Longer Hospitalizations and Higher In-Hospital Mortality for Acute Heart Failure during the COVID-19 Pandemic in Larger vs. Smaller Cardiology Departments: Subanalysis of the COV-HF-SIRIO 6 Multicenter Study.

Background: The coronavirus disease-2019 (COVID-19) pandemic is surging across Poland, leading to many direct deaths and underestimated collateral damage. We aimed to compare the influence of the COVID-19 pandemic on hospital admissions and in-hospital mortality in larger vs. smaller cardiology departments (i.e., with ≥ 2000 vs. < 2000 hospitalizations per year in 2019). Methods: We performed a subanalysis of the COV-HF-SIRIO 6 multicenter retrospective study including all patients hospitalized in 24 cardiology departments in Poland between January 1, 2019 and December 31, 2020, focusing on patients with acute heart failure (AHF) and COVID-19. Results: Total number of hospitalizations was reduced by 29.2% in larger cardiology departments and by 27.3% in smaller cardiology departments in 2020 vs. 2019. While hospitalizations for AHF were reduced by 21.8% and 25.1%, respectively. The length of hospital stay due to AHF in 2020 was 9.6 days in larger cardiology departments and 6.6 days in smaller departments (p < 0.001). In-hospital mortality for AHF during the COVID-19 pandemic was significantly higher in larger vs. smaller cardiology departments (10.7% vs. 3.2%; p < 0.001). In-hospital mortality for concomitant AHF and COVID-19 was extremely high in larger and smaller cardiology departments accounting for 31.3% vs. 31.6%, respectively. Conclusions: During the COVID-19 pandemic longer hospitalizations and higher in-hospital mortality for AHF were observed in larger vs. smaller cardiology departments. Reduced hospital admissions and extremely high in-hospital mortality for concomitant AHF and COVID-19 were noted regardless of department size.

Multimodal assessment of right ventricle overload-metabolic and clinical consequences in pulmonary arterial hypertension.

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.

Increased platelet content of SDF-1alpha is associated with worse prognosis in patients with pulmonary prterial hypertension.

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.

A questionnaire-based, multicenter registry of resistant and pseudo-resistant arterial

Introduction: Hypertensive patients with poor blood pressure (BP) control are commonly referred to tertiary centers with a diagnosis of resistant hypertension (RH). The aim of the study was to identify the causes of insufficient BP control and to assess the incidence of true resistant hypertension. Material and Methods: We ran a questionnaire-based, multicenter study (10 high volume tertiary centers in Poland) of patients referred with an initial diagnosis of RH. Only patients with ABPM-confirmed uncontrolled hypertension (systolic ≥140 mmHg and/or diastolic ≥90mmHg despite maximal doses of ≥3 medications, including a diuretic) were included. We assessed the causes of non-optimal BP control, a proportion of patients with excluded secondary hypertension, and the burden of hypertension-related complications. Results: We analyzed 124 patients aged 41-88, with a history of hypertension of 17.5±9 years. 90% of them had developed systemic complications, the most common being LV hypertrophy (73.4%) and LV diastolic dysfunction (63.4%). In only 47% all major causes of secondary hypertension were excluded. In 90.3% of subjects, at least one factor affecting BP control was identified. The most frequent factors were medication noncompliance (52.4%), metabolic syndrome (43.6%) excessive sodium intake (66.1%) and chronic administration of non-steroid anti-inflammatory drugs (40%). The incidence of real resistant hypertension was only 4.8%. Conclusions: Among patients referred with uncontrolled hypertension, the incidence of real resistant hypertension is small. A majority of these patients have multiple factors potentially responsible for poor BP control, the most common being medication non-adherence, use of drugs increasing BP, excessive salt intake and metabolic syndrome.

The significance of diminished sTWEAK and P-selectin content in platelets of patients with pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by proliferative changes in pulmonary arteries. There is growing evidence suggesting that soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and P-selectin could be involved in PAH development and progression. Here we investigate whether circulating platelets may be a source of sTWEAK and contribute to diminished availability of sTWEAK and P-selectin in PAH patients. We have prospectively enrolled two independent study groups of stable patients with confirmed PAH and age matched controls: derivation (10 PAH; 15 controls) and validation (20 PAH; 12 controls). P-selectin and sTWEAK concentrations were measured in platelet-poor plasma and platelet lysate. To avoid procedural bias, in each group we employed different protocols for platelet isolation. Consistently, both in derivation and validation groups PAH patients presented significantly lower sTWEAK content in platelets than control group with no significant differences in plasma levels. Similarly, patients presented comparable to controls plasma P-selectin concentrations and lower concentration in platelet lysate. Kaplan-Meier analysis revealed that patients with low platelet sTWEAK/total protein concentration ratio had more frequently detoriation of PAH in the follow-up (16.51 ±â€¯3.32 months), log-rank test, p = .03. Patients diagnosed with pulmonary arterial hypertension present diminished sTWEAK and P-selectin storage capacity in platelets. Thrombocytes appear to be a major source of sTWEAK that could be released upon local injury and its decreased availability could have an impact on pathophysiology and prognosis in PAH.

