Phosphatidylserines are known to sustain skeletal muscle activity during intense activity or hypoxic conditions, as well as preserve neurocognitive function in older patients. Our previous studies pointed out a potential cardioprotective role of phosphatidylserine in heart ischemia. Therefore, we investigated the effects of phosphatidylserine oral supplementation in a mouse model of acute myocardial infarction (AMI). We found out that phosphatidylserine increases, significantly, the cardiomyocyte survival by 50% in an acute model of myocardial ischemia-reperfusion. Similar, phosphatidylserine reduced significantly the infarcted size by 30% and improved heart function by 25% in a chronic model of AMI. The main responsible mechanism seems to be up-regulation of protein kinase C epsilon (PKC-ε), the main player of cardio-protection during pre-conditioning. Interestingly, if the phosphatidylserine supplementation is started before induction of AMI, but not after, it selectively inhibits neutrophil’s activation, such as Interleukin 1 beta (IL-1β) expression, without affecting the healing and fibrosis. Thus, phosphatidylserine supplementation may represent a simple way to activate a pre-conditioning mechanism and may be a promising novel strategy to reduce infarct size following AMI and to prevent myocardial injury during myocardial infarction or cardiac surgery. Due to the minimal adverse effects, further investigation in large animals or in human are soon possible to establish the exact role of phosphatidylserine in cardiac diseases.

(1) Background: Fibroblast growth factor 23 (FGF23) is associated with mortality in patients with heart failure (HF); however, less is known about mortality associations in patients with myocardial infarction (MI). (2) Methods: FGF23 was assessed in 180 patients with acute MI, 99 of whom presented with concomitant acute HF. Patients were followed up for one year, and outcome estimates by FGF23 were compared to GRACE score estimates. (3) Results: Log-transformed serum levels of intact FGF23 (logFGF23) did not differ between MI patients with and without HF, and no difference in logFGF23 was observed between 14 MI patients who died and those who survived. However, when only MI patients with concomitant HF were considered, logFGF23 was significantly higher among non-survivors compared to that in survivors. While logFGF23 was not associated with the outcome in the entire cohort, logFGF23 was fairly predictive for one-year mortality in patients with concomitant HF (AUC 0.78; 95%CI 0.61–0.95), where it outperformed GRACE score estimates (AUC 0.70; 95%CI 0.46–0.94). (4) Conclusions: FGF23 was associated with one-year mortality only in MI patients who concomitantly presented with HF, surpassing the predictive ability of GRACE score estimates. No associations were observed in patients without HF despite similar FGF23 levels at admission. Further studies are warranted to investigate whether FGF23 is causal for dismal outcome of HF.

Objectives: We aimed to evaluate the efficacy and safety of low-dose protamine in reducing access site-related complications during Transcatheter Aortic Valve Implantation (TAVI) as compared to full-dose protamine. Background: Access site-related complications represent an independent predictor of poor outcomes of TAVI. Data regarding heparin reversal with protamine and the dosage needed to prevent bleeding complications are scarce among patients undergoing TAVI. Methods: A total of 897 patients were retrospectively included in the study. Patients who underwent percutaneous coronary intervention within 4 weeks before or concomitantly with TAVI (n = 191) were given 0.5 mg protamine for each 100 units of unfractionated heparin. All other patients (n = 706) were considered as a control group and 1 mg protamine for each 100 units of heparin was administered. Results: The combined intra-hospital endpoint of death, life-threatening major bleeding, and major vascular complications were significantly more frequent in patients receiving low-dose protamine [29 (15.2%) vs. 50 (7.1%), p < 0.001]. After propensity matching (n = 130 for each group) for relevant clinical characteristics including anti-platelet therapy [19 (14.6%) vs. 6 (4.6%), p = 0.006], low-dose protamine predicted the combined endpoint (OR 3.54, 95%-CI 1.36–9.17, p = 0.009), and even in multivariable analysis, low-dose protamine continued to be a predictor of the combined endpoint in the matched model (OR 3.07, 95%-CI 1.17–8.08, p = 0.023) alongside baseline hemoglobin. Conclusions: In this propensity-matched retrospective analysis, a low-dose protamine regime is associated with a higher rate of major adverse events compared to a full-dose protamine regime following transfemoral TAVI.

