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Abstract: Apelin is a recently isolated novel endogenous ligand for the angiotensin-like 1 receptor (APJ). Initial experiments in animal models indicate that the cardiovascular system is the main target of the apelin–APJ system. Apelin plays an opposite role to the renin-angiotensin-aldosterone system as a compensatory mechanism. It is reduced in patients with heart failure, also of ischemic origin. However, only animal studies concern the role of the apelin–APJ system in myocardial ischemia. Less is known about the function of this adipokine in an acute phase of myocardial infarction in human. The apelin–APJ system could perhaps be involved in myocardial protection during acute myocardial ischemia. In the current review we have summarized recent data concerning the role of apelin in acute myocardial infarction and heart failure induced by ischemia. [Copyright &y& Elsevier]

Aims. The aim of the study was to determine whether a high dose of atorvastatin lowers blood pressure (BP) in normolipemic patients with well controlled primary arterial hypertension and if this effect is associated with alteration of biomarkers of endothelial function and oxidative stress. In this open-label study, normolipemic patients ( n=56) were randomized in the proportion of 2:1 to receive atorvastatin 80 mg daily for 3 months (statin-treated, ST n=39), or to previous therapy (statin-free, SF). BP was measured using a 24-h ambulatory BP measurement device. Plasma levels of 6-keto-PGF1α (prostacyclin metabolite), serum nitric oxide (NO) and levels of autoantibodies immunoglobulin G against oxidatively modified low-density lipoprotein (ox-LDL) were measured. Major findings. The mean change in systolic BP and diastolic BP for ST was – 5.7 mmHg (95% CI –4.1 to –7.2 mmHg) and –3.9 mmHg (95% CI –2.7 to –5.0 mmHg), respectively. Hypotensive statin effect was independent of lipid lowering. No change of BP in SF patients was observed. In ST, prostacyclin metabolites and NO concentrations were not significantly increased and autoantibodies against ox-LDL concentrations did not change. In ST, the decrease in BP correlated with increase in NO and decrease in autoantibodies against ox-LDL. Principal conclusion. High-dose atorvastatin resulted in reduction of BP independently of lipid-lowering effect, changes in endothelial function and oxidative stress, but it was related to the increase in NO and decrease in autoantibodies against ox-LDL. However, because of the open design of the study, these results should be carefully debated. [ABSTRACT FROM AUTHOR]

Background: In 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. Methods: Twenty-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. Results: Coupling 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 < 0.001). Conclusions: Coupling 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 [ABSTRACT FROM AUTHOR]

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. 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. 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. 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. [ABSTRACT FROM AUTHOR]

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 < 0.05). Patients with disease progression (death, WHO class worsening, or therapy escalation, n = 10) had a significantly higher platelet SDF-1/total platelet protein ratio (3.68*10–7 [2.45–4.62] vs. 1.69*10–7 [1.04–2.28], p = 0.001), with no significant differences between plasma levels. Kaplan–Meier analysis revealed that patients with higher platelet SDF-1/total platelet protein ratio had more frequently deterioration of PAH in the follow-up (15.24 ± 4.26 months, log-rank test, p = 0.01). Concentrations of IL-6, sIL-6 receptor and SDF-1 in plasma and platelets are elevated in PAH patients. Higher content of SDF-1 in platelets is associated with poorer prognosis. Our study, despite of limitation due to small number of enrolled patients, suggests that activated platelets may be an important source of cytokines at the site of endothelial injury, but their exact role in the pathogenesis of PAH requires further investigation. [ABSTRACT FROM AUTHOR]

