About half a century ago, Eugene Braunwald, a father of modern cardiology, shared a revolutionary belief that “time is muscle”, which predetermined never-ending effort to preserve the unaffected myocardium. In connection to that, researchers are constantly trying to better comprehend the ongoing changes of the ischemic myocardium. As the latest studies show, metabolic changes after acute myocardial infarction (AMI) are inconsistent and depend on many constituents, which leads to many limitations and lack of unification. Nevertheless, one of the promising novel mechanistic approaches related to iron metabolism now plays an invaluable role in the ischemic heart research field. The heart, because of its high levels of oxygen consumption, is one of the most susceptible organs to iron-induced damage. In the past few years, a relatively new form of programmed cell death, called ferroptosis, has been gaining much attention in the context of myocardial infarction. This review will try to summarize the main novel metabolic pathways and show the pivotal limitations of the affected myocardium metabolomics.

Introduction In these past few years tricuspid valve (TV) got its appreciation due to the latest focus of complications driven by tricuspid regurgitation (TR). Even though severe TR may require surgical repair, precise analyses performed by 3D echocardiographic tools to determine severe functional TR (FTR) are scarce. Aim To determine the accuracy of 3D echo-derived TV parameters in predicting severe FTR. Methods Prospective observational cohort study enrolled 90 patients (pts) with functional moderate (70%) or severe (30%) TR. Pts with FTR of various aetiologies (due to left-sided valvular heart disease, pulmonary arterial hypertension [invasively measured pulmonary capillary wedge pressure <15 mmHg]) were included in this study. Pts with ischemic heart disease (assessed by coronary angiography) were excluded from the analysis. TR severity was measured quantitatively: severe FTR was defined by 2 parameters: vena contracta ≥7 mm and TR effective regurgitant orifice area ≥40 mm2. The transthoracic echocardiography was performed and included the following 2D and 3D-derived TV parameters: the systolic and diastolic 4-chambers (septal – lateral), 2-chambers (anterior-posterior), major and minor axis TA diameters, TA area, perimeter, leaflet tenting height and volume. The 3D TV analysis was made using the 4D Auto TVQ quantification software package. Receiver Operating Characteristic (ROC) curves, area under the curve (AUC), specificity and sensitivity were analysed. Results Study cohort included 66% females; mean age was 65±11 years. The results of the ROC analysis are shown in Table 1. Of all TA 3D parameters, septal-lateral systolic (AUC 0.859) and diastolic (AUC 0.840) diameter, major axis systolic (AUC 0.816) and diastolic (AUC 0.810) diameter, as well as leaflet tenting volume (AUC 0.769) have the highest predictive value for severe FTR. 3D TA analysis provides 75–88% sensitivity for defying pts with severe FTR. Meanwhile, septal-lateral diameter, major axis diameter and annulus perimeter are the most specific to determine severe FTR. 2D echo-derived TA 4-chamber diastolic diameter index has a lower predictive value with worse sensitivity and specificity, compared to 3D parameters. Conclusions Analysis of three-dimensional echocardiographic parameters is an accurate method, suggesting that dilation of tricuspid annulus is a precise measure for identifying patients with severe FTR. Funding Acknowledgement Type of funding sources: None.

Introduction Evaluation of tricuspid annulus (TA) has many challenges due to its complex three-dimensional shape. The 3D-echocardiography is a gold standard method for accurate assessment of tricuspid valve (TV). Studies investigating TV geometry in different aetiologies of tricuspid regurgitation (TR) are still scarce. Aim The aim was to clarify the TV geometry characteristics in different aetiologies of functional TR (FTR). Methods Prospective observational cohort study enrolled 107 patients with functional moderate or severe TR and 10 healthy controls. FTR patients were divided into two groups according to the different aetiology of FTR: 1. TR caused by dominant left-sided valvular pathology (LSVP) – 68 patients (pts); 2. TR caused by precapillary pulmonary hypertension (PH) (invasively measured pulmonary capillary wedge pressure <15 mmHg) – 39 pts. Pts with ischemic heart disease (assessed by coronary angiography) were excluded from the analysis. The 3D-transthoracic echocardiography was performed and included the following parameters: the systolic and diastolic 4-chambers (septal–lateral), 2-chambers (anterior–posterior), major axis TA diameters, TA area, perimeter, leaflets tenting height and volume. All parameters have been indexed to body surface area. The 3D TV analysis was made using 4D Auto TVQ quantification software package (GE Healthcare, USA). The statistical analysis was performed using SPSS statistical software. Results Study cohort included 66% females; mean age was 65±11 years. TR severity, measured quantitatively, did not differ between FTR groups (ERA – 32±18 in LSVP vs 35±18 mm2 in PH group, p=0.219). The distribution of echocardiography parameters in study groups are shown in Table 1. All the 3D TV parameters were increased in both FTR groups when compared to controls. Precapillary PH was associated with larger leaflets tenting height, volume, and more increased indices of TA systolic and diastolic septal-lateral and major axis diameters. LVSP aetiology was associated with higher TA sphericity index. Conclusions Tricuspid valvular geometry differs between different aetiologies of functional TR. The implementation of 3D echocardiography is useful in the determination of TV geometry changes and might provide valuable tools in the evaluation of patients with functional TR. Funding Acknowledgement Type of funding sources: None.