Patients with Atrial Fibrillation and Chronic Kidney Disease More Often Undergo Angioplasty of Left Main Coronary Artery - a 867 Patient Study.

BACKGROUND/AIMS: Several studies have implicated atrial fibrillation (AF) as a contributing factor in chronic kidney disease (CKD) and cardiovascular events. The prevalence of coronary artery disease (CAD) in patients with AF varies substantially from 17% to 46.5%. There are only few studies concerning renal function in population with AF undergoing coronary angiography. The aim of the present study was to assess which type of AF is dominant in CKD population scheduled for coronary angiography and if it can influence patients' outcome, the association between renal impairment and the type of coronary procedures in AF patients and the influence of renal function on in-hospital mortality. METHODS: We retrospectively studied 867 patients with AF hospitalized due to coronary angiography in two year time. The cut off value of CKD was eGFR ≤ 60 ml/min./1.73m2 evaluated by CKD-EPI formula. RESULTS: A total of 867 patients with AF (44% women; mean age 72±10 years) were included in the analysis. The mean eGFR was 44±11ml/min./1.73m2 in patients with CKD and 89±18 ml/min./1.73m2 in patients with preserved renal function. Patients with CKD and AF were older (p< 0.001), had more often diabetes (p=0.009), heart failure (p< 0.001) and anaemia (p< 0.001). Patients with CKD and AF had more often permanent type of AF (p< 0.001). In CKD patients CHA2DS2VASc score was 4.3±1.5 and HAS-BLED score was 2.0±1.2 and it was significantly higher as compared to population with preserved renal function (p< 0.001, p=0.02, respectively). The use of oral anticoagulation was less frequent in CKD group (p< 0.001) although these patients had higher CHA2DS2VASc score. Patients with AF and CKD were more often admitted due to myocardial infarction (STEMI or NSTEMI) (p=0.02, p< 0.001, respectively) and more often underwent percutaneous coronary intervention (PCI) (p=0.01). Among coronary arteries the percutaneous coronary intervention (PCI) of left main artery was done more frequently in CKD patients (p=0.01). Among CKD population in-hospital mortality was significantly higher in patients with eGFR < 30 ml/min (p< 0.001). CONCLUSION: Patients with CKD had more often permanent type of AF. Percutaneous interventions of the left main coronary artery, the only elective procedures influencing patients' prognosis, were done more frequently in CKD patients with AF. In-hospital mortality was significantly higher in patients with severe renal impairment. Despite the higher risk of ischaemic stroke in CKD group the use of oral anticoagulation therapy was significantly less frequent and the patients were deprived of the confirmed benefits of such treatment.

Fibrinolysis for patients with intermediate-risk pulmonary embolism.

BACKGROUND: The role of fibrinolytic therapy in patients with intermediate-risk pulmonary embolism is controversial. METHODS: In a randomized, double-blind trial, we compared tenecteplase plus heparin with placebo plus heparin in normotensive patients with intermediate-risk pulmonary embolism. Eligible patients had right ventricular dysfunction on echocardiography or computed tomography, as well as myocardial injury as indicated by a positive test for cardiac troponin I or troponin T. The primary outcome was death or hemodynamic decompensation (or collapse) within 7 days after randomization. The main safety outcomes were major extracranial bleeding and ischemic or hemorrhagic stroke within 7 days after randomization. RESULTS: Of 1006 patients who underwent randomization, 1005 were included in the intention-to-treat analysis. Death or hemodynamic decompensation occurred in 13 of 506 patients (2.6%) in the tenecteplase group as compared with 28 of 499 (5.6%) in the placebo group (odds ratio, 0.44; 95% confidence interval, 0.23 to 0.87; P=0.02). Between randomization and day 7, a total of 6 patients (1.2%) in the tenecteplase group and 9 (1.8%) in the placebo group died (P=0.42). Extracranial bleeding occurred in 32 patients (6.3%) in the tenecteplase group and 6 patients (1.2%) in the placebo group (P<0.001). Stroke occurred in 12 patients (2.4%) in the tenecteplase group and was hemorrhagic in 10 patients; 1 patient (0.2%) in the placebo group had a stroke, which was hemorrhagic (P=0.003). By day 30, a total of 12 patients (2.4%) in the tenecteplase group and 16 patients (3.2%) in the placebo group had died (P=0.42). CONCLUSIONS: In patients with intermediate-risk pulmonary embolism, fibrinolytic therapy prevented hemodynamic decompensation but increased the risk of major hemorrhage and stroke. (Funded by the Programme Hospitalier de Recherche Clinique in France and others; PEITHO EudraCT number, 2006-005328-18; ClinicalTrials.gov number, NCT00639743.).