Purpose 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. Methods Thirty two patients (mean age 78.5 ± 7.9 years, 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 ± 6.7 months. Results 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 (p < 0.05). 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. Conclusions 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Introduction Even though thrombocytopenia following transcatheter aortic valve implantation (TAVI) has been described, further investigation of this phenomenon is needed. Aims To determine which factors may explain the fall in platelet count that occurs after implantation of a TAVI device, including markers of platelet and blood coagulation activation. Material and methods 32 patients without previous indications for dual antiplatelet therapy (mean age 78.5 ± 7.9 years, 62% females) with severe aortic valve stenosis (mean gradient 54.6 ± 16.9 mm Hg) who qualified for TAVI procedure (Edwards Sapien XT) were prospectively analyzed. Platelet counts were analyzed before the surgery, on the day of the procedure and for the three following postoperative days (POD 1 to 3). To assess platelet activation P-selectin (PS, serum) and platelet factor 4 (PF-4, CTAD plasma) were measured, whereas for the evaluation of coagulation activation prothrombin fragments 1 + 2 (F1 + 2, plasma) were assessed before the procedure, on POD-1 and POD-3 (ELISA). Results During the postoperative period a significant platelet count drop, the most evident on POD-2, was observed followed by a platelet count raise. The platelet count drop correlated directly with the amount of iodinated contrast agent ( r = 0.42, p = 0.016) and inversely with baseline mean platelet volume ( r = − 0.37, p = 0.046). Neither clinical nor perioperative parameters, except contrast medium, influenced platelet count decrease. No significant differences regarding the concentration of the evaluated markers in patients with and without thrombocytopenia were found. PF-4 and F1 + 2 significantly changed during the study ( p < 0.05). Greater acute PF-4 decrease correlated with greater acute platelet count drop ( r = 0.48, p = 0.043), and during the study slower PF-4 increase correlated with higher platelet count increase on POD-3 ( r = − 0.505, p = 0.032). Lower baseline PS correlated with lower baseline platelet count and higher platelet count increase on POD-3 ( r = 0.45, p = 0.04 and =− 0.55, p = 0.02, respectively). No significant correlations between F1 + 2 concentrations and platelet count changes have been found. Conclusions Platelet reduction shortly after TAVI procedure is related to the amount of contrast agent applied during the procedure. Platelet activation and blood coagulation along with impaired baseline platelet renewal might be the mechanisms of thrombocytopenia following TAVI procedure. [ABSTRACT FROM AUTHOR]

Introduction: Interleukin-6 (IL-6) is a cytokine with a complex function that is described as both pro- and anti-inflammatory. One factor that influences its function is the rs2228145 A/C single nucleotide polymorphism (SNP) of the IL-6 receptor (IL6R) gene. C allele carriers have a decreased inflammatory response and decreased prevalence of ischemic heart disease. The aim of the study was to investigate the association of the rs2228145 SNP of the IL6R gene with long-term total mortality in patients with ST-elevation myocardial infarction (STEMI) treated invasively.Material and Methods: We analyzed the data of consecutive patients with ST elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). Genotyping was performed with the TaqMan method. The analyzed end-point was total long-term mortality (median: 2875 days).Results: The registry comprised 553 patients (mean age: 62.4 ±11.9 years; 25.6% females, n = 142; TIMI 3 obtained in 91.7% of patients, n = 507). No significant differences in baseline characteristics were found between the genotypes. During long-term follow-up 171 (30.9%) patients died. There was non-significantly higher mortality in the rs2228145 AA homozygotes compared to C allele carriers (OR = 1.34, 95% CI: 0.93-1.93, p = 0.1).Conclusions: The rs2228145 polymorphism of IL6R was not significantly associated with long-term mortality after STEMI. However, AA homozygotes (high-risk genotype for ischemic heart disease) showed a trend towards adverse outcome compared to C allele carriers. The observed trend is promising, but it requires independent replication studies. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: Neutrophil gelatinase-associated lipocalin (NGAL), a widely accepted diagnostic marker of acute renal injury (AKI) may be involved in the development of atherosclerosis. Purpose: To assess the prognostic significance of serum and urinary NGAL and serum cystatin C in patients with stable angina undergoing percutaneous coronary intervention (PCI) on a 3-year follow-up. Methods: We included patients with stable angina undergoing PCI. Serum NGAL and cystatin C were evaluated before and 4h, 8h after PCI. Urinary NGAL was evaluated before and 12h and 24h after the procedure. The primary end-point was all-cause mortality on a 3-year follow-up. Results: Among 132 patients there were 63% of males (mean age 64,5±9,8 years). Mean eGFR was 86.2±28.5 ml/min. During follow-up 8% of the patients died. All-cause mortality was significantly higher in patients with increased urinary NGAL concentration 12h after PCI (p=0.04). Urinary NGAL 12h after PCI correlated with eGFR (p<0.05), with serum NGAL evaluated before and 4h and 8h after PCI (p<0.05) and with increased serum cystatin C evaluated 4 hours after PCI (p<0.05). Conclusions: Increased urinary NGAL concentration is a strong predictor of mortality in patients with stable angina who undergo PCI and may be used for the risk stratification in this population. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aim: The aim was to assess if the pharmacological treatment due to cardiovascular causes in dialysis patients is compliant with the European Guidelines. Methods: In total, 110 consecutive end-stage renal disease (ESRD) patients on regular dialysis were enrolled into the study. We divided the population into subgroups with coronary artery disease (CAD), chronic heart failure (CHF) and diabetes mellitus (DM). Results: We gathered information about drugs from 99 patients. The mean age was 61.8 ± 12.9 years (70% of males). There were 37 patients with CAD. Acetylsalicylic acid (ASA) was taken by 89% of the patients with CAD, clopidogrel by 25%, beta-blockers by 70%, angiotensin converting enzyme inhibitors (ACEIs) by 50%, angiotensin receptor blockers (ARBs) by 8%, and statins by 41%. Dual antiplatelet therapy was used after stent implantation (35%). There were 24 patients with CHF. Beta-blockers were taken by 71% of the patients, ACEIs by 45%, statins by 54%, and diuretics by 21% with CHF. There were 36 patients with DM. ASA was taken by 89% of the patients, clopidogrel and ticlopidine by 34%, beta-blockers were taken by 67%, ACE-inhibitors by 55%, and statins by 38% of the population with DM. The patients with DM were taking more ACEIs than those without DM ( p = 0.033). DM was associated with a statistically 21% higher odds of ACEI/ARB use, but CHF was associated with no increase in the odds of beta-blocker use and no increase in ACEI/ARB use. Conclusions: Dialysis patients with cardiovascular diseases are given less cardioprotective drugs such as ASA, beta-blockers, ACEIs, ARBs, and statins than they should be given according to the guidelines. [ABSTRACT FROM AUTHOR]

