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• Women appear to be more susceptible to CS in the setting of acute myocardial infarction compared with men with higher mortality risk. • Sex-related differences also exist with regard to other causes of CS. • In order to improve outcomes for women with CS, the underestimation of cardiovascular risk in women needs to be addressed. • In addition, more robust data on the optimal management of CS in women is urgently needed. • Until further evidence is obtained, adherence to guideline-directed therapies in women with CS must be mandated. [ABSTRACT FROM AUTHOR]

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]

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]

Introduction: In the course of acute myocardial infarction (AMI) cardiomyocyte injury, activation and destruction of endothelial cells together with inflammation lead to miRNA expression alterations. Aim: To assess levels of circulating cardiac-specific (miR-1) and endothelial-specific (miR-126) miRNAs in the acute phase of AMI and after a follow-up period. Material and methods: Seventeen AMI patients (mean age: 64.24 ±13.83 years, mean left ventricle ejection fraction (LVEF): 42.6 ±9.65%), treated with primary percutaneous coronary intervention within the first 12 h, had plasma miRNAs isolated (quantitative real-time PCR, Exiqon) on admission and after 19.2 ±5.9 weeks. Measurements were also performed in a control group of healthy volunteers matched for age and sex. Results: Concentrations of both miRNAs were significantly higher in AMI patients as compared to healthy controls: miR-1: 5.93 (3.15-14.92) vs. 1.46 (0.06-2.96), p = 0.04; miR-126: 4.5 (3.11-7.64) vs. 0.54 (0.36-0.99), p = 0.00003, respectively. Levels of both miRNAs significantly decreased after the follow-up period: miR-1: 5.93 (3.15-14.92) vs. 1.34 (0.04-2.34), p = 0.002; miR-126: 4.5 (3.11-7.64) vs. 1.18 (0.49-1.68), p = 0.0005). Moreover, miR-1 correlated positively with maximal troponin I concentration (r = 0.59, p = 0.02) and negatively with LVEF (r = --0.76, p = 0.0004). Conclusions: In our study, miR-1 emerged as a marker of cardiomyocyte injury and loss of myocardial contractility, whereas dynamics of miR-126 concentration may reflect endothelial activation and damage in the most extreme stage of atherosclerosis, followed by angiogenesis in ischemic myocardium. However, to fully elucidate the role of miR-1 and miR-126 as biomarkers of AMI and future therapeutic targets, further research is required. [ABSTRACT FROM AUTHOR]

Fluid therapy in congestive acute decompensated heart failure (ADHF) patients might be inappropriate and worsening the prognosis. The aim of our study was to analyze the effect of fluid administration on mortality in non-septic, ADHF patients with reduced ejection fraction. We analyzed 41 ADHF consecutive 'cold-wet' patients (mean age 69.3 ± 14.9 years, 27 men, LVEF 22.8 ± 11.1%, lactates 2.2 ± 1.6 mmol/L) without sepsis. At admission central venous pressure (CVP) was measured (17.6 ± 7.2 cm H 2 O), and ultrasound examination of inferior vena cava (IVC) was performed (IVC min. 18.6 ± 7.3 mm and IVC max. 24.6 ± 4.3 mm). Moreover, the groups were compared (survivors vs. non-survivors as well as 1st and 4th quartile of CVP). Altogether 17 (41%) patients died: 16 (39%) during a mean of 11.2 ± 7.8 days of hospitalization and 1 during a 30-day follow up. Patients in the lowest CVP quartile (<13 cm H 2 O) had significantly worse in-hospital survival as compared to patients in the highest quartile (>24 cm H 2 O), P = 0.012. Higher intravenous fluid volumes within the first 24 h were infused in patients in the lowest CVP quartile as compared to the highest CVP quartile (1791.7 ± 1357.8 mL vs. 754.5 ± 631.4 mL, P = 0.046). Moreover, more fluids were infused in a group of patients who died during a hospital stay and at 30-day follow up (1362.8 ± 752.7 mL vs. 722.7 ± 1046.5 mL, P = 0.004; 1348.8 ± 731.0 mL vs. 703.6 ± 1068.4 mL, P = 0.002, respectively). CVP-guided intravenous fluid therapy is a common practice which in high risk ADHF 'cold-wet' patients might be harmful and should rather be avoided. Lower CVP seems to be related with worse prognosis. [ABSTRACT FROM AUTHOR]

Abstract Background The aim of the study was to determine clinical and prognostic role of repeated heart-type fatty acid binding protein (hFABP) measurements in acute decompensated HF (ADHF) patients. Methods In seventy-seven ADHF patients (III and IV NYHA class, mean age 70 ± 12.7 years, mean left ventricle ejection fraction [LVEF] 29.73 ± 13.3%) plasma hFABPs concentrations (SunRed Biological Technology) were measured twice − on admission and at discharge (mean time of hospitalization 10.7 ± 4.9 days). Combined end point (CEP), assessed after mean 9.2 ± 7.3 months, was defined as death or the need of HF re-hospitalization. Results Median hFABP concentration on admission was significantly lower than at discharge. hFABP concentrations on admission significantly correlated with echocardiographic parameters of LV remodeling. Among fifty-six patients (72.7%) who reached CEP, significantly higher admission and discharge hFABP concentrations were found. Patients with plasma discharge hFABP concentrations higher than 7.8 ng/mL were at higher risk of CEP (log-rank test, p = 0.01). Logistic stepwise regression analysis revealed discharge hFABP, LVEF and left ventricle mass index independent and significant predictors of CEP (p < 0.05). Conclusions In ADHF patients plasma hFABP admission concentrations are related with LV remodeling. Persistently elevated hFABP concentrations have prognostic value, as may reflect continuous myocardial damage despite effective treatment and clinical improvement. Highlights • Mean hFABP levels increase during hospitalization in ADHF patients. • Baseline hFABP measurements correlate with echocardiographic parameters of LV remodeling. • Higher hFABP levels at discharge indicate poor out-of-hospital outcome in patients with ADHF. [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]

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 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]

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]

Purpose It has been established that endothelial dysfunction (ED) occurs after coronary artery bypass grafting (CABG). The aim of the study was to assess whether adiponectin may act as a novel marker of ED and its potential relations with new markers of ED: novel cell adhesion molecule CD146, a natural anti-thrombin glycoprotein – thrombomodulin (TM) and the well-established ED marker – Von Willebrand factor (VWF) in coronary artery disease (CAD) patients undergoing CABG. Material/methods 45 CAD patients undergoing elective CABG were included in the study. Results In the study group the concentration of adiponectin and CD146 before the surgery were significantly lower than in the control group – 6.06 μg/ml ± 3.06 vs. 19.0 μg/ml ± 6.4 and 303.2 ng/ml ± 28.7 vs. 328.1 ng/ml ± 22.6 ( p < 0.05). Significant increase of adiponectin and CD146 concentration 3 months after CABG vs. before the surgery was found. Adiponectin concentration 3 months after CABG correlated with VWF, TM, CD146, and a number of grafts. CD146 before and 3 months after CABG correlated significantly with adiponectin, VWF activity as well as the statins therapy after the surgery. Conclusions In CAD patients undergoing CABG new markers of endothelial cell dysfunction as adiponectin and CD146 are significantly lower compared to healthy volunteers. Significant increase in adiponectin and CD146 concentration 3 months after CABG vs. before the surgery was found. However adiponectin concentrations 3 months after CABG were still significantly lower compared to healthy individuals, whereas CD146 concentration returned to the values comparable to the control. [ABSTRACT FROM AUTHOR]