Despite the progress of its management, COVID-19 maintains an ominous condition which constitutes a threat, especially for the susceptible population. The cardiac injury occurs in approximately 30% of COVID-19 infections and is associated with a worse prognosis. The clinical presentation of cardiac involvement can be COVID-19-related myocarditis. Our review aims to summarise current evidence about that complication. The research was registered at PROSPERO (CRD42022338397). We performed a systematic analysis using five different databases, including i.a. MEDLINE. Further, the backward snowballing technique was applied to identify additional papers. Inclusion criteria were: full-text articles in English presenting cases of COVID-19-related myocarditis diagnosed by the ESC criteria and patients over 18 years old. The myocarditis had to occur after the COVID-19 infection, not vaccination. Initially, 1588 papers were screened from the database search, and 1037 papers were revealed in the backward snowballing process. Eventually, 59 articles were included. Data about patients’ sex, age, ethnicity, COVID-19 confirmation technique and vaccination status, reported symptoms, physical condition, laboratory and radiological findings, applied treatment and patient outcome were investigated and summarised. COVID-19-related myocarditis is associated with the risk of sudden worsening of patients’ clinical status, thus, knowledge about its clinical presentation is essential for healthcare workers.

Acute heart failure (AHF) is a life-threatening, heterogeneous disease requiring urgent diagnosis and treatment. The clinical severity and medical procedures differ according to a complex interplay between the deterioration cause, underlying cardiac substrate, and comorbidities. This study aimed to analyze the natural phenotypic heterogeneity of the AHF population and evaluate the possibilities offered by clustering (unsupervised machine-learning technique) in a medical data assessment. We evaluated data from 381 AHF patients. Sixty-three clinical and biochemical features were assessed at the admission of the patients and were included in the analysis after the preprocessing. The K-medoids algorithm was implemented to create the clusters, and optimization, based on the Davies-Bouldin index, was used. The clustering was performed while blinded to the outcome. The outcome associations were evaluated using the Kaplan-Meier curves and Cox proportional-hazards regressions. The algorithm distinguished six clusters that differed significantly in 58 variables concerning i.e., etiology, clinical status, comorbidities, laboratory parameters and lifestyle factors. The clusters differed in terms of the one-year mortality (p = 0.002). Using the clustering techniques, we extracted six phenotypes from AHF patients with distinct clinical characteristics and outcomes. Our results can be valuable for future trial constructions and customized treatment.

Acute heart failure (AHF) is a common and severe condition with a poor prognosis. Its course is often complicated by worsening renal function (WRF), exacerbating the outcome. The population of AHF patients experiencing WRF is heterogenous, and some novel possibilities for its analysis have recently emerged. Clustering is a machine learning (ML) technique that divides the population into distinct subgroups based on the similarity of cases (patients). Given that, we decided to use clustering to find subgroups inside the AHF population that differ in terms of WRF occurrence. We evaluated data from the three hundred and twelve AHF patients hospitalized in our institution who had creatinine assessed four times during hospitalization. Eighty-six variables evaluated at admission were included in the analysis. The k-medoids algorithm was used for clustering, and the quality of the procedure was judged by the Davies–Bouldin index. Three clinically and prognostically different clusters were distinguished. The groups had significantly (p = 0.004) different incidences of WRF. Inside the AHF population, we successfully discovered that three groups varied in renal prognosis. Our results provide novel insight into the AHF and WRF interplay and can be valuable for future trial construction and more tailored treatment.

Augmented peripheral chemoreceptor sensitivity (PChS) is a common feature of many sympathetically mediated diseases, among others, and it is an important mechanism of the pathophysiology of heart failure (HF). It is related not only to the greater severity of symptoms, especially to dyspnea and lower exercise tolerance but also to a greater prevalence of complications and poor prognosis. The causes, mechanisms, and impact of the enhanced activity of peripheral chemoreceptors (PChR) in the HF population are subject to intense research. Several methodologies have been established and utilized to assess the PChR function. Each of them presents certain advantages and limitations. Furthermore, numerous factors could influence and modulate the response from PChR in studied subjects. Nevertheless, even with the impressive number of studies conducted in this field, there are still some gaps in knowledge that require further research. We performed a review of all clinical trials in HF human patients, in which the function of PChR was evaluated. This review provides an extensive synthesis of studies evaluating PChR function in the HF human population, including methods used, factors potentially influencing the results, and predictors of increased PChS.

The assessment of functional severity of moderate coronary stenoses is challenging. Coronary angiography remains the standard technique for diagnosis, although, due to its limitations, it is frequently insufficient to detect relevant myocardial ischemia. Fractional flow reserve (FFR) is defined as the ratio between the mean hyperemic coronary artery pressure distal to the lesion and mean pressure in the aorta. The FFR measurement is currently supported by guidelines to evaluate the hemodynamic significance of lesions. Proper identification of patients that have the potential to benefit from revascularization is crucial. Based on already published literature, we focus on the long-term follow-up of patients with FFR-driven treatment. We also provide a review of specific clinical cases such as borderline FFR values, comorbidities or lesions in anatomical risk locations, in which interpretation can be challenging during the physiological assessment. The aim of this paper is to provide an overview of the evidence of FFR implementation in daily clinical practice and determine issues that raise doubts.

Heart failure (HF) patients experience elevated sympathetic tone and abnormal peripheral chemoreceptor (PChR) function (elevated sensitivity [PChS] and tonicity [PChT]), which can be attributed to a reduction in cardiac output (CO) and resultant hypoperfusion of the carotid bodies. Left ventricular assist devices (LVADs) are known to increase CO, and can be used as a unique model to examine the impact of acute hemodynamic changes on PChR. Fourteen HF patients with LVADs underwent assessment of PChS (using the transient hypoxia test) and PChT (using low-dose dopamine infusion) under different LVAD flow parameters, previously determined using right heart catheterization to achieve significantly distinct CO levels. PChS did not differ between the low- vs high-flow conditions (0.61 [0.49;0.74] vs. 0.67 [0.33;0.9] L/min/SpO2%, p = 0.36) as well as PChT (0.97 [-0.36;1.96] vs. 0.81 [-1.67;2.2] L/min-1, p = 0.81).). In 9 patients, central venous pressure (CVP) decreased in response to higher pump speeds. In this group, PChS more frequently increased and was significantly higher than in the remaining patients. ΔCVP was also inversely related to ΔHVR (R = 0.75, p = 0.002). Acute changes in CO, as well as pulse pressure, did not affect PChS or PChT. Surprisingly, we observed a strong correlation between a decrease in CVP in response to higher LVAD speed and an increase in PChS, which can be explained by the function of low-pressure baroreceptors. These findings provide unique data on PChR function under different hemodynamic conditions in the LVAD population.