Background and Objectives: Inflammation is a recognized factor in disease progression in both heart failure (HF) patients with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Neutrophils take part in maintaining the pro-inflammatory state in HF. Hypercholesterolemia is stated to heighten neutrophil production, which contributes to accelerated cardiovascular inflammation. HF pathogenesis differences in the different HF phenotypes are yet to be investigated. Aim: To determine differences in complete blood count, C-reactive protein (CRP) concentration and lipidogram between chronic HF patients with an absence/presence of myocardial infarction (MI) history and preserved/reduced EF. Materials and Methods: We separated the patients (n = 266) according to chronic HF phenotype: (1) HFrEF patients (n = 149) into groups according to presence of MI: those who had had no MI (n = 91) and those with MI (n = 58); (2) chronic HF without MI according to left ventricular ejection fraction (LVEF): LVEF ≥ 50%, n = 117; LVEF < 50%, n = 91. Laboratory and clinical readings (age, weight, pulse, blood pressure, and body mass index (BMI)) were taken from the patients’ medical histories. Results: Mean corpuscular hemoglobin concentration (MCHC) was lower and red cell distribution width—coefficient of variation (RDW-CV) was higher in the lower EF group without a history of MI (337.32 (10.60) and 331.46 (13.13), p = 0.004; 13.6 (11.5–16.9), and 14.7 (12.6–19.1), p = 0.001). Lymphocyte percentage and lymphocyte-to-monocyte ratio (LYM/MON) were lower in the lower EF group without a history of MI (30.48 (10.87), 26.98 (9.08), p = 0.045; 3.33 (1.22–9.33), 3 (0.44–6.5), p = 0.011). In the group according to LVEF without MI neutrophil count positively correlated with weight (rp = 0.196, p = 0.024); lymphocyte count correlated with RDW-CV (rs = −0.223; p = 0.032) and body mass index (rp = 0.186, p = 0.032). RDW-CV and monocyte count correlated with NT-proBNP and serum creatinine (rs = 0.358, p = 0.034; rs = 0.424, p < 0.001 and rs = 0.354, p = 0.012; rs= 0.205, p = 0.018 respectively). CRP concentration (6.9 (1.46–62.97), 7 (1–33.99), p = 0.012) was higher and HDL concentration was lower (0.96 (0.44–2.2), 0.92 (0.56–1.97), p = 0.010) in HFrEF with MI in comparison with the group without MI. LVEF correlated with MCHC and RDW-CV (rs = 0.273, p = 0.001; rs = −0.404, p < 0.001). HDL cholesterol concentration was lower (0.96 (0.44–2.2); 0.92 (0.56–1.97, p = 0.010) and CRP concentration (6.9 (1.46–62.97), 7 (1–33.99), p = 0.012) was higher in the HFrEF with MI group. Uric acid concentration correlated with platelet-to-lymphocyte ratio and LYM/MON (rs = 0.321, p = 0.032; rs = −0.341, p = 0.023). Creatinine concentration correlated with monocyte percentage and count (rp = 0.312, p = 0.001; rp = 0.287, p = 0.003). A correlation between CRP and MCHC (rs = 0.262, p = 0.008) was observed. Conclusions: Our findings revealed the higher pro-inflammatory condition in HFrEF group without MI in comparison with HFpEF without MI. LYM/MON can be appropriate as additional reading for evaluation of functional condition in HFrEF group without MI. It seems inflammation environment could be higher in HFrEF with MI in disease history in comparison with those without MI. HDL concentration inversely correlated with monocyte count and the percentages could show the relationship between the low-grade inflammation and lipid metabolism in HFrEF. Both MCHC and RDW-CV may be relevant in assessing the chronic HF patients’ condition.