Morbidity in end-stage renal disease ( ESRD) diabetic patients is worse than in patients without diabetes mellitus ( DM). This study aims to compare clinical, laboratory, and echocardiographic features between the ESRD patients with and without DM. Fifty-eight ESRD patients on dialysis were prospectively divided into two groups according to the presence of DM. Demographic, clinical, laboratory, and echocardiographic features (ejection fraction and wall motion score index) were compared between the two groups. Overall, 20 out of 58 patients (37.8%) with ESRD had DM. There were no significant differences between the patients with DM and those without DM when it comes to age (60.6 ± 10.6 vs. 59.0 ± 10.6 years, P = 0.665), ejection fraction (52.6% ± 12.8% vs. 54.2% ± 12.8%, P = 0.59), and wall motion score index (1.21 ± 0.3 vs.1.15 ± 0.3, P = 0.37). In multivariant analysis of the interventricular septum, posterior wall thickness and left atrium size correlated positively with DM. There was also no statistical difference in myocardial perfusion disturbances on real-time contrast echocardiography between the groups with and without DM (12 (60%) patients vs. 14 patients (36.8%), P = 0.079). Among diabetics 77.8% had significant atherosclerotic changes, while in the group without DM, only 38.1%, P = 0.01. From the laboratory parameters ferritin and high-sensitivity C-reactive protein levels were significantly higher in the group with DM, P = 0.014 and P = 0.026, respectively. Patients with ESRD and DM have significantly bigger left atrial size, thicker left ventricular walls, and higher serum ferritin and high-sensitivity C-reactive protein levels than the patients without DM. The aforementioned features may be possible risk factors for the development of adverse cardiac events in patients on hemodialysis. [ABSTRACT FROM AUTHOR]

Background/aims: The aim of this study was to determine the correlation between renal function and 6-year mortality in patients with acute myocardial infarction (AMI), treated successfully with primary percutaneous coronary intervention (PCI), and to examine whether Cockcroft-Gault (C-G) formula or Modification of Diet in Renal Disease (MDRD) study equation or CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation is the best predictor of very late mortality. Methods: A prospective cohort study with 6-year follow-up of a homogenous group of 193 patients, with ST-segment elevation AMI treated with successful primary PCI. Glomerular filtration rate (GFR) estimated by C-G formula, MDRD, and CKD-EPI equation were analyzed. Results: The patients with chronic kidney disease (CKD) had a much lower cumulative survival rate than those without it ( p < 0.05). A larger area under the receiver-operating characteristic curve for death with respect to GFR for C-G formula was observed. In the multivariate analysis, only GFR ≥ 55 mL/min according to C-G formula was independently associated with lower mortality. Conclusion: CKD is associated with higher mortality after a successful primary PCI during a 6-year follow-up. C-G formula is better than MDRD and CKD-EPI equations at predicting mortality after AMI. [ABSTRACT FROM AUTHOR]

