Although disturbance of redox homeostasis might be responsible for COVID-19 cardiac complications, this molecular mechanism has not been addressed yet. We have proposed modifying the effects of antioxidant proteins polymorphisms (superoxide dismutase 2 (SOD2), glutathione peroxidase 1 (GPX1), glutathione peroxidase 3 (GPX3) and nuclear factor erythroid 2-related factor 2, (Nrf2)) in individual susceptibility towards the development of cardiac manifestations of long COVID-19. The presence of subclinical cardiac dysfunction was assessed via echocardiography and cardiac magnetic resonance imaging in 174 convalescent COVID-19 patients. SOD2, GPX1, GPX3 and Nrf2 polymorphisms were determined via the appropriate PCR methods. No significant association of the investigated polymorphisms with the risk of arrhythmia development was found. However, the carriers of variant GPX1*T, GPX3*C or Nrf2*A alleles were more than twice less prone for dyspnea development in comparison with the carriers of the referent ones. These findings were even more potentiated in the carriers of any two variant alleles of these genes (OR = 0.273, and p = 0.016). The variant GPX alleles were significantly associated with left atrial and right ventricular echocardiographic parameters, specifically LAVI, RFAC and RV-EF (p = 0.025, p = 0.009, and p = 0.007, respectively). Based on the relation between the variant SOD2*T allele and higher levels of LV echocardiographic parameters, EDD, LVMI and GLS, as well as troponin T (p = 0.038), it can be proposed that recovered COVID-19 patients, who are the carriers of this genetic variant, might have subtle left ventricular systolic dysfunction. No significant association between the investigated polymorphisms and cardiac disfunction was observed when cardiac magnetic resonance imaging was performed. Our results on the association between antioxidant genetic variants and long COVID cardiological manifestations highlight the involvement of genetic propensity in both acute and long COVID clinical manifestations.

Right ventricular (RV) dysfunction is common and linked to poor outcomes across conditions such as heart failure (HF), acute coronary syndromes, pulmonary embolism, and pulmonary hypertension. While imaging, electrocardiogram (ECG), and invasive tests remain central to RV assessment, circulating biomarkers offer a rapid, non-invasive, and reliable alternative. These biomarkers reflect key pathophysiological processes, including myocardial injury, stress, fibrosis, inflammation, congestion, and multiorgan involvement. High-sensitivity troponins and natriuretic peptides (BNP, NT-proBNP) are already widely used, while emerging biomarkers—such as CA125, copeptin, galectin-3, and others—may enhance diagnostic accuracy and risk stratification. Some, like CA125 and NT-proBNP, have shown promise in guiding post-discharge therapy. However, challenges remain regarding the specificity of biomarkers for RV dysfunction and their role across different clinical contexts. This review provides an integrated overview of RV dysfunction, with a focus on the diagnostic and therapeutic potential of both established and novel biomarkers.

Background: This study investigates the potential mechanisms behind changes in cardiac structure and function in long COVID patients. Methods: This study involved 176 consecutive outpatients in follow-up care (average age 55.9 years; 58.5% male) who experienced symptoms for over 12 weeks (average 6.2 ± 2.7 months), following coronavirus infection (COVID-19). Results: The patients with long COVID and cardiovascular manifestations were significantly more hospitalized (88.5% vs. 75.9%) and had longer hospital stays. Significant echocardiography changes were observed in the left ventricular ejection fraction (LVEF) (59.6 ± 5.4% vs. 62.5 ± 3.8%); longitudinal strain (LS) in the sub-endocardium and intra-myocardium layers (−20.9 vs. −22.0% and −18.6 vs. −19.5%); circumferential strain (CS) in the sub-epicardium layers (−9.6 vs. −10.5%); and CS post-systolic shortening (CS PSS) (0.138 vs. 0.088 s). Additionally, pathological cardiac magnetic resonance (CMR) findings were seen in 58.2% of the group of patients with long COVID and cardiovascular manifestation; 43.3% exhibited positive late gadolinium enhancement (LGE), 21.0% had elevated native T1 mapping, and 22.4% had elevated native T2 mapping. Conclusions: Most patients with long COVID showed structural and functional changes in their cardiovascular systems, primarily caused by prolonged inflammation. Using multimodality imaging is important for uncovering the mechanisms to predict chronic myocarditis, early-stage heart failure, and pre-ischemic states, which can lead to serious complications. Recognizing the specific cardiovascular phenotypes associated with long COVID is essential in order to provide timely and appropriate treatment.

