Background: This systematic review seeks to evaluate the role of epicardial adipose tissue

Ischemic stroke is associated with a tremendous economic and societal burden, and only a few therapies are currently available for the treatment of this devastating disease. The main therapeutic approaches used nowadays for the treatment of ischemic brain injury aim to achieve reperfusion, neuroprotection and neurorecovery. Therapeutic angiogenesis also seems to represent a promising tool to improve the prognosis of cerebral ischemia. This review aims to present the modern concepts and the current status of regenerative therapy for ischemic stroke and discuss the main results of major clinical trials addressing the effectiveness of stem cell therapy for achieving neuroregeneration in ischemic stroke. At the same time, as a glimpse into the future, this article describes modern concepts for stroke prevention, such as the implantation of bioprinted scaffolds seeded with stem cells, whose 3D geometry is customized according to carotid shear stress.

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Wound healing is a complex restorative process of the altered cutaneous tissue, which is impaired by numerous local and systemic factors, leading to chronic non-healing lesions with few efficient therapeutic options. Stem cells possess the capacity to differentiate into various types of cell lines. Furthermore, stem cells are able to secrete cytokines and growth factors, modulating inflammation and ultimately leading to angiogenesis, fibrogenesis, and epithelization. Because of their paracrine activity, these cells are able to attract other cell types to the base of the wound, improving the formation of new skin layers. Mesenchymal stem cells derived from the adipose tissue, bone marrow, and placenta, offer numerous ways of implementation. The process of harvesting, growing, and administrating stem cells depends on the site and type of the cells, but recent trial results showed improvement of wound healing independent of the administration site. Bioengineered skin substitutes are validated for treatment of chronic wounds with direct application on the skin surface. These offer physical scaffolding for the migrating cells and promote secretion of growth factors, thus facilitating rapid wound healing. Obtaining further clinical data is essential, but stem cell therapy may become a first-line therapeutic choice for the treatment of non-healing chronic wounds.

An unstable plaque has a high risk of thrombosis and at the same time for a fast progression of the stenosis degree. Also, “high-risk plaque” and “thrombosis-prone plaque” are used as synonym terms for characterization of a vulnerable plaque. The imaging biomarkers for vulnerable coronary plaques are considered to be spotty calcifications, active remodeling, low-density atheroma and the presence of a ring-like attenuation pattern, also known as the napkin-ring sign. Computed cardiac tomography can determine the plaque composition by assessing the plaque density, which is measured in Hounsfield units (HU). The aim of this manuscript was to provide an update about the most frequently used biomarkers of vulnerability in a vulnerable plaque with the help of computed cardiac tomography.

Introduction:While the role of inflammation in acute coronary events is well established, the impact of inflammatory-mediated vulnerability of coronary plaques from the entire coronary tree, on the extension of ventricular remodeling and scaring, has not been clarified yet.Materials and methods:The present manuscript describes the procedures of the VIABILITY trial, a descriptive prospective single-center cohort study. The main purpose of this trial is to assess the link between systemic inflammation, pan-coronary plaque vulnerability (referring to the plaque vulnerability within the entire coronary tree), myocardial viability and ventricular remodeling in patients who had suffered a recent ST-segment elevation acute myocardial infarction (STEMI). One hundred patients with STEMI who underwent successful revascularization of the culprit lesion in the first 12 hours after the onset of symptoms will be enrolled in the study. The level of systemic inflammation will be evaluated based on the serum biomarker levels (hs-CRP, matrix metalloproteinases, interleukin-6) in the acute phase of the myocardial infarction (MI) and at 1 month. Pan-coronary plaque vulnerability will be assessed based on serum biomarkers known to be associated with increased plaque vulnerability (V-CAM or I-CAM) and at 1 month after infarction, based on computed tomographic angiography analysis of vulnerability features of all coronary plaques. Myocardial viability and remodeling will be assessed based on 3D speckle tracking echocardiography associated with dobutamine infusion and LGE-CMR associated with post-processing imaging methods. The study population will be categorized in 2 subgroups: subgroup 1 - subjects with STEMI and increased inflammatory response at 7 days after the acute event (hs-CRP ≥ 3 mg/dl), and subgroup 2 - subjects with STEMI and no increased inflammatory response at 7 days (hs-CRP < 3 mg/dl). Study outcomes will consist in the rate of post-infarction heart failure development and the major adverse events (MACE) rate.Conclusion:VIABILITY is the first prospective study designed to evaluate the influence of infarct-related inflammatory response on several major determinants of post-infarction outcomes, such as coronary plaque vulnerability, myocardial viability, and ventricular remodeling.

