Heart failure (HF) is a common complication of various cardiac diseases, and its incidence constantly increases. This is caused mainly by aging of populations and improvement in the treatment of coronary artery disease. As HF patients age, they tend to develop comorbidities, creating new problems for health-care professionals. Sarcopenia, defined as the loss of muscle mass and function, and cachexia, defined as weight loss due to an underlying illness, are muscle wasting disorders of particular relevance in the heart failure population, but they go mostly unrecognized. The coexistence of chronic HF and metabolic disorders facilitates the development of cachexia. Cachexia, in turn, significantly worsens a patient’s prognosis and quality of life. The mechanisms underlying cachexia have not been explained yet and require further research. Understanding its background is crucial in the development of treatment strategies to prevent and treat tissue wasting. There are currently no specific European guidelines or recommended therapy for cachexia treatment in HF (“cardiac cachexia”).

Frailty syndrome (FS) is an independent predictor of mortality in cardiovascular disease and is found in 15–74% of patients with heart failure (HF). The syndrome has a complex, multidimensional aetiology and contributes to adverse outcomes. Proper FS diagnosis and treatment determine prognosis and support the evaluation of treatment outcomes. Routine FS assessment for HF patients should be included in daily clinical practice as an important prognostic factor within a holistic process of diagnosis and treatment. Multidisciplinary team members, particularly nurses, play an important role in FS assessment in hospital and primary care settings, and in the home care environment. Raising awareness of concurrent FS in patients with HF patients and promoting targeted interventions may contribute to a decreased risk of adverse events, and a better prognosis and quality of life.

We are constantly looking for new parameters and markers that can help in the assessment of patients with various diseases, including cardiac disorders; this can translate into better care and improved prognosis. Suppression of tumorigenicity 2 (ST2) has recently gained interest as a potential biomarker in many fields: it is involved in many inflammatory diseases and allergies, including asthma, rheumatoid arthritis and inflammatory bowel disease, and it participates in cardiovascular pathophysiology. Suppression of tumorigenicity 2 is being investigated as a promising biomarker in heart diseases. The interaction of interleukin 33 (IL-33) and ST2L is part of a cardioprotective pathway that prevents fibrosis and inhibits inflammatory response, hypertrophy and apoptosis of cardiomyocytes. In this review, we try to summarize the current knowledge about the usefulness of soluble ST2 (sST2) in cardiology. Clinical data show promising results for the possibility of using sST2 in various diseases, such as arrhythmia, hypertension, myocarditis, acute aortic syndrome, and coronary artery disease (CAD). This novel biomarker may also play a role in heart transplantation and perioperative care.

The COVID-19 pandemic has caused more than 3 million deaths worldwide. Recently developed genetically engineered vaccines are the most critical solution for controlling the pandemic. Clinical trials on a large number of participants confirmed their safety and efficacy. However, with the growing number of vaccinated people, new infrequent adverse effects have been reported, not described in the medicinal product characteristics. We would like to report a case of acute pancreatic injury that occurred shortly after administering Pfizer BioNTech COVID-19 mRNA vaccine (Comirnaty). The report points out the potential need for close monitoring of patients reporting abdominal pain after vaccination (unresponsive to standard oral painkillers) because such symptom can be associated with acute pancreatitis.

New parameters and markers are constantly being sought to help better assess patients with heart failure (HF). ST2 protein has gained interest as a potential biomarker in cardiovascular disease. It is known that the IL-33/ST2L system belongs to the cardioprotective pathway, which prevents the fibrosis, hypertrophy, and apoptosis of cardiomyocytes and also inhibits the inflammatory response. Soluble ST2 (sST2) is involved in the immune response and secreted in response to the mechanical overload of the myocardium, thus providing information on the processes of myocardial remodeling and fibrosis. A total of 110 hospitalized patients diagnosed with heart failure with reduced ejection fraction (HFrEF) were included in the study. Clinical and biochemical parameters were studied. During the follow-up, 30.9% patients died and 57.3% patients reached the composite endpoint. Using ROC curves, the reference cut-off point for sST2 was determined to be 45.818 pg/mL for all-cause deaths. Significantly higher concentrations of inflammatory parameters and natriuretic peptides were found in the group of patients with higher sST2 concentrations. sST2 protein is an independent risk factor for all-cause deaths of patients with HFrEF.

Several studies have shown increased rates of cardiovascular disease (CVD) in patients suffering from inflammatory bowel disease (IBD), particularly in cases of early atherosclerosis and myocardial infarction. IBD most frequently begins at an early age, patients usually present normal weight and remain under constant care of a physician, as well as of a nutritionist. Therefore, the classical risk factors of CVD are not reflected in the higher prevalence of CVD in the IBD population. Still, both groups are characterised by chronic inflammation and display similar physiopathological mechanisms. In the course of IBD, increased concentrations of pro-inflammatory cytokines, such as C-reactive protein (CRP) and homocysteine, may lead to endothelial dysfunctions and the development of CVD. Furthermore, gut microbiota dysbiosis in patients with IBD also constitutes a risk factor for an increased susceptibility to cardiovascular disease and atherosclerosis. Additionally, diet is an essential factor affecting both positively and negatively the course of the aforementioned diseases, whereas several dietary patterns may also influence the association between IBD and CVD. Thus, it is essential to investigate the factors responsible for the increased cardiovascular (CV) risk in this group of patients. Our paper attempts to review the role of potential inflammatory and nutritional factors, as well as intestinal dysbiosis and pharmacotherapy, in the increased risk of CVD in IBD patients.