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Purpose: The goal of the study was to identify markers of organ function used in daily routines that could potentially aid in the overall evaluation of the cardiovascular system in patients with right-ventricle heart failure due to pulmonary arterial hypertension (PAH) and left-ventricle heart failure. We analyzed correlations between parameters from right heart catheterization (RHC), cardiopulmonary exercise test (CPET), and selected laboratory parameters of thyroid, liver, kidneys function and iron homeostasis., Patients and Methods: A retrospective analysis included 107 patients (mean age 57.6 ​± ​16.2; 34.6 ​% women), comprising 57 patients with PAH (mean age 54.0 ​± ​18.2; 49.1 ​% women) and 50 patients with heart failure with reduced ejection fraction (HFrEF) ​< ​40 ​% (mean age 61.6 ​± ​12.7; 18 ​% women). All patients underwent CPET. Each patient in the PAH group had RHC performed. Fifteen patients from the HFrEF group underwent RHC, which confirmed the suspicion of pulmonary hypertension (HFrEF-SPH)., Results: CPET and laboratory parameters' analysis showed strong correlations between ventilation/carbon dioxide production (VE/VCO 2 ) slope and NT-proBNP in HFrEF without secondary PH and HFrEF-SPH groups. In the PAH group, VE/VCO 2 slope correlated with liver and thyroid function but also with morphological parameters of red-cell system. Analysis of correlations between laboratory and hemodynamic parameters revealed significant correlations between pulmonary arterial pressure, pulmonary vascular resistance (PVR) and red-cell parameters, especially strong with fT4 in the PAH group., Conclusions: In HFrEF-SPH patients, laboratory parameters strongly correlated with pulmonary pressures and pulmonary capillary wedge pressure (PCWP)., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Background: Myocardial infarction (MI) remains a major burden for healthcare systems. Therefore, we intended to analyze the determinants of cost management of patients hospitalized for MI in Poland., Methods: Data on patients hospitalized and discharged with the diagnosis of acute MI were derived from the public payer claims database. Adult patients, reported between October 1, 2017 and December 31, 2019, were included. Costs of hospitalization for acute MI and cumulative one-year follow-up were analyzed., Results: The median (IQR) of the total direct cost was €3804.7 (2674.1-5712.7) per patient and 29% (€1113.6 [380.5-2490.4]) of these were costs related to the use of post-hospitalization healthcare resources. The median cost of cardiovascular disease management was €3624.7 (2582.1-5258.5), and 26% of this sum were follow-up costs. The analysis of the total cost for individual years showed a slight increase in median costs in subsequent years: €3450.7 (2407.8-5205.2) in 2017, €3753.8 (2642.6-5681.9) in 2018, and €3944.9 (2794.8-5844.4) in 2019. Male sex, heart failure, atrial fibrillation, diabetes, kidney disease, chronic obstructive pulmonary disease, and history of stroke in addition to hospitalization in a department other than cardiology or internal disease were independently related to the cost of MI patient management., Conclusions: The high cost of management of MI patients was independently related to sex, heart failure, atrial fibrillation, diabetes, kidney disease, chronic obstructive pulmonary disease, and history of stroke as well as hospitalization in other than cardiology or internal disease department.

Background: The exact role of individual inflammatory factor in heart failure with reduced ejection fraction (HFrEF) remains elusive. The study aimed to evaluate three monocyte subsets (classical-CD14 ++ CD16 - , intermediate-CD14 ++ CD16 + , and nonclassical-CD14 + CD16 ++ ) in HFrEF patients and to assess the effect of the cardiac resynchronization therapy (CRT) on the changes in monocyte compartment., Methods: The study included 85 patients with stable HFrEF. Twenty-five of them underwent CRT device implantation with subsequent 6-month assessment. The control group consisted of 23 volunteers without HFrEF., Results: The analysis revealed that frequencies of non-classical-CD14 + CD16 ++ monocytes were lower in HFrEF patients compared to the control group (6.98 IQR: 4.95-8.65 vs. 8.37 IQR: 6.47-9.94; p = 0.021), while CD14 ++ CD16 + and CD14 ++ CD16 - did not differ. The analysis effect of CRT on the frequency of analysed monocyte subsets 6 months after CRT device implantation showed a significant increase in CD14 + CD16 ++ (from 7 IQR: 4.5-8.4 to 7.9 IQR: 6.5-9.5; p = 0.042) and CD14 ++ CD16 + (from 5.1 IQR: 3.7-6.5 to 6.8 IQR: 5.4-7.4; p = 0.017) monocytes, while the frequency of steady-state CD14 ++ CD16 - monocytes was decreased (from 81.4 IQR: 78-86.2 to 78.2 IQR: 76.1-81.7; p = 0.003)., Conclusions: HFrEF patients present altered monocyte composition. CRT-related changes in the monocyte compartment achieve levels observed in controls without HFrEF.

