Search Results (832)

Hereditary ataxias are a highly heterogenous group of diseases characterized by loss of coordination. In this study, we investigated a family of random-bred dogs, in which two siblings were affected by a slowly progressive ataxia. They presented with clinical signs of progressive cerebellar ataxia, hypermetria, and absent menace response. The MRI revealed generalized brain atrophy, reduced cortical demarcation, hypoplastic corpus callosum, and cerebellar folia thinning, highly suggestive of a neurodegenerative disorder. We sequenced the genomes of the two affected dogs and their unaffected parents. Filtering for protein-changing variants that had homozygous alternate genotypes in the affected dogs, heterozygous genotypes in the parents, and homozygous reference genotypes in 1576 control genomes yielded a single missense variant in the RAB24 gene, XM_038534663.1:c.239G>T or XP_038390591.1:p.(Gly80Val). Genotypes at this variant showed the expected co-segregation with the ataxia phenotype in the investigated family. The predicted amino acid affects the conserved RabF4 motif. Glycine-80 resides at the protein surface and the introduction of a hydrophobic isopropyl side chain of the mutant valine might impede solvent accessibility. Another missense variant in RAB24, p.Glu38Pro, was previously reported to cause a clinically similar form of cerebellar ataxia in Gordon Setters and Old English Sheepdogs. Taken together, the available data suggest that RAB24:p.Gly80Val represents the causal variant in the studied dogs. To the best of our knowledge, this is only the second report of a potentially pathogenic RAB24 variant in any species and further supports that RAB24 should be considered a candidate gene in human ataxia patients with unclear molecular etiology. Full article

In this report of two cases, we describe two patients with spinal involvement of gout. The first case involved a 67-year-old female who presented to the emergency department with a one-week history of weakness in both the upper and lower limbs, despite no prior history of gout. Cervical spine MRI revealed spinal cord compression at the C4 level from a posterior lesion. During surgery, chalky white deposits consistent with gouty tophi were observed in the ligamentum flavum within the epidural space at C4. These intraoperative findings correlated with elevated serum uric acid levels. The second case concerned a 68-year-old male who presented with a five-day history of right lower limb pain along with bilateral knee discomfort. Radiologic and laboratory evaluations revealed elevated inflammatory markers, negatively birefringent crystals in knee joint aspirate, spondylodiscitis at the L5-S1 level, and a right-sided synovial cyst at the T10–T11 level causing spinal cord compression. Following the initiation of anti-gout therapy, the patient experienced significant clinical improvement, normalization of inflammatory markers, and radiologic resolution of the thoracic synovial cyst. Full article

Introduction: Breast density is a well-recognized factor in breast cancer risk assessment, with higher density linked to increased malignancy risk and reduced sensitivity of conventional mammography. Background parenchymal enhancement (BPE), observed in contrast-enhanced imaging, reflects physiological contrast uptake in non-pathologic breast tissue. While extensively characterized in breast MRI, the role of BPE in contrast-enhanced mammography (CEM) remains uncertain due to inconsistent findings regarding its correlation with breast density and cancer risk. Unlike breast density—standardized through the ACR BI-RADS lexicon—BPE lacks a uniform classification system in CEM, leading to variability in clinical interpretation and research outcomes. To address this gap, we introduce the BPE-CEM Standard Scale (BCSS), a structured four-tiered classification system specifically tailored to the two-dimensional characteristics of CEM, aiming to improve consistency and diagnostic alignment in BPE evaluation. Materials and Methods: In this retrospective single-center study, 213 patients who underwent mammography (MG), ultrasound (US), and contrast-enhanced mammography (CEM) between May 2022 and June 2023 at the “A. Perrino” Hospital in Brindisi were included. Breast density was classified according to ACR BI-RADS (categories A–D). BPE was categorized into four levels: Minimal (< 10% enhancement), Light (10–25%), Moderate (25–50%), and Marked (> 50%). Three radiologists independently assessed BPE in a subset of 50 randomly selected cases to evaluate inter-observer agreement using Cohen’s kappa. Correlations between BPE, breast density, and age were examined through regression analysis. Results: BPE was Minimal in 57% of patients, Light in 31%, Moderate in 10%, and Marked in 2%. A significant positive association was found between higher breast density (BI-RADS C–D) and increased BPE (p < 0.05), whereas lower-density breasts (A–B) were predominantly associated with minimal or light BPE. Regression analysis confirmed a modest but statistically significant association between breast density and BPE (R² = 0.144), while age showed no significant effect. Inter-observer agreement for BPE categorization using the BCSS was excellent (κ = 0.85; 95% CI: 0.78–0.92), supporting its reproducibility. Conclusions: Our findings indicate that breast density is a key determinant of BPE in CEM. The proposed BCSS offers a reproducible, four-level framework for standardized BPE assessment tailored to the imaging characteristics of CEM. By reducing variability in interpretation, the BCSS has the potential to improve diagnostic consistency and facilitate integration of BPE into personalized breast cancer risk models. Further prospective multicenter studies are needed to validate this classification and assess its clinical impact. Full article