An implantable pump Lenus pro® in the treatment of pulmonary arterial hypertension with intravenous treprostinil.

BACKGROUND: Subcutaneous treprostinil is a prostacyclin analogue used to treat pulmonary arterial hypertension (PAH). Due to local pain it can cause a deterioration of heart related quality of life (HRQoL) or even abandonment of treatment. The aim of this paper was to assess the feasibility of treatment with intravenous treprostinil administered by means of the Lenus Pro® implantable pump. METHODS: This was a retrospective, multi-center study involving 12 patients (8 females) with PAH treated with a subcutaneous infusion of treprostinil with intolerable pain at the infusion site. Clinical evaluation, including HRQoL assessment with SF-36 questionnaire was performed, before pump implantation and 2-9 months after. The median time of follow-up time was 14 months (4-29 months). RESULTS: After implantation of the Lenus Pro® pump, no statistically significant changes were observed in the 6-min walking distance and NT-proBNP. After implantation 50% of patients were in II WHO functional class (33% before, p = 0,59). There was a significant improvement in HRQoL within the Physical Component Score (28 ± 7 vs 38 ± 8 pts., p < 0,001) and in specific domains of SF-36 form: physical role (31 ± 7 pts. vs. 41 ± 12 pts., p = 0,03), bodily pain (31 ± 12 vs. 50 ± 14 pts., p = 0,02), and vitality (37 ± 8 pts. vs. 50 ± 14 pts., p = 0,03). During the periprocedural period, one patient developed a recurrent haematoma at the implantation site. During follow-up in one patient, the drug delivering cannula slipped out of the subclavian vein, what required repositioning repeated twice, and in another patient an unexpected increase in the drug administration rate was observed. CONCLUSIONS: In patients with PAH who do not tolerate subcutaneous infusion of treprostinil, the use of the Lenus Pro® implantable pump results in significant subjective improvement of vitality and physical aspect of the HRQoL with acceptable safety profile.

Predictors of Long-Term Mortality in Patients Hospitalized in an Intensive Cardiac Care Unit.

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.

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage.

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/VO2, VE/VCO2, VE/VCO2 slope and peak PetCO2. 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.

Is real time contrast echocardiography useful for assessment of the right ventricular morphology, function, and perfusion?

BACKGROUND: Contrast-enhanced echocardiography (CE) is recommended to assess left ventricular function and perfusion but is rarely used to assess the right ventricle (RV). We used CE to assess RV function and perfusion and evaluated whether RV perfusion defects varied in different patient groups with RV failure due to pressure overload. METHODS: We studied 17 patients with acute pulmonary embolism (PE), 19 patients with chronic pulmonary arterial hypertension (CPH), and 7 healthy volunteers. The examination included RV opacification (RVO) and myocardial CE. RV end-diastolic area (RVEDA), RV end-systolic area (RVESA), fractional area change (FAC), and wall-motion score index (WMSI) were assessed before and after contrast agent administration. Perfusion was evaluated qualitatively and quantitatively. RESULTS: RVEDA, RVESA, FAC, and regional contractility were comparable before and after contrast agent injection. Significant perfusion defects were seen in PE and CPH (18/39 segments and 37/51 segments, respectively, vs. 0/21 segments in healthy volunteers; P < 0.0001). Wall-perfusion score index (WPSI) was higher in PE and CPH compared to healthy volunteers (1.5 ± 0.3 and 1.8 ± 0.4 vs. 1.0 ± 0.0; P = 0.02 and P = 0.0003, respectively). Linear correlations were noted between WMSI, FAC and WPSI (r = 0.5, P = 0.014 and r = -0.55, P = 0.005, respectively). Quantitative perfusion assessment revealed perfusion defects in the apical segment in the PE group. The mean region of interest value was insignificantly reduced in PE and CPH groups. CONCLUSION: Contrast-enhanced echocardiography is feasible and may be useful for RVO and perfusion assessment in patients with RV dysfunction due to systolic overload. The SonoVue contrast agent was well tolerated by stable patients with PE and CPH.