Background: Deficiency in vitamin D₃ and its metabolites has been linked to dismal outcomes in patients with chronic diseases, including cardiovascular disease and heart failure (HF). It remains unclear if a vitamin D₃ status is a prognostic feature in patients with acute decompensated HF. Methods: We assessed serum levels of 25-OH-vitamin D₃ and 1,25-(OH)₂-vitamin D₃ in 139 patients with acute HF who had been admitted to the intermediate care unit of a maximum care hospital. The follow-up period was one year. After exclusion of patients with sampling errors and those who were lost to follow-up, 118 patients remained in the final study cohort. Outcome estimates by 25-OH-vitamin D₃ and 1,25-(OH)₂-vitamin D₃ levels were compared to the Seattle Heart Failure (SHF) Model. Results: More than two-thirds (79.7%) of the patients showed inadequate 25-OH-vitamin D₃ levels (i.e., <30 ng/mL) upon admission. Low levels of 1,25-(OH)₂-vitamin D₃ (i.e., <19.9 pg/mL) were observed in 16.1% of patients. Of the 118 HF patients, 22 (19%) died during the following 12 months. There were no differences in vitamin D₃ levels between patients who died and those who survived, neither in 25-OH-vitamin D₃ (23.37 ± 19.14 ng/mL vs. 19.11 ± 12.25 ng/mL; p = 0.19) nor in 1,25-(OH)₂-vitamin D₃ levels (31.10 ± 19.75 ng/mL vs. 38.25 ± 15.73 ng/mL; p = 0.02); therefore, vitamin D₃ levels alone did not predict one-year survival (AUC [25-OH-vitamin D₃] 0.50; 95% CI 0.34–0.65; AUC [1,25-(OH)2-vitamin D₃] 0.62; 95% CI 0.48–0.76). Moreover, whilst the SHF model exhibited acceptable discriminatory ability for predicting one-year mortality (AUC 0.79; 95% CI 0.66–0.91), adding vitamin D levels on admission to the SHF score did not improve its discriminatory value. Conclusion: Our data do not support the use of vitamin D₃ screening in patients admitted with acute decompensated HF to aid prognostication.

Background/Objective: Cardiac magnetic resonance (CMR) is the reference method for right ventricular (RV) volume and function analysis, but time-consuming manual segmentation and corrections of imperfect automatic segmentations are needed. This study sought to evaluate the applicability of an echocardiographically established truncated cone–rhomboid pyramid formula (CPF) for simplified RV quantification using CMR. Methods: A total of 70 consecutive patients assigned to RV analysis using CMR were included. As standard method, the manual contouring of RV-short axis planes was performed for the measurement of end-diastolic volume (EDV) and end-systolic volume (ESV). Additionally, two linear measurements in four-chamber views were obtained in systole and diastole: basal diameters at the level of tricuspid valve (Dd and Ds) and baso-apical lengths from the center of tricuspid valve to the RV apex (Ld and Ls) were measured for the calculation of RV-EDV = 1.21 × Dd² × Ld and RV-ESV = 1.21 × Ds ² × Ls using CPF. Results: RV volumes using CPF were slightly higher than those using standard CMR analysis (RV-EDV index: 86.2 ± 29.4 mL/m² and RV-ESV index: 51.5 ± 22.5 mL/m² vs. RV-EDV index: 81.7 ± 24.1 mL/m² and RV-ESV index: 44.5 ± 23.2 mL/m²) and RV-EF was lower (RV-EF: 41.1 ± 13.5% vs. 48.4 ± 13.7%). Both methods had a strong correlation of RV volumes (ΔRV-EDV index = −4.5 ± 19.0 mL/m²; r = 0.765, p < 0.0001; ΔRV-ESV index = −7.0 ± 14.4 mL/m²; r = 0.801, p < 0.0001). Conclusions: Calculations of RV volumes and function using CPF assuming the geometrical model of a truncated cone–rhomboid pyramid anatomy of RV is feasible, with a strong correlation to measurements using standard CMR analysis, and only two systolic and diastolic linear measurements in four-chamber views are needed.

Background/Objectives: Percutaneous left atrial appendage occlusion (LAAO) has become an alternative to oral anticoagulation in selected patients with atrial fibrillation. The results of transcatheter LAAO were evaluated by conventional cardiac angiography (CCA), fluoroscopy, and 2D and 3D transesophageal echocardiography (TEE). Methods: In 47 consecutive patients (76 ± 8 years), LAAO was performed with the Amplatzer^TM device. CCA and 2D and 3D TEE were performed for LAA measurements. The eccentricity of the device landing zone was assessed by 3D TEE as the ratio of the maximal and minimal diameters. The device size was selected depending on the CCA maximal diameter. The postprocedural device lobe morphology was classified by fluoroscopy as “square” type (sign of undersizing), “tire” type (optimal deformation), and “strawberry” type (sign of oversizing). After 6 months, TEE was repeated to evaluate peri-device leaks (PDLs). Results: The postprocedural device morphology was “square” type in 9 (19%), “tire” type in 28 (60%), and “strawberry” type in 10 patients (21%). After 6 months, peri-device leaks were observed in 11 patients (23%), with the lowest incidence in the “tire”-type group (11%) compared with “square” type (56%) and “strawberry” type (30%) (p = 0.019). The 3D TEE eccentricity index with a cut-off value of ≤1.29 (indicating a more circular morphology) was a very specific predictor for excluding postprocedural device deformation of the “strawberry” type (AUC = 0.689; sensitivity 48.7%, specificity 100%). Conclusions: Undersizing as well as oversizing of the LAA occluder, as characterized by deformation type by fluoroscopy, was associated with postprocedural PDLs. The eccentricity of the LAA landing zone by 3D TEE may indicate inadequate size selection of the Amplatzer^TM device leading to oversizing in patients with a more eccentric LAA.