Objective: In this study, we aimed to examine the prognostic impact of decreased kidney function at admission on the occurrence of new-onset atrial fibrillation (AF) in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). Methods: The study enrolled 3,115 consecutive patients with STEMI. Kidney function was assessed by estimation of the glomerular filtration rate (eGFR) at admission. Patients with cardiogenic shock at admission, patients on hemodialysis, and patients with a medical history of previous AF (paroxysmal, persistent, or permanent) were excluded. The follow-up period was six years. Results: New-onset AF occurred in 215 (6.9%) patients, 75 (34.9%) patients presented with AF, and 140 (65.1%) patients developed AF after pPCI. The median time of AF occurrence in patients who did not present with AF was 4.5 (interquartile range 1-25) hours after pPCI. New-onset AF was associated with a higher short- and long-term mortality. In the multiple logistic regression analysis, all stages of reduced kidney function were independent predictors for the occurrence of new-onset AF, and negative prognostic impact increased with the deterioration of kidney function: eGFR <90 mL/min/m(2), hazard ratio (HR) 1.96, 95% confidence interval (CI) 1.42-2.89, p=0.011; eGFR 60-89 mL/min/m(2), HR 1.54, 95% CI 1.13-2.57, p=0.045; eGFR 45-59 mL/min/m(2-), HR 2.09, 95% CI 1.24-2.85, p=0.023; eGFR 30-44 mL/min/m(2-), HR 2.93, 95% CI 1.64-5.29, p<0.001; eGFR 15-29 mL/min/m(2-), HR 5.51, 95% CI 2.67-11.39, p<0.001. Conclusion: Decreased kidney function was significantly associated with the occurrence of new-onset AF, and its impact increased with the deterioration in kidney function, starting with an eGFR value of 90 mL/min/m(2). New-onset AF was an independent predictor of long-term allcause mortality in the analyzed patients.

Background: Patients with ST-segment elevation myocardial infarction (STEMI) and COVID-19 infection have a worse clinical course and prognosis. The prognostic significance of the timing of STEMI in relation to COVID-19 infection was not investigated. Objectives: To assess whether the time of STEMI development in relation to COVID-19 infection (concurrent or following the infection) influenced the short-term prognosis. Methods: This was an observational study of consecutive COVID-19 patients with STEMI admitted to the COVID-hospital Batajnica (February 2021–March 2022). The patients were divided into the “STEMI first” group: patients with STEMI and a positive polymerase chain reaction test for COVID-19, and the “COVID-19 first” group: patients who developed STEMI during COVID-19 treatment. All patients underwent coronary angiography. The primary endpoint was in-hospital all-cause mortality. Results: The study included 87 patients with STEMI and COVID-19 ( M _age , 66.7 years, 66% male). The “STEMI first” group comprised 54 (62.1%) patients, and the “COVID-19 first” group included 33 (37.9%) patients. Both groups shared a comparatively high burden of comorbidities, similar angiographic and procedural characteristics, and high percentages of performed percutaneous coronary interventions with stent implantation (90.7% vs. 87.9%). In-hospital mortality was significantly higher in the “COVID-19 first” group compared to the “STEMI first” group (51.5% vs. 27.8%). Following adjustment, the “COVID-19 first” group had a hazard ratio of 3.22 (95% confidence interval, 1.18–8.75, p = .022) for in-hospital all-cause death, compared with the “STEMI first” group (reference). Conclusion: Clinical presentation with COVID-19 infection, followed by STEMI (“COVID-19 first”), was associated with greater short-term mortality compared to patients presenting with STEMI and testing positive for COVID-19 (“STEMI first”).

Background: Malignant arrhythmias, ventricular tachycardia or ventricular fibrillation (VT/VF) in acute myocardial infarction (AIM) carry ominous prognosis including sudden cardiac death (SCD). It is not clear whether the timing of VT/VF occurrence always affects the poor prognosis of patients with AMI. Aim: To investigate the prognosis of patients who undergoing primary percutaneous coronary intervention (PCI) in accordance with timing of VT/VF and to find the power predictors of their occurrence. Methods: 307 consecutive patients in PREDICT-VT study (NCT03263949), 57.9±10.6 year old, 72.3% males were analysed. Of these patients, 27.7% had VT/VF from the symptoms onset, within 48 hours of AIM (early VT/VF group). 8.1% of patients had VT/VF after 48h, during one year follow up (late VT/VF group). Results: The frequency of VT/VF occurrence was high between symptoms onset and the end of 2nd month and during 5th and 6th month of AIM. The parameters of conventional echocardiography were significantly impaired in late VT/VF group, as well as parameters of longitudinal strain (LS) (table). Moreover, the MACE (cardiovascular mortality, SCD, new infarction, emergency revascularisation, and hospitalized heart failure) was the highest in late VT/VF group (p=0.000). The most significant predictor of late VT/VF was systolic LS (cut off −12.72%, ROC 0.680, Sen 71%, Sp 64%, p=0.006). Conclusions: Although late VT/VF occurrence after primary PCI were less frequent than early VT/VF occurrence, patients with late VT/VF had a very poor prognosis. The most power predictor of late VT/VF were systolic longitudinal strain. Funding Acknowledgement: Type of funding source: Public hospital(s). Main funding source(s): Clinical Center of Serbia