Serum levels of CD163 and TWEAK in patients with pulmonary arterial hypertension.

BACKGROUND: Inflammation may play a pivotal role in the pathogenesis of pulmonary arterial hypertension (PAH). We evaluated the concentrations of serum sTWEAK, its scavenger receptor sCD163 and sTWEAK/sCD163 ratio in patients with PAH. DESIGN: The study enrolled 26 stable patients with PAH confirmed by right heart catheterization and 24 healthy volunteers matched for age, sex and body weight. All patients underwent transthoracic echocardiography, cardiopulmonary exercise test, 6-min walk test, measurement of lung diffusing capacity for the carbon monoxide (DLCO) and venous blood tests. Concentrations of sTWEAK and sCD163 were determined using ELISA kits. RESULTS: The PAH patients were characterized by significantly higher median serum sCD163 levels (1072 vs 890ng/ml, p=0.04) together with lower serum sTWEAK concentrations (200 vs 278.1pg/ml, p=0.003) comparing to control subjects. sTWEAK/sCD163 ratio was therefore significantly lower in PAH group (0.18 vs 0.33, p=0.0005). No correlation was found between sTWEAK and sCD163 concentrations in both groups. We observed statistically significant inverse correlation between peak VO2 consumption and sCD163 concentrations (r=-0.52, p<0.05) and positive with sTWEAK/sCD163 ratio (r=0.45, p<0.05) in PAH group. Moreover, sTWEAK/sCD163 ratio positively correlated with % of predicted values of DLCO (r=0.42, p<0.05). CONCLUSIONS: Patients with PAH present altered serum sTWEAK and sCD163 levels. The sTWEAK/sCD163 ratio appears to be a better indicator of the severity of PAH as compared to sTWEAK or sCD163 alone. The exact role of sCD163 or interaction between CD163 and sTWEAK in the initiation or progression of PAH as well as their potential prognostic significance remains to be established.

Pentraxin 3 as a marker of development and severity of stable coronary artery disease.

PURPOSE: Inflammation plays a crucial role in the development of atherosclerotic plaques. Pentraxin 3 (PTX3) is produced at the site of inflammation and has been identified as a specific marker of atherosclerosis, vascular inflammation, and progression of the coronary artery disease (CAD). The aim of the study was to establish if PTX3 has potential relations with classical markers of cardiovascular risk, and if PTX3 may act as an independent risk factor of CAD occurrence and advancement. MATERIALS AND METHODS: The study included 98 patients with stable CAD confirmed in coronary angiography (CAD group) (median age 65 interquartile range [IQR] 61-72 years; 72 â€‹% men). The control group consisted of 40 patients without CAD. RESULTS: The CAD group had significantly higher PTX3 concentration compared to the control group. There was a correlation with age, male gender, lipid profile and intima-media thickness. There was no correlation between PTX3 concentration and the number of coronary vessels with significant atherosclerotic lesions and the advancement of atherosclerotic lesions on the Gensini scoring scale. The cut-off point was determined for 0.89 â€‹ng/ml for the exclusion of angiographically significant atherosclerotic lesions. CONCLUSIONS: Patients with CAD have significantly higher concentration of PTX3. There was no correlation between PTX3 and the advancement of angiographically significant atherosclerotic lesions in coronary arteries. Low PTX3 concentration may serve as an indicator for the absence of atherosclerosis.

Right-Ventricle Heart Failure in PAH vs. HFrEF with Secondary PH: Hemodynamic, Ergospirometric, and Organ Function Correlations.

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/VCO2) slope and NT-proBNP in HFrEF without secondary PH and HFrEF-SPH groups. In the PAH group, VE/VCO2 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).

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 Importance of Lung Ultrasound and IGFBP7 (Insulin-like Growth Factor Binding Protein 7) Assessment in Diagnosing Patients with Heart Failure.

