Left ventricular remodeling (LVR) after anterior ST-segment elevation myocardial infarction (STEMI) is associated with adverse cardiovascular outcomes. We aimed to determine whether detailed electrocardiographic (ECG) features provide incremental predictive value beyond clinical characteristics for LVR after anterior STEMI. We retrospectively analyzed 1079 patients with anterior STEMI, including a derivation cohort of 831 patients (training, n = 665; internal validation, n = 166) and a temporal internal validation cohort of 248 patients. An exploratory cohort of 730 patients with non-anterior STEMI was also included. LVR was defined as a ≥20% increase in left ventricular end-diastolic volume from baseline to 6 months. After feature selection, two extreme gradient boosting models were constructed for risk prediction at hospital discharge: Model 1 included three clinical predictors, whereas Model 2 additionally included eight ECG features. No ECG features were retained in the exploratory non-anterior STEMI analysis. Model 2 had a higher area under the receiver operating characteristic curve (AUC) than Model 1 in both the internal validation cohort (0.869 vs. 0.787; p = 0.039) and the temporal validation cohort (0.792 vs. 0.638; p = 0.001). Model 2 also showed greater estimated net benefit in decision curve analysis and improved risk reclassification. Detailed ECG features may provide additional prognostic information beyond the clinical predictors examined in this study. The web-based calculator is intended for research use only, pending external validation.
Regular physical activity (PA) is strongly associated with cardiovascular health; however, its associations with cardiovascular function may differ according to the domain, intensity, and context in which it is performed. This exploratory cross-sectional study investigated associations between domain- and intensity-specific PA and heart rate (HR) responses to standardized exercise in 605 adults from northeastern Hungary. Participants had a mean age of 42.50 ± 12.23 years, 65.5% were women, and 60.7% were overweight or obese. PA was assessed using the long-form IPAQ, and HR responses were evaluated using the YMCA 3 min step test. Multiple linear regression models were adjusted for demographic, clinical, behavioural, and socioeconomic covariates, with genetic scores examined in sensitivity analyses. Higher total PA was associated with lower ΔHR, HRaft, and HRmax% (standardized β = −0.222 to −0.207; all q < 0.001). Moderate-intensity PA showed the strongest intensity-specific associations (β = −0.237 to −0.223; all q < 0.001), whereas vigorous PA was associated only with ΔHR after FDR correction, and walking PA showed no significant associations. In the mutually adjusted domain model, leisure-time and domestic/gardening PA were each associated with lower values of all three principal HR outcomes, whereas work- and transport-related PA were not. Exploratory activity-specific associations for cycling, vigorous gardening, and moderate leisure-time PA did not remain significant after FDR correction. These exploratory findings suggest that the intensity and domain composition of habitual PA may be relevant to its associations with post-exercise HR measures and warrant further investigation in independent studies.
Immune checkpoint inhibitor-associated myocarditis (ICI-AM) is rare but potentially fatal. We retrospectively reviewed pre-existing clinical records of 42 patients diagnosed with ICI-AM at Renmin Hospital of Wuhan University between October 2023 and March 2025 and classified them as mild (grade 1–2, n = 29) or severe (grade 3–4, n = 13). Baseline characteristics, electrocardiographic findings, biomarkers, treatment patterns, and clinical outcomes were summarized descriptively. Follow-up information was retrospectively obtained from available clinical records, with an administrative follow-up end date of 31 January 2026. Severe ICI-AM was characterized by more frequent dyspnea, concomitant myasthenia gravis, electrocardiographic abnormalities, and higher troponin, CK-MB, and myoglobin levels, together with more frequent corticosteroid, intravenous immunoglobulin, and additional immunosuppressive treatment. Concomitant myositis was also more frequently observed in severe cases. During follow-up, 13 patients (31.0%) died, including 6 of 13 (46.2%) patients with severe ICI-AM and 7 of 29 (24.1%) with mild ICI-AM. Severe ICI-AM showed a more clinically overt phenotype, frequent neuromuscular involvement, and substantial all-cause mortality. These descriptive findings highlight the clinical heterogeneity of ICI-AM and require further investigation in larger prospective multicenter studies.
Acute myocarditis encompasses a broad clinical spectrum, ranging from mild chest pain with preserved ventricular function to fulminant heart failure, malignant ventricular arrhythmias, cardiogenic shock and sudden cardiac death. Recent advances have shifted its definition from a primarily histopathological entity toward an integrated clinical syndrome in which multimodality imaging, biomarkers and endomyocardial biopsy contribute to diagnosis and risk assessment. Cardiac magnetic resonance has become central to non-invasive tissue characterization while endomyocardial biopsy remains a relevant approach in high-risk or treatment-refractory patients, allowing identification of histological subtypes that may require specific therapy. Management is largely determined by clinical severity and aetiology, ranging from supportive care and guideline-directed heart failure therapy to immunosuppression, targeted antimicrobial treatment and temporary mechanical circulatory support in fulminant cases. Increasing evidence also highlights the relationship between myocarditis-like episodes and inherited cardiomyopathies, particularly desmosomal disease, in which recurrent “hot phases” may represent an early manifestation of a genetic substrate. Based on a structured literature search, this narrative review summarizes current concepts in the classification, diagnosis, complications and management of acute myocarditis with particular emphasis on heart failure and fulminant presentations, risk stratification and genetic susceptibility. Throughout the text, established treatments are kept separate from emerging mechanism-based strategies, which are still supported by limited evidence.
Background: STMN1 regulates microtubule dynamics, cytoskeletal remodeling, and cell migration, but its role in atherosclerosis remains unclear. Methods: eQTL-based two-sample Mendelian randomization was used to assess associations between genetically predicted STMN1 expression and coronary or cerebral atherosclerosis. Functional validation was performed in high-cholesterol diet-fed ApoE−/− mice with AAV9-mediated STMN1 knockdown and in ox-LDL-treated mouse aortic smooth muscle cells with siRNA-mediated STMN1 silencing. Virtual screening was conducted to identify candidate STMN1-binding compounds. Results: Higher genetically predicted STMN1 expression was associated with increased risk of both coronary and cerebral atherosclerosis. In vivo, STMN1 knockdown reduced aortic lesion burden, plaque lipid deposition, plaque area, and inflammatory cytokine expression, while increasing collagen content without significantly altering serum lipid levels. In vitro, STMN1 silencing suppressed ox-LDL-induced inflammation, migration, and MMP2/MMP9 expression. R428 was identified as the top-ranked candidate compound. Conclusions: STMN1 may promote atherosclerosis by regulating vascular inflammation, smooth muscle cell migration, and matrix remodeling.
