Endomyocardial biopsy as the cornerstone of diagnostics has been re-evaluated throughout the years, leaving unanswered questions on the precedence of it. The reported incidence of myocarditis has increased during the pandemic of coronavirus disease 2019 (COVID-19), reinforcing discussions on appropriate diagnostics of myocarditis. By analysis of evidence-based literature published within the last demi-decade, we aimed to summarize the most recent information in order to evaluate the current role of endomyocardial biopsy in diagnostics and management of myocarditis. For the most part, research published over the last five years showed ongoing uncertainty regarding the use, informativeness, safety and necessity of performing a biopsy. Special circumstances, such as fulminant clinical course or failure to respond to empirical treatment, were reconfirmed as justified indications, with a growing applicability of non-invasive diagnostic approaches for most other cases. We concluded that endomyocardial biopsy, if performed properly and with adjunct diagnostic methods, holds a critical role for treatment correction in specific histological subtypes of myocarditis and for differential diagnosis between immune-mediated myocarditis and secondary infections due to immunosuppressive treatment. A high level of possible misdiagnosing was detected, indicating the need to review terminology used to describe findings of myocardial inflammation that did not meet Dallas criteria.

Background: Atrial fibrillation (AF) is the most common arrhythmia and typically occurs in elderly patients with other cardiovascular and extracardiac diseases. However, up to 15% of AF develops without any related risk factors. Recently, the role of genetic factors has been highlighted in this particular form of AF. Aims: The aims of this study were to determine the prevalence of pathogenic variants in early-onset AF in patients without known disease-related risk factors and to identify any structural cardiac abnormalities in these patients. Materials and Methods: We conducted exome sequencing and interpretation in 54 risk factor-free early-onset AF patients and further validated our findings in a similar AF patient cohort from the UK Biobank. Results: Pathogenic/likely pathogenic variants were found in 13/54 (24%) patients. The variants were identified in cardiomyopathy-related and not arrhythmia-related genes. The majority of the identified variants were TTN gene truncating variants (TTNtvs) (9/13 (69%) patients). We also observed two TTNtvs founder variants in the analysed population—c.13696C>T p.(Gln4566Ter) and c.82240C>T p.(Arg27414Ter). Pathogenic/likely pathogenic variants were found in 9/107 (8%) individuals from an independent similar AF patient cohort from the UK Biobank. In correspondence with our Latvian patients, only variants in cardiomyopathy-associated genes were identified. In five (38%) of the thirteen Latvian patients with pathogenic/likely pathogenic variants, dilation of one or both ventricles was identified on a follow-up cardiac magnetic resonance scan. Conclusions: We observed a high prevalence of pathogenic/likely pathogenic variants in cardiomyopathy-associated genes in patients with risk factor-free early-onset AF. Moreover, our follow-up imaging data indicate that these types of patients are at risk of developing ventricular dilation. Furthermore, we identified two TTNtvs founder variants in our Latvian study population.

Background and Objectives: Recurrence of atrial fibrillation (AF) within six months after sinus rhythm restoration with direct current cardioversion (DCC) is a significant treatment challenge. Currently, the factors influencing outcome are mostly unknown. Studies have found a link between genetics and the risk of AF and efficacy of rhythm control. The aim of this study was to examine the association between eight single-nucleotide variants (SNVs) and the risk of AF development and recurrence after DCC. Materials and Methods: Regarding the occurrence of AF, 259 AF cases and 108 controls were studied. Genotypes for the eight SNVs located in the genes CAV1, MYH7, SOX5, KCNN3, ZFHX3, KCNJ5 and PITX2 were determined using high-resolution melting analysis and confirmed with Sanger sequencing. Six months after DCC, a telephone interview was conducted to determine whether AF had recurred. A polygenic risk score (PRS) was calculated as the unweighted sum of risk alleles. Multivariate regression analyses were performed to assess SNV and PRS association with AF occurrence and recurrence after DCC. Results: The risk allele of rs2200733 (PITX2) was significantly associated with the development of AF (p = 0.012, OR = 2.31, 95% CI = 1.206–4.423). AF recurred in 60% of patients and the allele generally associated with a decreased risk of AF of rs11047543 (SOX5) was associated with a greater risk of AF recurrence (p = 0.014, OR = 0.223, 95% CI = 0.067–0.738). A PRS of greater than 7 was significantly associated (p = 0.008) with a higher likelihood of developing AF after DCC (OR = 4.174, 95% CI = 1.454–11.980). Conclusions: A higher PRS is associated with increased odds of AF recurrence after treatment with DCC. PITX2 (rs2200733) is significantly associated with an increased risk of AF. The protective allele of rs11047543 (SOX5) is associated with a greater risk of AF recurrence. Further studies are needed to predict the success of rhythm control and guide patient selection towards the most efficacious treatment.

The conference of the ‘Implantable Cardioverter Defibrillator for Life’ Initiative—Fighting against Sudden Cardiac Death in Emerging Economies was jointly organized by the European Heart Rhythm Association and the Hungarian Society of Cardiology.

Background: Accurate assessment of aerobic capacity is essential for performance monitoring in masters athletes, particularly in high-intensity team sports. The objective of this study was to evaluate the validity and agreement of three indirect maximal oxygen uptake (VO₂max) protocols (Åstrand–Ryhming, YMCA, and Polar OwnIndex Fitness test) against the gold-standard cardiopulmonary exercise testing (CPET) in masters basketball players. Methods: A cross-sectional comparative study included 50 male masters basketball players (aged 51–81 years, M = 64.3 ± 7.9). Validity was determined by comparing results from the three indirect protocols to direct VO₂max measurement via CPET. Agreement was assessed using Pearson correlations (r), systematic error, mean absolute error (MAE), and Bland–Altman limits of agreement. Results: The Åstrand–Ryhming test and YMCA tests showed the closest agreement with CPET (systematic error < 4%, MAE ≈ 17–18%, r > 0.50). The Polar OwnIndex test substantially overestimated VO₂max (mean error ≈ 30%, MAE = 32%). The Åstrand–Ryhming test at low workload yielded the strongest correlation (r = 0.75). Conclusions: The Åstrand–Ryhming and YMCA submaximal tests demonstrated acceptable validity and low systematic bias for estimating VO₂max in masters basketball players, positioning them as practical alternatives to CPET. Conversely, the Polar OwnIndex test showed poor agreement and clinically significant overestimation. These findings support the use of submaximal cycling protocols for fitness monitoring and tailored training prescription in this specific older athlete population. Future longitudinal research is warranted to confirm their ability to track fitness changes over time in this population.

This chapter is structured as a historical overview of the history of the development of defibrillators and the most prominent personalities who contributed to the development of the modern concept of resuscitation. Defibrillators in medical practice can be external or implanted. The devices, known as automated external defibrillators, automate the diagnosis of a patient’s rhythm and the process of stopping arrhythmias, meaning they can be used successfully by nonspecialists. In Europe, 350,000–700,000 people suffer from sudden cardiac arrest every year. On average, it is 55–113 per 100,000 people. Most of these people are usually at home, but about 10–20% of victims are in a public place at the time. Defibrillation within 3–5 minutes of cardiac arrest can increase survival by 50–70%. For every minute that defibrillation is delayed, the chance of survival decreases by 10–12%. A significant contribution to the development of the defibrillation concept was made by Peter Kristians Abildgård, Albert Salisbury Hyman, William Bennett Couwenhoven, Paul Morris Zoll, James Francis Pantridge, and many others. Clinical studies confirm that public access defibrillators (PADs), when available and used correctly during out-of-hospital cardiac arrest, were associated with a 40% median survival rate.