Background: In daily practice, there are problems with adequately diagnosing the cause of dyspnea in patients with heart failure with preserved and mildly reduced ejection fractions (HFpEF and HFmrEF). This study aimed to assess the usefulness of lung ultrasound in diagnosing HFpEF and HFmrEF and determine its correlation with IGFBP7 (insulin-like growth factor binding protein 7), NTproBNP (N-terminal pro-B-type natriuretic peptide), and echocardiographic markers. Methods: The research was conducted on 143 patients hospitalized between 2018 and 2020, admitted due to dyspnea, and diagnosed with HFpEF and HFmrEF. Venous blood was collected from all participants to obtain basic biochemical parameters, NTproBNP, and IGFBP7. Moreover, all participants underwent echocardiography and transthoracic lung ultrasound. Two years after hospitalization a follow-up telephone visit was performed. Results: The number of B-lines in the LUS ≥ 16 was determined with a sensitivity of-73% and specificity of-62%, indicating exacerbation of heart failure symptoms on admission. The number of B-lines ≥ 14 on admission was determined as a cut-off point, indicating an increased risk of death during the 2-year follow-up period. The factors that significantly impacted mortality in the study patient population were age and the difference between the number of B-lines on ultrasound at admission and at hospital discharge. IGFBP7 levels had no significant effect on the duration of hospitalization, risk of rehospitalization, or mortality during follow-up. Conclusions: Lung ultrasonography provides additional diagnostic value in patients with HFpEF or HFmrEF and exacerbation of heart failure symptoms. The number of B-lines ≥ 14 may indicate an increased risk of death.

Pulmonary embolism in COVID-19 pneumonia patients admitted to temporary hospital - The follow-up study.

PURPOSE: Coronavirus disease 2019 (COVID-19) is linked with major coagulation disorders, especially higher risk of developing pulmonary embolism (PE). Our study summarizes COVID-19 patients' management with concomitant PE during the first weeks of pandemic and underlines the importance of D-dimer concentration assessment at admission in terms of prognosis. MATERIAL AND METHODS: Study group consisted of 107 outpatients (mean age 68.91 â€‹± â€‹12.83 years) admitted to the Temporary COVID-19 Hospital in Bialystok, Poland with confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and suspicion of PE based on elevated D-dimer concentration (>500 â€‹µg/l) and/or low saturation rate (<90%). The clinical follow-up lasted 6 months. Death or re-hospitalization were used as composite clinical endpoint (CEP). RESULTS: Cumulative incidence of PE was 62.3% (73/107 patients). Most of the patients were in the intermediate PE risk group according to the pulmonary embolism severity index (PESI) score. The mean total computed tomography (CT) lung involvement of COVID-19 findings was 48.42 â€‹± â€‹27.71%. Neither D-dimers nor NT-proBNP concentrations correlated significantly with the percentage of lung abnormalities in CT. Patients with baseline D-dimer concentration higher than 1429 â€‹µg/l had worse prognosis in 6-months observation, log-rank test, p â€‹= â€‹0.009. CONCLUSIONS: Ongoing SARS-CoV-2 infection along with massive involvement of lung tissue and concomitant thrombi in pulmonary arteries are challenging for physicians. It seems that simple D-dimer concentration assessment at admission may be a helpful tool not only to predict PE but also to estimate the long-term prognosis.

The impact of specific pulmonary arterial hypertension therapy on cardiac fluorodeoxyglucose distribution in PET/MRI hybrid imaging-follow-up study.

BACKGROUND: PET/MRI hybrid imaging in pulmonary arterial hypertension (PAH) provides important prognostic information identifying patients who might benefit from early therapy escalation, as right ventricle (RV) metabolic alterations are linked with hemodynamics and might precede clinical deterioration. Now, we hypothesize that adequate PAH therapy escalation may result in reversal of unfavourable increased glucose uptake of RV, which is associated with improved prognosis. METHODS: Out of twenty-six initially clinically stable PAH patients who had baseline PET/MRI scans, twenty (49.9 ± 14.9 years) had second PET/MRI after 24 months. SUVRV/SUVLV ratio was used to estimate and compare cardiac glucose uptake. Occurrences of clinical endpoints (CEP), defined as death or clinical deterioration, were assessed during 48-month follow-up from baseline. RESULTS: In first 24 months of observation, sixteen patients had CEP and needed PAH therapy escalation. At follow-up visits, we observed significant improvement of RV ejection fraction (45.1 ± 9.6% to 52.4 ± 12.9%, p = 0.01), mean pulmonary artery pressure (50.5 ± 18.3 to 42.8 ± 18.6 mmHg, p = 0.03), and SUVRV/SUVLV, which tended to decrease (mean change -0.20 ± 0.74). Patients with baseline SUVRV/SUVLV value higher than 0.54 had worse prognosis in 48 months observation (log-rank test, p = 0.0007); follow up SUVRV/SUVLV > 1 predicted CEP in the following 24 months, regardless of previously escalated treatment. CONCLUSIONS: PAH therapy escalation may influence RV glucose metabolism, what seems to be related with patients' prognosis. PET/MRI assessment may predict clinical deterioration regardless of previous clinical course, however its clinical significance in PAH requires further studies. Importantly, even mild alterations of RV glucose metabolism predict clinical deterioration in long follow-up. Clinical Trial Registration ClinicalTrials.gov, NCT03688698, 05/01/2016, https://clinicaltrials.gov/ct2/show/study/NCT03688698?term=NCT03688698&draw=2&rank=1.