Background/Aims: To assess the impact of diabetes mellitus (DM) on clinical outcome in patients with end-stage renal disease (ESRD) on a 3-year follow-up. Methods: 58 ESRD patients were divided into 2 groups according to the presence of DM. We analyzed following end points: death, cardiac arrest, myocardial infarction, stroke, hospitalizations due to cardiovascular causes, revascularization, and combined end point. Results: Among diabetics, 14 (77.8%) had significant atherosclerotic changes, in the group without DM only 8 (38.1%), p = 0.01. In the group without DM, 14 (46.7%) patients reached combined end point, while in the group with DM 16 (53.3%) patients, p = 0.0013. There were no statistical differences in mortality (p = 0.423). Conclusion: Survival of hemodialyzed diabetic patients is not inferior to nondiabetics; however, morbidity is significantly higher due to adverse cardiac events. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: Background: We aimed to assess apelin—novel endogenous ligand for the angiotensin-like 1 receptor in patients with ST-elevation myocardial infarction (STEMI) and to compare its value with B-type natriuretic peptide (BNP). Methods: In 78 consecutive patients with first STEMI treated with primary PCI, plasma apelin-36 (RIA) and BNP (MEIA) concentrations were measured twice: on admission and on the fifth day of hospitalization. Left ventricle ejection fraction (LVEF) was assessed on admission and composite endpoint (CEP)—after 1year follow-up. Results: During the 5-day interval median plasma BNP level significantly increased and median plasma apelin concentration significantly decreased. BNP, but not apelin, correlated with low LVEF (<50%). In ROC analysis only BNP measurements were diagnostic for low LVEF. In ANOVA test, in patients with CEP, a significant decrease in apelin (but not BNP) concentrations measured in 5-day interval was found. ROC analysis identified only second BNP measurement as significant to estimate adverse outcome 0.627 in the prediction of CEP (95% confidence interval=0.507–0.736). Conclusion: Following STEMI there is a decrease of plasma apelin-36 concentration and an increase of plasma BNP concentration. BNP is better, than apelin diagnostic value for the detection of impaired LVEF. Both BNP and apelin have prognostic value, although both needs further evaluation. [ABSTRACT FROM AUTHOR]

Aim: The aim of this study was to assess the prognostic significance of myocardial contrast echocardiography (MCE) in patients with end-stage renal disease (ESRD) on a 3-year follow-up and to compare the value of MCE with demographic, clinical, and laboratory parameters. Methods: Fifty-eight ESRD patients on regular dialysis were prospectively screened for coronary artery disease (CAD) using perfusion assessment on real-time MCE. We analyzed the following end points during the 3-year follow-up: death, cardiovascular complications, and combined end point, which consisted of adverse cardiac events mentioned above. All features were compared between the two groups with and without perfusion disturbances on MCE. Results: No adverse events related to MCE administration have been observed. Twenty-seven (47%) patients with ESRD demonstrated perfusion defects on MCE. The patients with perfusion defects on MCE comparison with those without perfusion disturbances were older ( p = 0.008) and had lower ejection fraction (EF) ( p = 0.0001) and higher wall motion index (WMSI) ( p = 0.0001). After the 3-year follow-up, the incidence of death ( p = 0.00018), cardiovascular end points, revascularizations [both percutaneous coronary intervention (PCI) and coronary artery bypass grafts (CABG) p = 0.0016 and p = 0.004, respectively], and composite end point ( p = 0.0015) was significantly higher in patients with perfusion defect on MCE. Conclusions: In patients with ESRD, MCE appears to be a safe and useful tool for risk stratification. MCE facilitates decision for coronary angiography. [ABSTRACT FROM AUTHOR]

