Backgrounds: Omega-3 supplements are endorsed for heart failure (HF) patients to reduce hospitalizations and mortality, offering anti-inflammatory and cardioprotective benefits. Methods: A comprehensive search was conducted in various databases until November 2022. Eligible studies included clinical trials on patients with HF. Data extraction covered study details, omega-3 specifics, outcomes, and limitations. The JADAD scale was used to assess the risk of bias in randomized controlled trials. Results: The review process involved 572 records from database searches, resulting in 19 studies after eliminating duplicates and screening. These studies assessed the impact of omega-3 on various clinical outcomes, such as mortality, hospitalization, cardiac function, and quality of life. Studied duration varied from weeks to years. Omega-3 supplementation demonstrated potential benefits such as improved heart function, reduced inflammation, and decreased risk of cardiovascular events. Conclusion: Omega-3 supplementation could benefit heart disease treatment, potentially reducing therapy duration and improving outcomes. Starting omega-3 supplementation for HF patients seems favorable.

ACE2’s impact on the severity of COVID-19 is widely discussed but still controversial. To estimate its role in aspects of the main risk factors and comorbidities, we involved post-COVID-19 patients in Ternopil region (Ukraine). The recruitment period was from July 2020 to December 2021. Medical records, treatment modalities, and outcomes were recorded and analyzed. The serum human ACE2 protein was measured with Cusabio ELISA kits (Houston, TX, USA). Statistical analysis was performed with SPSS21.0 software (SPSS Inc., Chicago, IL, USA). The level of the ACE2 serum protein was significantly higher (p < 0.001) in patients with mild symptoms compared to a more severe course of the disease, and inversely had changed from 1 to 90 days after recovery. In patients with mild COVID-19, ACE2 levels significantly decreased over time, while among critical patients, it increased by 34.1 percent. Such results could be explained by ACE2 shedding from tissues into circulation. Loss of the membrane-bound form of the enzyme decreases the virus’ entry into cells. Our studies did not identify a sex-related ACE2 serum level correlation. The most common comorbidities were hypertension, cardiovascular diseases, respiratory diseases, and diabetes mellitus. All abovementioned comorbidities except respiratory diseases contribute to the severity of the disease and correlate with ACE2 blood serum levels.

Coronavirus disease (COVID-19) causes various vascular and blood-related reactions, including exacerbated responses. The role of endothelial cells in this acute response is remarkable and may remain important beyond the acute phase. As we move into a post-COVID-19 era (where most people have been or will be infected by the SARS-CoV-2 virus), it is crucial to define the vascular consequences of COVID-19, including the long-term effects on the cardiovascular system. Research is needed to determine whether chronic endothelial dysfunction following COVID-19 could lead to an increased risk of cardiovascular and thrombotic events. Endothelial dysfunction could also serve as a diagnostic and therapeutic target for post-COVID-19. This review covers these topics and examines the potential of emerging vessel-on-a-chip technology to address these needs. Vessel-on-a-chip would allow for the study of COVID-19 pathophysiology in endothelial cells, including the analysis of SARS-CoV-2 interactions with endothelial function, leukocyte recruitment, and platelet activation. “Personalization” could be implemented in the models through induced pluripotent stem cells, patient-specific characteristics, or genetic modified cells. Adaptation for massive testing under standardized protocols is now possible, so the chips could be incorporated for the personalized follow-up of the disease or its sequalae (long COVID) and for the research of new drugs against COVID-19.