Comparison of reorganized versus unaltered cardiology departments during the COVID-19 era: A subanalysis of the COV-HF-SIRIO 6 study.

BACKGROUND: Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, numerous cardiology departments were reorganized to provide care for COVID-19 patients. We aimed to compare the impact of the COVID-19 pandemic on hospital admissions and in-hospital mortality in reorganized vs. unaltered cardiology departments. METHODS: The present research is a subanalysis of a multicenter retrospective COV-HF-SIRIO 6 study that includes all patients (n = 101,433) hospitalized in 24 cardiology departments in Poland between January 1, 2019 and December 31, 2020, with a focus on patients with acute heart failure (AHF). RESULTS: Reduction of all-cause hospitalizations was 50.6% vs. 21.3% for reorganized vs. unaltered cardiology departments in 2020 vs. 2019, respectively (p < 0.0001). Considering AHF alone respective reductions by 46.5% and 15.2% were registered (p < 0.0001). A higher percentage of patients was brought in by ambulance to reorganized vs. unaltered cardiology departments (51.7% vs. 34.6%; p < 0.0001) alongside with a lower rate of self-referrals (45.7% vs. 58.4%; p < 0.0001). The rate of all-cause in-hospital mortality in AHF patients was higher in reorganized than unaltered cardiology departments (10.9% vs. 6.4%; p < 0.0001). After the exclusion of patients with concomitant COVID-19, the mortality rates did not differ significantly (6.9% vs. 6.4%; p = 0.55). CONCLUSIONS: A greater reduction in hospital admissions in 2020 vs. 2019, higher rates of patients brought by ambulance together with lower rates of self-referrals and higher all-cause in-hospital mortality for AHF due to COVID-19 related deaths were observed in cardiology departments reorganized to provide care for COVID-19 patients vs. unaltered ones.

A 39-Year-Old Woman with Ventricular Electrical Storm Treated with Emergency Cardiac Defibrillation Followed by Multidisciplinary Management.

BACKGROUND Ventricular electrical storm (VES) is a treatment-resistant ventricular arrhythmia associated with high mortality. This report is of a 39-year-old woman with VES treated with emergency cardiac defibrillation followed by multidisciplinary management. CASE REPORT A 39-year-old woman, previously diagnosed with eosinophilia of unknown origin and recurrent non-sustained ventricular tachycardias, was admitted to the Department of Invasive Cardiology with VES after an initial antiarrhythmic approach, analgesia, and defibrillation in the Emergency Department. The patient had a temporary pacing wire implanted, but overdrive therapy was not successful. The medical treatment and multiple defibrillations did not stop the arrythmia. Due to the hemodynamic instability, extracorporeal membrane oxygenation (ECMO) was performed at the Department of Cardiac Surgery. Consequently, the patient was stabilized and an electrophysiology exam and RF ablation of arrhythmogenic focus were conducted in the Department of Cardiology. One day after the procedure, the patient had pulmonary edema caused by pericardial tamponade. The patient was successfully operated on in the Department of Cardiac Surgery. Then, the next complication appeared - a femoral artery embolism - which was treated in the Department of Vascular Surgery. After patient stabilization and exclusion of serious neurological damage, an implantable cardioverter-defibrillator (ICD) was implanted for secondary prevention of sudden cardiac death (SCD). CONCLUSIONS This case has shown the importance of the rapid diagnosis of VES and emergency management with cardiac defibrillation. Multidisciplinary clinical follow-up is required to investigate and treat any reversible causes and to ensure long-term stabilization of cardiac rhythm.