic findings, the patients were divided into two sub-groups: 187 pts (85 %) with patent RA after PCI and 33 pts (15 %) with RAO. Both sub-groups significantly statistically differed with regard to the frequency of local hematomas—15 versus 27.3 % (p = 0.02), the frequency of applying IIbIIIa inhibitors in PCI—6.4 versus 15.1 % (p = 0.015) and procedure duration—0.59 ± 0.37 versus 0.77 ± 0.38 (p = 0.014), respectively. In a multifactorial analysis the only factor influencing RA patency promptly after the procedure was PCI duration (p

Background: Anaemia is present in 12–30% of patients with acute coronary syndromes (ACS). Many studies have shown that admission anaemia is an independent predictor of in-hospital or short-term mortality in patients with ACS. However, there is limited data on the long-term prognostic importance of anaemia in this group of patients. Aim: To establish the relation between haemoglobin concentration on admission and six-year all-cause mortality in patients with ST-segment elevation myocardial infarction (STEMI) treated invasively. Methods: We retrospectively studied 551 patients with the diagnosis of STEMI referred to the catheterisation laboratory of our hospital and treated with successful primary percutaneous coronary intervention. Patients were divided into two groups according to admission haemoglobin concentration (< 13 g/dL in males and < 12 g/dL in females). Results: A total of 551 patients with STEMI (164 female, 30%) were included in the analysis, mean age was 63 ± 12 years. Anaemia on admission was present in 11% (n = 61) of the patients. Of the entire cohort, renal failure was present in 25% (n = 138), and diabetes in 16% (n = 88). Admission haemoglobin concentration was significantly associated with age (r = –0.2663, p < 0.05), blood pressure (systolic blood pressure [SBP]: r = 0.1940, diastolic blood pressure [DBP]: r = 0.2023, p < 0.05), glucose concentration (r = –0.1218, p < 0.05), white blood cells count (r = 0.1230, p < 0.05), cholesterol concentration (r = 0.1253,p < 0.05), estimated glomerular filtration rate (eGFR; r = 0.1819, p < 0.05), Killip-Kimball class (r = –0.1387, p < 0.05) and TIMI risk score for STEMI (r = –0.2647, p < 0.05). During follow-up, 27% (n = 130) of the patients died. The mortality rate was significantly higher in the patients with admission anaemia (47% vs. 24%, p = 0.0002). The patients with anaemia were older (p = 0.0007), had lower blood pressure (SBP: p = 0.007; DBP: p = 0.01), higher heart rate (p = 0.03), higher glycaemiaconcentration (p = 0.003), higher C-reactive protein concentration (p = 0.0007) and lower white blood cells count (p = 0.03). Patients with anaemia had more frequently renal failure (eGFR < 60 mL/min/1.73 m 2 ) (p = 0.02) and a significantly higher TIMI risk score for STEMI (p = 0.01). In multivariate analysis, all-cause mortality was associated with: anaemia on admission (OR = 2.29; 95% CI 1.20–4.36; p = 0.011), low ejection fraction (OR = 2.97; 95% CI 1.78–4.96; p < 0.001) and age (OR = 1.65 [per 10 years]; 95% CI 1.34–2.03; p < 0.001). Anaemia on admission remained an independent predictor of six-year mortality. Conclusions: Admission anaemia significantly influences all-cause mortality in patients with STEMI treated invasively ina six-year follow-up and may be used for risk stratification in this population.