To date, only animal studies have been concerned with apelin involvement in acute myocardial ischemia. The aim of this study was to investigate apelin measurements in low-risk patients with first ST-elevation myocardial infarction (STEMI) and to assess if apelin may feature as a marker of left ventricular (LV) injury and prognosis. In 78 consecutive patients (mean age 67 ± 11.5 years, 24 women) with first STEMI treated with primary percutaneous coronary intervention, plasma apelin-36 concentrations were measured twice: on admission and on the 5th day of hospitalization. Left ventricle ejection fraction (LVEF) was applied as marker of LV injury. Composite endpoint (CEP), which included death, stroke, and recurrent ischemic event, was assessed after 1 year follow-up. On the first day, median apelin-36 concentration was 2138.5 pg/ml and on the 5th day was significantly lower, 2008.3 pg/ml ( P = 0.002). There were no significant differences found in apelin-36 concentrations between patients with normal and low LVEF. In both groups significant reductions were found in apelin-36 concentrations measured in 5-day intervals ( P = 0.04 and P = 0.008, respectively). After a 1-year follow-up, only one patient died and 19 patients (24.3%) had reached CEP. No difference in baseline apelin-36 concentrations were found in the group of patients who reached CEP compared with those without CEP. However, in both groups concentrations significantly decreased after 5 days ( P = 0.04 and P = 0.013, respectively). Apelin-36 concentrations are reduced in lowrisk first STEMI patients during the first days regardless of the degree of LV dysfunction and prognosis. [ABSTRACT FROM AUTHOR]

Abstract: We hypothesize that higher morbidity of patients with ST-segment elevation myocardial infarction (STEMI) in the out-of-office hours differences in outcome after myocardial infarction may depend on the concentrations of inflammatory cytokines. The aim of the study was to determine the relation between the time of percutaneous coronary intervention (PCI) and local concentration of interleukin 6 (IL-6) and its soluble receptors (sIL-6R and sgp130) in patients with STEMI. Methods and results: The study included 32 patients with invasively treated left anterior descending artery occlusion and no significant co-morbidities. Blood samples were drawn from coronary sinus and aorta before and after intervention. Patients admitted in the afternoon (13–20) presented significantly higher mean IL-6 levels in all samples than patients admitted in the morning. There was a positive correlation between time of intervention and concentrations of IL-6 in all samplings, but also with transcardiac IL-6 gradient at the end of procedure and IL-6 increase during PCI. We did not find any significant association between time of PCI and concentrations of sIL-6R and sgp130, time from pain to balloon, angiographic parameters or medical history. Conclusions: Coronary concentration of IL-6 in patients with STEMI is significantly higher in the afternoon than in the morning. This might be involved in increased morbidity of those patients. [Copyright &y& Elsevier]

Background. Myocardial ischaemia in patients with end-stage renal disease (ESRD) develops both due to the epicardial coronary artery stenosis and to the microvascular injury. We aimed to evaluate coronary blood flow in ESRD patients by means of the thrombolysis in myocardial infarction (TIMI) frame count method (TFC). In patients with ESRD, implementation of the TFC as a marker of the coronary flow abnormalities have not been previously investigated. [ABSTRACT FROM PUBLISHER]

Abstract: Interleukin 6 (IL-6) is a pleiotropic cytokine involved in both inflammatory reaction and myocardial response to stress. Its effects largely depend on the concentration of the soluble receptors (sIL-6R and sgp130). We investigated the production of IL-6, sIL-6R and sgp130 by the heart during ischemia and reperfusion. Methods: The levels of IL-6 were determined in blood of 34 patients with first myocardial infarction (STEMI), left anterior descending (LAD) artery occlusion, otherwise normal coronaries, without significant co-morbidities and 16 comparable subjects with stable ischemic heart disease and lesion in LAD. Blood samples from coronary sinus (CS) and aorta (Ao) were drawn before percutaneous intervention (PCI), immediately after and at the end of the procedure. Venous blood from 30 healthy volunteers served as control. Results: STEMI patients presented high IL-6 concentrations that increased further after reperfusion when its levels in CS became significantly higher than in Ao. In both groups prior to the PCI there were significantly higher concentrations of sIL-6R in Ao than in CS. This difference disappeared immediately after reperfusion. STEMI patients who experienced cardiovascular complications had higher IL-6 concentration and higher transcardiac sIL-6R gradient than patients with event-free hospitalisation. This association was confirmed in multivariate logistic regression analysis. Myocardial infarction increases concentration of IL-6 that is further elevated by reperfusion. A transcardiac gradient of sIL-6R during ischemia may indicate that large amounts of soluble IL-6 receptors are bound to the infarcted heart and thus affect signal transduction. IL-6 and initial sIL-6R gradient may portend complications in STEMI patients. [Copyright &y& Elsevier]