Background and Aim: We aimed to evaluate the prevalence and determinants of different stress coping strategies in Polish patients suffering from heart failure with reduced ejection fraction (HFREF)., Methods: This manuscript is a sub-study of the CAPS-LOCK-HF multicentre psychological status assessment of patients with HFREF. Patients with > six-month history of HFREF and clinical stability for ≥ three months and left ventricular ejection fraction (LVEF) < 45% were enrolled in the study. Demographic and clinical variables were obtained from medical records, while a standardised Coping Inventory for Stressful Situations (CISS) was applied to all subjects., Results: The study comprised 758 patients (599 men; 79%) with a median age of 64 years (IQR 58-71). Median LVEF was 33% (25-40). Subjects most commonly used task-oriented coping strategies (median CISS score 55 points; IQR 49-61), followed by avoidance (45 points; 39-50) and emotion-oriented coping strategies (41 points; 34-48). Distraction-based avoidance coping strategies (20 points; 16-23) were more pronounced than social diversion strategies (16 points; 14-19). Multiple regression analysis showed that higher New York Heart Association (NYHA) class and lower systolic blood pressure were independent predictors of task-oriented style. Emotion-oriented coping was more common among females and higher NYHA classes, and in patients who did not take angiotensin-converting enzyme inhibitors. Patients who used avoidance-oriented strategies were more frequently those in sinus rhythm on assessment and those who had less history of neoplastic disease., Conclusions: Patients with HFREF most commonly use favourable task-oriented coping strategies. However, female patients and those with higher NYHA classes tend to use potentially detrimental emotion-oriented coping strategies.

Background: CCN family of proteins has been implicated in various processes in cardiovascular physiology and pathology, including angiogenesis, regeneration and fibrosis. In this study we assessed long term changes of CCN1 and CCN2 gene products abundance in the failing ventricular myocardium., Methods: Male, 12-14-weeks-old C57BL6/J and C57BL6/J (IL-6-/-) mice were used. To assess short term changes, a transient reversible ischemia model was utilized. Heart failure was caused by ligation of anterior descending coronary artery. The presence of systolic dysfunction was confirmed by echocardiography and left ventricular ANP RNA expression. Molecular analysis was performed on left ventricular samples from animals sacrificed 12-14 weeks after infarction. Western blotting and QT-PCR were used to investigate abundance of CCN proteins and RNAs, respectively., Results: Short ischemia resulted in marked increase of CCN1 transcript. However, three months after myocardial infarction (MI), remote myocardium showed a markedly increased expression of CCN1 protein, but not RNA. In the case of CCN2, the RNA was distinctly up-regulated, whereas the protein presented only modest, non-significant increase in failing myocardium. Expression of CCN2 RNA closely correlated with expression of ANP. Long-term telmisartan administration after infarction decreased the expression of CCN1 protein. Interleukin 6 (IL-6) deficiency caused increased CCN2 protein abundance in control animals, but the difference was absent after MI. Infarction did not increase CCN1 protein in the hearts of IL-6 deficient mice., Conclusion: CCN genes are activated in heart failure. Their regulation is multidimensional both transcriptional and posttranscriptional. The involved pathways include angiotensin II and IL-6., (Copyright © 2014 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)

