Value of APACHE II, SOFA and CardShock scoring as predictive tools for cardiogenic shock: A single-centre pilot study.

AIMS: The aim of this study was to determine the value of the Acute Physiology and Chronic Health Evaluation II (APACHE II), Sequential Organ Failure Assessment (SOFA) and CardShock scoring systems in predicting the risk of in-hospital, 30 day and 3 year mortality in patients with cardiogenic shock (CS). METHODS: This was a single-centre observational study conducted between May 2016 and December 2017. Data from consecutive patients with CS admitted to the intensive cardiac care unit (ICCU) were included in the analysis. RESULTS: The study group comprised 63 patients with CS {median age 71.0 [interquartile range (IQR), 59-82]; 42 men}: 32 patients with ischaemic and 31 with non-ischaemic aetiology. The median APACHE II, SOFA and CardShock scores were 13 (IQR, 9.9-19.0) points, 8.0 (IQR, 6.0-10.0) points and 3.0 (IQR, 2.0-5.0) points, respectively. The in-hospital, 30 day and 3 year mortality rates were 39.7%, 41.3% and 77.8%, respectively. APACHE II and SOFA scores were significantly higher in the group of patients who died at 30 days (P = 0.043 and P = 0.045, respectively). The CardShock score was higher in patients with CS who died in hospital (P = 0.007) and within 30 days (P = 0.004). No score was statistically significant for 3 year mortality. Area under the curve (AUC) analysis showed that the CardShock score had the highest value in predicting in-hospital and 30 day mortality relative to APACHE II and SOFA, with a cut-off score of 5 points [AUC: 0.70; 95% confidence interval (CI): 0.59-0.81; P = 0.001] and 4 points (AUC: 0.71; 95% CI: 0.60-0.82; P < 0.001), respectively. The Bayesian Weibull model demonstrated the utility of all scales in estimating short-term risk in patients with CS, with the impact of APACHE II and SOFA on patient life expectancy decreasing to a non-significant level at approximately 32 days and CardShock at 33 days. The forest plots derived from the Bayesian logistic regression analysis show significant estimated coefficients with 94% highest density interval (HDI) for in-hospital and 30 day mortality. The use of invasive or non-invasive ventilation, a higher heart rate and a less negative fluid balance showed an unfavourable prognosis. Survival was associated with being in the pre-CS class, with a higher glomerular filtration rate and a higher platelet count. CONCLUSIONS: APACHE II and SOFA could be used for the risk stratification of patients with CS admitted to the ICCU. CardShock proved to be a more appropriate tool for assessing short-term prognosis in patients with CS of all aetiologies, suggesting that there is potential for its promotion for use in daily clinical practice.

The use of andexanet alpha in the Polish setting: An interdisciplinary protocol. Expert consensus statement of the Polish Cardiac Society.

Andexanet alfa (AA) is a recombinant inactive analog of human activated factor X (FXa), effectively reversing the effects of its inhibitors - rivaroxaban and apixaban, which are available in Poland. The drug was approved for clinical use registration after the publication of the results of the ANNEXA-4 trial (Andexanet Alfa, a Novel Antidote to the Anticoagulation Effects of FXa Inhibitors 4), in which its efficacy in restoring hemostasis in life-threatening hemorrhages in patients receiving using the aforementioned anticoagulants was demonstrated. Hence, AA is now recommended for patients on apixaban or rivaroxaban therapy with massive and uncontrollable hemorrhages, including hemorrhagic strokes (HS) and gastrointestinal bleeding. Drug-specific chromogenic anti-Xa assays are generally best suited for estimating rivaroxaban and apixaban plasma levels, aside from direct assessment of their concentrations. The absence of anti-Xa activity, determined using these assays, allows us to rule out the presence of clinically relevant plasma concentrations of any FXa inhibitor. On the other hand, the dose of AA should not be modified based on the results of coagulation tests, as it depends solely on the time that elapsed since the last dose of FXa inhibitor and oon the dose and type of FXa inhibitor. AA is administered as an intravenous (i.v.) bolus, followed by an i.v. infusion of the drug. The maximum reversal of anti-Xa activity occurs within two minutes of the end of the bolus treatment, with the continuation of the continuous i.v. infusion allowing the effect to be maintained for up to two hours afterwards. Because anticoagulant activity can reappear after the infusion is completed, it is currently unclear at what point after AA administration FXa inhibitors or heparin should be re-administered. In Poland AA is starting to become available and its urgent need to administer it to patients with severe bleeding on apixaban or rivaroxaban.