ACE2 impact on the severity of COVID-19 is widely discussed but still controversial. To estimate its role in aspects of the main risk factors and comorbidities, we involved post-COVID-19 patients in Ternopil region (Ukraine). Recruitment period was July 2020 to December 2021. Medical records, treatment modalities and outcomes were recorded and analyzed. Serum human ACE2 protein was measured with Cusabio ELISA kits (Houston, TX, USA). Statistical analysis was performed with SPSS21.0 software (SPSS Inc., Chicago, IL, USA). The level of ACE2 serum protein was significantly higher (p < 0.001) in patients with mild symptoms compared to more severe course of disease, and inversely had changed from 1 to 90 days after recovery. In patients with mild COVID-19, ACE2 level significantly decreased over time, while among critical patients, it increased by 34.1percent. Such results could be explained by ACE2 shedding from tissues into circulation. Loss of the membrane-bound form of the enzyme decreases the virus entry into cells. Our studies did not identify any sex-related ACE2 serum levels correlation. The most common comorbidities were hypertension, cardiovascular diseases, respiratory diseases and diabetes mellitus. All comorbidities except respiratory diseases contribute to the severity of disease and correlate with ACE2 blood serum level.

The complex network of blood vessels plays a key role in transporting oxygen and nutrients and maintaining homeostasis in the human body. The inner walls of all blood and lymphatic vessels are lined by the endothelium, a monolayer of endothelial cells (ECs) oriented along the direction of blood flow. ECs play a pivotal role in vascular homeostasis, including regulating vascular tone, delivering oxygen and nutrients, modulating pro‐inflammatory molecules and pro‐inflammatory immune responses, and performing other vital functions. Therefore, the study of EC biology and vascular responses is key for a deeper understanding of vascular biology and the development of new therapeutics. Most studies in vivo and in vitro present technical challenges, either complexity or oversimplification, respectively, which slow down advances in the field. Therefore, 3D models and microfluidics offer a complementary alternative that integrates shapes similar to those observed in vivo , with the advantages of an in vitro system. Here, we present a robust and reproducible vessel‐on‐a‐chip (VOC) composed of an EC monolayer and a microvascular microenvironment maintained by a peristaltic pump to ensure continuous media circulation and physiological levels of shear stress. In addition, we validated this model for in vitro studies of vascular inflammation by monitoring EC status. We observed cellular alignment after shear stress exposure, increased E‐selectin expression, and TNF‐induced morphological changes in ECs. This new VOC is a promising approach to studying EC mechanobiology and inflammation and opens new avenues for its versatile use in vascular biology, inflammation, and immune and cancer cell migration in a controlled, scalable manner. © 2025 The Author(s). Current Protocols published by Wiley Periodicals LLC. Basic Protocol 1 : 3D Vessel Formation within a microfluidic organ‐on‐a‐chip system Basic Protocol 2 : Evaluation of shear stress Basic Protocol 3 : Evaluation of inflammation

The clinical course of coronavirus disease 2019 (COVID-19) strongly affects blood coagulation. In our work, we focused on analyzing the molecular markers of hemostasis system activation in blood plasma of patients recovered after COVID-19. We examined the concentrations of soluble fibrin (SF), D-dimer, fibrinogen, protein C (PC) and prethrombin-1 (Pre-1) in blood plasma samples of seropositive patients recovered post-COVID-19 (PCD, n = 191). PCD patients were divided into high-risk group (HRG, n = 163) and non-risk group (NRG, n = 28) according to WHO recommendations. Blood plasma samples of seronegative healthy volunteers were collected as the reference group (n = 19). The fibrinogen, SF and Pre-1 concentrations were increased in blood plasma of PCD patients in comparison to the reference group. Increasing of fibrinogen and Pre-1 concentrations correlated with COVID-19 severity. The fibrinogen and SF concentrations remained high more than two months after recovery in HRG and elevated after two months post recovery in NRG. D-dimer concentrations were elevated in 8% of patients and protein C levels were decreased in 11% of PCD patients. We observed long-term prethrombotic state in PCD patients that was more expressed in HRG and correlated with severity of the disease. SF, Pre-1 and elevated fibrinogen concentrations were selected as useful thrombosis markers in PCD patients. Monitoring the main coagulation markers can indicate the risk of intravascular thrombus formation in PCD patients.