Coronary stenting may create local inflammatory reaction. Interleukin 6 effects depend on the presence of soluble receptors (sIL-6R and sgp130) that facilitate or impede interleukin 6 signal transduction. Concentrations of interleukin 6 and its soluble receptors were assessed in aorta and coronary sinus after stenting in optimally treated stable angina patients scheduled for elective stenting. Baseline levels of interleukin 6 and its soluble receptors in patients did not differ from healthy controls. Initial levels of sIL-6R in aorta were significantly higher than in coronary sinus but this difference disappeared after intervention. Stenting caused interleukin 6 concentration increase to a similar extent both in coronary sinus and in aorta. Moreover, there was significantly higher sgp130 concentration in coronary sinus than in aorta. Coronary intervention increases concentration of interleukin 6 in patients with stable angina. It affects the cardiac level of interleukin 6 soluble receptors what may influence the local inflammatory reaction. [ABSTRACT FROM AUTHOR]

Abstract: Background: In ST-elevation myocardial infarction (STEMI) B-type natriuretic peptide (BNP) holds promise for risk stratification. Aim of this study was to assess prognostic value of plasma BNP measurement and to compare with other powerful prognostic markers — TIMI Risk Score (TRS) and C-reactive protein (CRP) in patients with first STEMI treated with primary PCI (pPCI). Methods: 86 patients, admitted within initial 12 h of the first STEMI. Admission plasma levels of BNP were measured by MEIA method. Serum levels of CRP were measured using immunoturbidimetric assays. Composite end point (CEP) was assessed after 7 months. Results: Median plasma BNP value was higher in patients with CEP, compared with those without CEP (p <0.001). Patients with plasma BNP >99.2 pg/mL were at significantly higher risk for CEP (the highest sensitivity and specificity). CRP level >10.6 mg/dL was also associated with poor outcome. TRS has not influenced the occurrence of CEP. In the analysis of logistic regression the BNP value >99.2 pg/mL was the strongest predictor of CEP. ROC analysis identified BNP measurement as significant to estimate adverse outcome 0.950 in the prediction of CEP (95% Confidence interval=0.878–0.985). Conclusion: Admission plasma BNP concentrations provide incremental prognostic information in patients with first STEMI treated with pPCI. [Copyright &y& Elsevier]

The widespread introduction of fibrinolytics and recently also PTCA in the treatment of myocardial infarction has changed the picture of modern cardiology. But this therapy also raises new problems and challenges. One of them is the occurrence of extensive tissue injury caused by reperfusion. Reinstitution of oxygen to the ischemic tissues initiates various processes leading to generation of reactive oxygen species (ROSs). Acting on the plasma membrane ROS damage its organization and release various proinflammatory agents. Different proteins, including receptors, ionic channels, transporters or components of transduction pathways are substrates of oxidation by ROSs. Their changed structure results in altered functioning and disruption of vital cellular processes. Another key factor of reperfusion injury is activation and infiltration of infarcted area by polymorphonuclear leukocytes (PMNs). Multiple studies identified consecutive stages of PMN activation and substances being involved in it. Main interest lies in cellular adhesion molecules, particularly selectins and β2 integrins, as their antagonists were repeatedly found to diminish neutrophil activation and infarct size. Nevertheless new publications strike at the foundations of the established order and confront the relation between neutrophil infiltration and infarct size. PMNs are linked by close ties to other cells involved in inflammatory response. Seemingly also in cardiac ischemia–reperfusion injury, the activity of neutrophils is modulated by lymphocytes and macrophages. The article describes mutual interactions between different factors involved in the reperfusion injury that may enable preparing new treatments, hopefully as effective and successful as reperfusion therapy. [ABSTRACT FROM AUTHOR]

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 CHA2DS2VASc 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 CHA2DS2VASc score was not used until now in predicting the effectiveness of electrical cardioversion. Aim To assess the value of CHA2DS2VASc 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 CHA2DS2VASc 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 CHA2DS2VASc score ( P = 0.002). The CHA2DS2VASc 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 CHA2DS2VASc 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 CHA2DS2VASc score ≥ 2 than in patients with a CHA2DS2VASc score of 0 or 1 ( OR 3.06; CI: 1.03-9.09; P = 0.044). Conclusion The CHA2DS2VASc 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. [ABSTRACT FROM AUTHOR]