Echocardiographic Assessment of Right Ventricular-Arterial Coupling in Predicting Prognosis of Pulmonary Arterial Hypertension Patients.

In response to an increased afterload in pulmonary arterial hypertension (PAH), the right ventricle (RV) adapts by remodeling and increasing contractility. The idea of coupling refers to maintaining a relatively constant relationship between ventricular contractility and afterload. Twenty-eight stable PAH patients (mean age 49.5 ± 15.5 years) were enrolled into the study. The follow-up time of this study was 58 months, and the combined endpoint (CEP) was defined as death or clinical deterioration. We used echo TAPSE as a surrogate of RV contractility and estimated systolic pulmonary artery pressure (sPAP) reflecting RV afterload. Ventricular-arterial coupling was evaluated by the ratio between these two parameters (TAPSE/sPAP). In the PAH group, the mean pulmonary artery pressure (mPAP) was 47.29 ± 15.3 mmHg. The mean echo-estimated TAPSE/sPAP was 0.34 ± 0.19 mm/mmHg and was comparable in value and prognostic usefulness to the parameter derived from magnetic resonance and catheterization (ROC analysis). Patients who had CEP (n = 21) had a significantly higher mPAP (53.11 ± 17.11 mmHg vs. 34.86 ± 8.49 mmHg, p = 0.03) and lower TAPSE/sPAP (0.30 ± 0.21 vs. 0.43 ± 0.23, p = 0.04). Patients with a TAPSE/sPAP lower than 0.25 mm/mmHg had worse prognosis, with log-rank test p = 0.001. the echocardiographic estimation of TAPSE/sPAP offers an easy, reliable, non-invasive prognostic parameter for the comprehensive assessment of hemodynamic adaptation in PAH patients.

The relationships among monocyte subsets, miRNAs and inflammatory cytokines in patients with acute myocardial infarction.

BACKGROUND: Acute myocardial infarction (AMI) causes irreversible myocardial damage and release of inflammatory mediators, including cytokines, chemokines and miRNAs. We aimed to investigate changes in the levels of cytokines (IL-6, TNF-α and IL-10), miRNAs profiles (miR-146 and miR-155) and distribution of different monocyte subsets (CD14++CD16-, CD14++CD16+, CD14+CD16++) in the acute and post-healing phases of AMI. METHODS: In eighteen consecutive AMI patients (mean age 56.78 ± 12.4 years, mean left ventricle ejection fraction - LVEF: 41.9 ± 9.8%), treated invasively, monocyte subsets frequencies were evaluated (flow cytometry), cytokine concentrations were analyzed (ELISA) as well as plasma miRNAs were isolated twice - on admission and after 19.2 ± 5.9 weeks of follow-up. Measurements were also performed among healthy volunteers. RESULTS: AMI patients presented significantly decreased frequencies of classical cells in comparison to healthy controls (median 71.22% [IQR: 64.4-79.04] vs. 84.35% [IQR: 81.2-86.7], p = 0.001) and higher percent of both intermediate and non-classical cells, yet without statistical significance (median 6.54% [IQR: 5.14-16.64] vs. 5.87% [IQR: 4.48-8.6], p = 0.37 and median 5.99% [IQR: 3.39-11.5] vs. 5.26% [IQR: 3.62-6.2], p = 0.42, respectively). In AMI patients both, analyzed plasma miRNA concentrations were higher than in healthy subjects (miR-146: median 5.48 [IQR: 2.4-11.27] vs. 1.84 [IQR: 0.87-2.53], p = 0.003; miR-155: median 25.35 [IQR: 8.17-43.15] vs. 8.4 [IQR: 0.08-16.9], p = 0.027, respectively), and returned back to the values found in the control group in follow-up. miR-155/miR-146 ratio correlated with the frequencies of classical monocytes (r=0.6, p = 0.01) and miR-155 correlated positively with the concentration of inflammatory cytokines - IL-6 and TNF-α. CONCLUSIONS: These results may suggest cooperation of both pro-inflammatory and anti-inflammatory signals in AMI in order to promote appropriate healing of the infarcted myocardium.

Persistently elevated plasma heart-type fatty acid binding protein concentration is related with poor outcome in acute decompensated heart failure patients.

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 ±â€¯12.7 years, mean left ventricle ejection fraction [LVEF] 29.73 ±â€¯13.3%) plasma hFABPs concentrations (SunRed Biological Technology) were measured twice - on admission and at discharge (mean time of hospitalization 10.7 ±â€¯4.9 days). Combined end point (CEP), assessed after mean 9.2 ±â€¯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.