Background: Acute heart failure (AHF) is a life-threatening condition associated with poor prognosis., Aim: To investigate the long term prognosis and identify prognostic factors among patients who were discharged after an episode of cardiogenic pulmonary oedema., Methods: We enrolled 84 patients (M: 56%, n = 47) who were discharged with cardiogenic pulmonary oedema as a diagnosis. Clinical, biochemical and echocardiographic variables were collected and analysed. The completeness of two- and five-year follow-up was 100% and 96%, respectively., Results: The median (IQR) age was 74 years (64-81), left ventricular ejection fraction was 35% (27-45), blood pressure on admission was 140/90 mm Hg (115-180/70-100), estimated glomerular filtration rate was 60 mL/min/1.73 m2 (45-73). Forty per cent (n = 34) of the patients had a history of atrial fibrillation (AF), however, AF was directly involved with pulmonary oedema only in 4% (n = 3) of the cases. Acute myocardial infarction (AMI) accounted for 34% (n = 29) of all the causes of pulmonary oedema and was associated with a better two-year prognosis compared to other causes of pulmonary oedema (p = 0.018). Two- and five-year mortality was 45% (n = 38) and 72% (n = 58), respectively. Co-morbidities were common. Ischaemic heart disease and arterial hypertension were present in 83% and 70% of the patients, respectively. Multivariable analysis identified increased left ventricular mass (RR 3.609, 95% CI 1.235-10.547, p = 0.017) and treatment with long-acting vasodilator drugs (LAVDs) (RR 4.881, 95% CI 1.618-14.727, p = 0.004) as independent negative prognostic factors, whereas in-hospital therapy with beta-blockers created a distinctly protective effect (RR 0.123, 95% CI 0.033-0.457, p = 0.002) in the two-year follow-up. Five-year mortality was independently associated with older age (RR 1.08, 95% CI 1.02-1.14, p = 0.005) and treatment with LAVDs (RR 6.4, 95% CI 1.47-28.14, p = 0.012), while percutaneous coronary intervention (RR 0.17, 95% CI 0.05-0.58, p = 0.004) significantly decreased the risk., Conclusions: AHF is a heterogeneous syndrome with a very high remote mortality. LAVDs administered during the hospital stay as well as older age on admission correlate with higher long-term overall mortality. In the age of percutaneous coronary intervention, AMI aetiology of pulmonary oedema is no longer a negative prognostic factor for the long-term prognosis.

Previous studies have reported the upregulation of CCN proteins early after acute heart injury. The aim of the present work was to evaluate the expression of the CCN1 and CCN2 proteins and their regulation by angiotensin II in the atrial myocardium of a chronically failing heart. Male adult mice were subjected to ligation of the left coronary artery to produce myocardial infarction (the MI group), and 16 of them were treated for 12 weeks with the AT1 receptor antagonist telmisartan (the MI-Tel group). Sham-operated mice served as controls. The expression of proteins was evaluated by immunohistochemistry 12 weeks after the operation. In shamoperated mice, stainings for CCN1 and CCN2 proteins were positive within atrial cardiomyocytes. CCN1-positive reaction revealed diffused cytoplasmic localization, while CCN2 was present mainly within the perinuclear cytoplasm. CCN1 was upregulated in the MI group, while CCN2 remained at basal level. Telmisartan prevented the upregulation of CCN1 and decreased CCN2 level. We compared the experimental data with the expression of CCN1 and CCN2 proteins in human right atrial appendages. We found an inverse, but not significant, relation between the level of either protein and the left ventricular ejection fraction. This suggests a similar atrial regulation of CCN1 and CCN2 expression also in humans. We conclude that in the murine atria, CCN1 and CCN2 proteins are expressed constitutively. In chronic heart failure, CCN proteins tend to be upregulated, which may be related to the action of angiotensin II.

The number of patients suffering from heart failure is constantly increasing. One of its main causes is coronary artery disease, especially myocardial infarction. Progression of heart failure depends both on the extent of ischaemic injury and the course of subsequent adaptive processes. Genetic methods may help to find individuals at high risk of developing heart failure. There are multiple genes influencing circulatory system, some of their alleles may potentially affect progression of the disease. Among the most promising targets are genes of the renin-angiotensin-aldosterone system: insertion/deletion (L/D) polymorphism of angiotensin converting enzyme gene, polymorphisms of angiotensinogen, angiotensin receptors (AT1 and AT2) and aldosterone syntase genes. Other genetic factors, which may affect are different gene variants of adrenergic receptors (beta1, beta2, alpha2C), AMP deaminase-1, endothelin-1, endothelial nitric oxide syntase, precursors of natriuretic peptides and inflammatory factors (TNF-alpha, IL-6, MCP-1, TGF, MMP-2). Furthermore, the response to drugs may depend on genetic background, that is why pharmacogenetics creates new possibilities to tailor the best therapy for each patients with heart failure. Therefore research in the field of genetic factors affecting the development of heart failure has not only scientific, but also practical value.