Background: The impact of nutritional status on the early outcome of subjects with acute myocardial infarction (AMI) is still not completely elucidated. This study aimed to assess the correlation between nutritional status, as expressed by the CONUT and PIN scores, and (1) clinical and laboratory characteristics, (2) complication rates, and (3) length of hospitalization, in patients with AMI. Materials and methods: We included 56 consecutive patients with AMI who underwent primary percutaneous intervention and stenting. Evaluation of the nutritional status was comprised in the calculation of the CONUT and PNI scores. The study population was divided into 2 groups according to the calculated CONUT score, as follows: group 1 – CONUT score <3 points (normal to mildly impaired nutritional status) and group 2 – CONUT score ≥3 points (moderate to severe malnutrition). The primary end-point of the study was the rate of in-hospital complications (left ventricular free wall rupture, hemodynamic instability requiring inotropic medication, high-degree atrioventricular block, the need for temporary cardiostimulation, supraventricular and ventricular arrhythmias and in-hospital cardiac arrest). The secondary end-points included the duration of hospitalization and the length of stay in the intensive cardiac care unit. Results: In total, 56 patients (44.64% with STEMI, 55.35% with NSTEMI) with a mean age of 61.96 ± 13.42 years, 58.92% males were included in the study. Group distribution was: group 1 – 76.78% (n = 43), group 2 – 23.21% (n = 23). There were no differences between the two groups regarding age, gender, cardiovascular risk factors, or comorbidities. PNI index in group 1 was 54.4 ± 10.4 and in group 2 41.1 ± 2.8, p <0.0001. Serum albumin was significantly lower in group 1 – 4.1 ± 0.3 vs. group 2 – 3.6 ± 0.3 (p <0.0001), similarly to total cholesterol levels (group 1 – 194.9 ± 41.5 vs. group 2 – 161.2 ± 58.2, p = 0.02). The complete blood cell count showed that group 2 presented lower levels of hematocrit (p = 0.003), hemoglobin (p = 0.002), and lymphocytes (p <0.0001) compared to group 1, but a significantly higher platelet count (p = 0.001), mean platelet volume (p = 0.03), neutrophil/lymphocyte (p <0.0001) and platelet/lymphocyte (p <0.0001) ratios, indicating enhanced blood thrombogenicity and inflammation. Regarding in-hospital complications, group 2 presented a higher rate of hemodynamic instability (group 1 – 11.6% vs. group 2 – 38.4%, p = 0.02). The overall hospitalization period was 7.7 ± 1.4 days in group 1 vs. 10.2 ± 4.8 days in group 2, p = 0.06; while the duration of stay in the intensive cardiac care unit was 2.6 ± 0.5 days in group 1 vs. 4.0 ± 2.5 days in group 2, p = 0.02. Conclusions: This study proved that nutritional deficit in acute myocardial patients who undergo revascularization is associated with an increased rate of in-hospital complications and with a longer observation time in a tertiary intensive cardiac care unit.

(1) Background: The prediction of recurrent events after acute myocardial infarction (AMI) does not sufficiently integrate systemic inflammation, coronary morphology or ventricular function in prediction algorithms. We aimed to evaluate the accuracy of inflammatory biomarkers, in association with angiographical and echocardiographic parameters, in predicting 1-year MACE after revascularized AMI. (2) Methods: This is an extension of a biomarker sub-study of the VIP trial (NCT03606330), in which 225 AMI patients underwent analysis of systemic vulnerability and were followed for 1 year. Hs-CRP, MMP-9, IL-6, I-CAM, V-CAM and E-selectin were determined at 1 h after revascularization. The primary end-point was the 1-year MACE rate. (3) Results: The MACE rate was 24.8% (n = 56). There were no significant differences between groups in regard to IL-6, V-CAM and E-selectin. The following inflammatory markers were significantly higher in MACE patients: hs-CRP (11.1 ± 13.8 vs. 5.1 ± 4.4 mg/L, p = 0.03), I-CAM (452 ± 283 vs. 220.5 ± 104.6, p = 0.0003) and MMP-9 (2255 ± 1226 vs. 1099 ± 706.1 ng/mL p = 0.0001). The most powerful predictor for MACE was MMP-9 of >1155 ng/mL (AUC-0.786, p < 0.001) even after adjustments for diabetes, LVEF, acute phase complications and other inflammatory biomarkers. For STEMI, the most powerful predictors for MACE included I-CAM >239.7 ng/mL, V-CAM >877.9 ng/mL and MMP-9 >1393 ng/mL. (4) Conclusions: High levels of I-CAM and MMP-9 were the most powerful predictors for recurrent events after AMI for the overall study population. For STEMI subjects, the most important predictors included increased levels of I-CAM, V-CAM and MMP-9, while none of the analyzed parameters had proven to be predictive. Inflammatory biomarkers assayed during the acute phase of AMI presented a more powerful predictive capacity for MACE than the LVEF.