Fatigue is a common, non-specific symptom that often impairs patients’ quality of life. Even though fatigue may be the first symptom of many serious diseases, it is often underestimated due to its non-specific nature. Iron metabolism disorders are a prominent example of conditions where fatigue is a leading symptom. Whether it is an iron deficiency or overload, tiredness is one of the most common features. Despite significant progress in diagnosing and treating iron pathologies, the approach to chronic fatigue syndrome in such patients is not precisely determined. Our study aims to present the current state of knowledge on fatigue in patients with deteriorated iron metabolism.

Vascular aging is a physiological, multifactorial process that involves every type of vessel, from large arteries to microcirculation. This manifests itself as impaired vasomotor function, altered secretory phenotype, deteriorated intercellular transport function, structural remodeling, and aggravated barrier function between the blood and the vascular smooth muscle layer. Iron disorders, particularly iron overload, may lead to oxidative stress and, among other effects, vascular aging. The elevated transferrin saturation and serum iron levels observed in iron overload lead to the formation of a non-transferrin-bound iron (NTBI) fraction with high pro-oxidant activity. NTBI can induce the production of reactive oxygen species (ROS), which induce lipid peroxidation and mediate iron-related damage as the elements of oxidative stress in many tissues, including heart and vessels’ mitochondria. However, the available data make it difficult to precisely determine the impact of iron metabolism disorders on vascular aging; therefore, the relationship requires further investigation. Our study aims to present the current state of knowledge on vascular aging in patients with deteriorated iron metabolism.

(1) Background: Atrial fibrillation (AF) in acute myocardial infarction (AMI) could worsen the prognosis. Yet, there is no definitive answer to whether new-onset AF (NOAF) is a more aggravating diagnosis than other types of that arrhythmia. The purpose of our study was to compare in-hospital clinical course and outcomes of NOAF patients contrary to patients with other pre-existing types of AF. (2) Methods: AMI patients hospitalized in the high-volume cardiological center within 2017–2018 were included in the study. NOAF was noticed in 106 (11%) patients, 95 (10%) with an AF history and AF during AMI formed the AF group, 60 (6%) with an AF history but without AF during AMI constituted the Prior-AF group, and 693 (73%) patients were without an AF before and during AMI. Medical history, routinely monitored clinical parameters, and in-hospital outcomes were analyzed between the groups. (3) Results: NOAF patients, contrary to others, initially had the highest high-sensitivity troponin I (hsTnI), B-type natriuretic peptide (BNP), C-reactive protein (CRP), and glucose levels, and the lowest potassium concentration, with the worst profile of changes for that parameter within the first four days of hospitalization. NOAF patients had the highest rate of ST-elevated AMI (40%), the longest hospitalization (p < 0.001), and the highest in-hospital mortality (p < 0.001). Not NOAF, but other AF groups (AF and Prior-AF groups) were more burdened with the previous comorbidities. (4) Conclusions: NOAF could be a distinct phenomenon in AMI patients, identifying those with the worst clinical in-hospital course and outcomes as compared to other types of AF.

Background/Objectives: Atrial fibrillation (AF) is the most frequent arrhythmia in the adult population associated with a high rate of severe consequences leading to significant morbidity and mortality worldwide. Therefore, its prompt recognition is of high clinical importance. AF detection often remains challenging due to unspecific symptoms and a lack of reliable biomarkers for its prediction. Herein, novel bioanalytical methodologies, such as metabolomics, offer new opportunities for a better understanding of the underlying pathological mechanisms of cardiovascular diseases, including AF. The metabolome, considered a complete set of small molecules present in the organism, directly reflects the current phenotype of the studied system and is highly sensitive to any changes, including arrhythmia’s onset. A growing body of evidence suggests that metabolite profiling has prognostic value in AF prediction, highlighting its potential role not only in early diagnosis but also in guiding therapeutic interventions. By identifying specific metabolites as a disease biomarker or recognising particular metabolomic pathways involved in the AF pathomechanisms, metabolomics could be of great clinical value for further clinical decision-making, risk stratification, and an individual personalised approach. The presented narrative review aims to summarise the current state of knowledge on metabolomics in AF with a special emphasis on its implications for clinical practice and personalised medicine.

Mitral valve prolapse (MVP) could associate with malignant ventricular arrhythmias (VAs). Mitral annular disjunction, a putative mechanism for an arrhythmic substrate, leads to excessive mobility, stretch, and damage of some segments. Speckle tracking echocardiography (STE), with particular attention to the segmental longitudinal strain and myocardial work index (MWI), could be an indicator of the segments we aimed to check. Seventy-two MVP patients and twenty controls underwent echocardiography. Complex VAs documented prospectively after the enrollment was qualified as the primary endpoint, which was noticed in 29 (40%) patients. Pre-specified cut-off values for peak segmental longitudinal strain (PSS) and segmental MWI for basal lateral (−25%, 2200 mmHg%), mid-lateral (−25%, 2500 mmHg%), mid-posterior (−25%, 2400 mmHg%), and mid-inferior (−23%, 2400 mmHg%) segments were accurate predictors of complex VAs. A combination of PSS and MWI increased the probability of the endpoint, reaching the highest predictive value for the basal lateral segment: odds ratio 32.15 (3.78–273.8), p < 0.001 for PSS ≥ −25% and MWI ≥ 2200 mmHg%. STE may be a valuable tool for assessing the arrhythmic risk in MVP patients. Excessively increased segmental longitudinal strain with an augmented regional myocardial work index identifies patients with the highest risk of complex VAs.

Background: Hereditary hemochromatosis (HH) is a genetic condition with fatigue as an essential but not precisely assessed symptom. While some well-specified scales for fatigue assessment in some pathologies exist, data on their usefulness in HH need to be collected. This research aimed to evaluate fatigue in HH using the Fatigue Assessment Scale (FAS), Fatigue Severity Scale (FSS), and Chalder Fatigue Scale (CFQ). Methodology: Seventy-nine HH patients underwent a questionnaire containing items about detailed medical history and the FAS, FSS, and CFQ scales. Twenty-five sex- and age-matched healthy persons constituted the control group (controls); additionally, thirty blood donors (donors) were compared. Results: The fatigue indices were significantly worse in the HH patients than in the controls and donors (HH vs. controls p-value: FAS = 0.003, FSS < 0.001, and CFQ = 0.003; HH vs. donors p-value: FAS = 0.025, FSS < 0.001, and CFQ = 0.041). There were no differences between the severity of fatigue and the specific genotype or the age of the patients. The HH women presented more severe fatigue than the men. High internal consistency and reliability for each scale were revealed: the Cronbach alpha values were as follows: FAS 0.92, FSS 0.95, and CFQ 0.93. Additionally, the construct validity and factorial validity of the implemented scales were confirmed. Conclusions: The HH patients exhibited significantly worse fatigue across all the scales. The FAS, FSS, and CFQ are simple and reliable diagnostic tools for assessing and quantifying fatigue for clinical and research purposes.