Background and Objectives: Early repolarization pattern (ERP) has recently been shown to be related with an increased risk of ventricular arrhythmias in susceptible individuals. Materials and Methods: We studied the ERP-associated ECG changes, with potential clinical relevance, in 220 young (age 22.1 ± 1.6 years), healthy, male subjects using 12-lead ECG recordings. A total of 38 subjects (17.3%) fulfilled the diagnostic criteria for ERP, and a total of 90 ECG characteristics were compared between the groups of subjects with and without ERP. Results: None of the ECGs were pathological, and 22 ECG parameters differed significantly (p < 0.05) between the subjects with and without ERP. Among them, the P wave-related parameters (e.g., average P wave duration: 101.5 ± 9.2 ms vs. 106.8 ± 9.9 ms, p = 0.004) and the presence of fragmented QRS complexes (67.6% vs. 92.1%, p = 0.002) revealed a potential propensity for atrial and ventricular arrhythmogenesis. The time-domain parameters of repolarization, those not corrected for QRS duration, showed shorter values (e.g., Tpeak-Tend interval: 70.9 ± 8.1 ms vs. 67.8 ± 8.0 ms, p = 0.036), reflecting the accelerated repolarization. Conclusions: Certain ECG characteristics seem to be more associated with ERP. The clinical significance of this finding at the individual level needs further prospective investigations.

This review aims to discuss the apparent reduction in pulmonary cancer incidence in the general population during and shortly after the COVID-19 pandemic from a biological and pathophysiological mechanistic point of view. While the epidemiological evidence points to a disruption in the early- and mid-stage diagnostic process, which causes a shift to late-stage lung cancer discovery with no impact on its actual prevalence, an alternative hypothesis based on the intersection of viral and cancer biology could have a real effect on lung carcinogenesis as an independent phenomenon. By weaving together population-level trends, mechanistic insights, and translational oncology, we discuss whether the pandemic-associated decline in lung cancer diagnoses reflects primarily a temporary diagnostic artifact or whether it also reveals biologically relevant intersections between SARS-CoV-2 and pulmonary oncogenesis. The COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has exerted profound and multifaceted effects on global healthcare systems, altering patterns of disease detection, management, and outcomes across nearly all medical disciplines. These disruptions generated what has been termed a “diagnostic deficit”, producing a backlog of undetected cancers that have only partially been recovered in subsequent years. This phenomenon, sometimes described as a “COVID-19 debt” in oncology, is thought to contribute to excess late-stage diagnoses and potentially worse medium-term survival outcomes. Beyond the disruption of medical systems, the pandemic also raised a more speculative but biologically intriguing question: could SARS-CoV-2 infection itself, through direct or indirect mechanisms, influence lung cancer biology? Our review aims to critically synthesize the evidence across seven domains to address this dual hypothesis. (1) We examine the observed effects of the pandemic on cancer incidence, highlighting global registry and health-system data; (2) we review SARS-CoV-2 infection biology, including viral entry, replication, protein functions, and treatment implications; (3) we summarize the pathogenesis of lung cancer; (4) we explore the role of immune checkpoints in tumor immune evasion, followed by (5) analyses of immune dysregulation in acute infection and (6) in long COVID; and (7) finally, we evaluate proposed oncogenic mechanisms of SARS-CoV-2, integrating molecular virology with cancer immunology. We conclude that the “diagnostic deficit” phenomenon was a reality during and immediately post-pandemic. However, a definitive answer to the questions related to the impact of the infection as an independent phenomenon would require advanced research information covering the biology of the viral infection and lung cancer oncogenesis: processes that are not currently implemented in routine clinical laboratory investigations.

Background: Exercise-induced modifications in ECG parameters among individuals with an early repolarization pattern (ERP) have not been evaluated in detail. We aimed to assess this phenomenon, with potential associations with arrhythmogenesis. Methods: Twenty-three young, healthy males with ERP (ERP+) participated in this study, alongside a control group, which consisted of nineteen healthy males without ERP (ERP−). ECGs at baseline, at peak exercise (Bruce protocol), and during the recovery phase were analyzed and compared between the two groups. Results: The treadmill test demonstrated strong cardiovascular fitness, with similar chronotropic and pressor responses in both groups. In the baseline ECGs, the QRS complex and the QT interval were shorter in the ERP+ group. During exercise, the P-wave duration was significantly longer and the QRS was narrower in the ERP+ group. In the recovery phase, there was a longer P wave and a narrower QRS in the ERP+ group. During the treadmill test, the J wave disappeared or did not meet the criteria required for ERP diagnosis. Conclusions: The slowed intra-atrial conduction found during exercise could be predictive of atrial arrhythmogenesis in the setting of ERP. The disappearing of J waves during exercise, due to increased sympathetic activity, has potential clinical significance.

Background and Objectives: Persistent cough, dyspnea, chest tightness, and exercise limitation after SARS-CoV-2 infection are common in people with asthma but are not specific to uncontrolled asthma. This critical narrative review evaluates inhaled corticosteroid (ICS) delivery optimization after COVID-19 while distinguishing direct post-COVID evidence from established asthma evidence. Materials and Methods: PubMed/MEDLINE was searched from January 2020 through 6 July 2026 for literature on asthma after COVID-19, ICS, inhaler technique, adherence, device selection, small-airway disease, chronic cough, rehabilitation, and severe-asthma care; relevant GINA (Global Initiative for Asthma), WHO (World Health Organization), NICE (National Institute for Health and Care Excellence), ERS (European Respiratory Society), and ATS (American Thoracic Society) guidance was also reviewed. The narrative synthesis drew on 89 cited sources, grouped by relevance, study design, and evidentiary directness. Results: Direct post-acute evidence is limited and predominantly observational. Post-acute asthma-control outcomes vary across cohorts; observational evidence suggests increased exacerbation risk, particularly after severe or hospitalized COVID-19. In the most directly relevant observational study, Tichopad et al. evaluated 654 patients with asthma and COVID-19 and found that a higher combined adherence/inhaler-technique score was associated with better recovery of lung-function measures and quality of life, without establishing causality. Evidence for adherence assessment, inhaler-technique correction, device-patient matching, and appropriate ICS-containing therapy is stronger in established asthma care. Extra-fine formulations may improve peripheral deposition in selected asthma phenotypes, whereas post-COVID air trapping alone does not establish corticosteroid responsiveness. Conclusions: COVID-19 history should trigger better asthma assessment, not automatic treatment intensification. Persistent symptoms should prompt confirmation of asthma relevance, assessment of objective and inflammatory features when appropriate, verification of adherence, inhaler technique, and device suitability, and consideration of non-asthma mechanisms before pharmacological escalation.