Background. There is a raising awareness that heart failure (HF) is a highly heterogeneous, multiorgan syndrome with an increasing global prevalence and still poor prognosis. The comorbidities of HF are one of the key reasons for presence of various phenotypes with different clinical profile and outcome. Heterogeneity of skeletal muscles (SMs) quantity and function may have an impact on patient's phenotype. Aim. We intended to compare clinical characteristics of phenotypes defined by a combination of various SM mass taken as a fat-free compartment from DEXA scans and different levels of SUCR (Spot Urinary Creatinine). All-cause mortality with mortality predicted by MAGGIC in such phenotypes were compared. Methods. In 720 HF patients with reduced ejection fraction (age: 52.3 ± 10 years, female: 14%, NYHA: 2.7 ± 0.7, LVEF: 24.3 ± 7.3%), admitted to the hospital for heart transplantation candidacy assessment, morning SUCR along with body composition scanning (DEXA) was performed. All study participants were dichotomized twice, first by low or normal appendicular muscle mass index (ASMI) and second by SUCR (Spot Urinary Creatinine) < and ≥of 1.34 g/L. Four study groups (phenotypes) were created as combinations of lower or higher SUCR and low or normal ASMI. Results. Low ASMI was found in 242 (33.6%) patients, while the remaining 478 had normal muscle mass. In 446 patients (61.9%), SUCR was <1.34 g/L. During 3 years of follow-up, 223 (31.0%) patients died (all-cause). The phenotype of lower both ASMI and SUCR was associated with the highest mortality. The death rate in phenotype with both low ASMI and SUCR exceeded by 70% the risk estimated by MAGGIC. This difference was significant as judged by the 95% confidence interval for MAGGIC estimation. In Cox regression analysis adjusted for MAGGIC and parameters known to increase risk, the relative risk of patients with phenotype of low both ASMI and SUCR was elevated by 45–55% as compared to patients with all other phenotypes. The protective role of higher SUCR in patients with muscle wasting was, therefore, confirmed in Cox analysis. Conclusions. Measurement of SUCR in HF patients can identify clinical phenotypes with skeletal muscle wasting but strikingly different risk of death that is actually not captured by MAGGIC score. The higher level of SUCR was associated with similar risk independently of presence of muscle wasting. As the analysis of SUCR is cheap and easy to perform, it should be further tested as a potentially useful biomarker, which may precisely phenotype HF patients independently of their skeletal muscle status. [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]

The objective of this study was to determine the associations between insulin-like growth-factor-binding protein 7(IGFBP7) concentrations and concentrations of troponin T(TnT), N-terminal pro-B-type natriuretic peptide(NT-proBNP) and the parameters of kidney function in patients with stable ischemic heart disease(IHD). The IHD group consisted of 88 patients, and the population group comprised 66 subjects without a history of IHD. IGFBP7, TnT and NTproBNP concentrations were measured. The IGFBP7 value was considerably higher in the IHD group (1.76 ± 1 ng/mL vs. 1.43 ± 0.44 ng/mL, respectively, p = 0.019). Additionally, IHD subjects had a significantly higher concentration of TnT and NTproBNP. In both groups there was a significant correlation between IGFBP7 and serum parameters of kidney function (creatinine concentration: population gr. r = 0.45, p < 0.001, IHD gr. r = 0.86, p < 0.0001; urea concentration: population gr. r = 0.51, p < 0.0001, IHD gr. r = 0.71, p < 0.00001). No correlation between IGFBP7 and microalbuminuria or the albumin to creatinine ratio in urine was found. Moreover, there was a significant correlation between IGFBP7 concentration and markers of heart injury/overload-TnT and NT-BNP(r = 0.76, p < 0.001 and r = 0.72, p < 0.001, respectively). Multivariate regression analysis in joint both revealed that the IGFBP7 concentration is independently associated with urea, creatinine and TnT concentrations (R2 for the model 0.76). IHD patients presented significantly higher IGFBP7 concentrations than the population group. Elevated IGFBP7 levels are associated predominantly with markers of kidney function and myocardial damage or overload. [ABSTRACT FROM AUTHOR]