Background: Spectrin proteins are critical cytoskeleton components that maintain cellular structure and mediate intracellular transport. Pathogenic variants in SPTBN1, encoding βII-spectrin, have been associated with various neurodevelopmental disorders, including developmental delay, intellectual disability, autism spectrum disorder, and epilepsy. Here we report a Korean infant with infantile epileptic spasms syndrome (IESS) and an SPTBN1 mutation and provide a review of this mutation. Methods: The genomic data of the patient were analyzed by whole exome sequencing. A comprehensive literature review was conducted to identify and analyze all reported SPTBN1 variants, resulting in a dataset of 60 unique mutations associated with neurodevelopmental phenotypes. Case Presentation: A 10-month-old Korean female presented with IESS associated with a de novo heterozygous SPTBN1 mutation (c.785A>T; p.Asp262Val). The patient exhibited global developmental delay, microcephaly, hypotonia, spasticity, and MRI findings of diffuse cerebral atrophy and corpus callosum hypoplasia. Electroencephalography revealed hypsarrhythmia, confirming the diagnosis of IESS. Seizures persisted despite initial treatment with vigabatrin and steroids. Genetic analysis identified a likely pathogenic variant within the calponin homology 2 (CH2) domain of SPTBN1. Conclusions: This is the first report of an association between IESS and an SPTBN1 CH2 domain mutation in a Korean infant. This finding expands the clinical spectrum of SPTBN1-related disorders and suggests domain-specific effects may critically influence phenotypic severity. Further functional studies are warranted to elucidate the pathogenic mechanisms of domain-specific variants. Full article

Pathogenic variants in the MAP1B gene have been associated with neurological impairment, including intellectual disability, attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder, brain malformations, cognitive hearing loss, short stature, and dysmorphic features. However, few cases with detailed clinical characterization have been reported. We describe a 12-year-old boy carrying a loss-of-function MAP1B variant, presenting with severe elimination disorders despite normal intelligence. He was referred to the genetics service due to persistent elimination issues, including daytime urinary incontinence, nocturnal enuresis, and fecal incontinence. He had normal motor and cognitive development, with an IQ of 99; however, he also presented with ADHD, short stature, microcephaly, and myopia. Brain MRI revealed bilaterial subependymal periventricular nodular heterotopia (PVNH). Audiometry showed normal bilateral hearing. Testing fragile X syndrome (FXS) and karyotype analyses yielded normal results. Whole exome sequencing (WES) revealed a nonsense pathogenic variant in MAP1B (c.895 C>T; p.Arg299*). No other family members showed a similar phenotype; however, a great-uncle and a great-aunt had a history of nocturnal enuresis until age 10. The patient’s deceased mother had short stature and psychiatric disorders, and a history of consanguinity was reported on the maternal side. This case broadens the phenotypic spectrum associated with MAP1B syndrome, suggesting that elimination disorder, frequently reported in FXS, should also be evaluated in MAP1B pathogenic variant carriers. In addition, the presence of short stature also appears to be part of the syndrome. Full article

Background/Objectives: Elevated troponin levels are widely recognized as key biomarkers of myocardial injury and are frequently used in clinical decision making. However, not all instances of troponin elevation indicate true cardiac damage. In some cases, biochemical or immunological interferences may lead to false-positive results. These situations may lead to unnecessary diagnostic interventions and clinical uncertainty, ultimately impacting patient management negatively. This study aims to investigate the underlying mechanisms of false-positive troponin elevation in pediatric patients, focusing on factors such as macrotroponin formation, autoantibodies, and heterophile antibody interference. Methods: This retrospective study analyzed data from 13 pediatric patients who presented with elevated cardiac troponin levels between 2017 and 2024. Clinical evaluations included transthoracic echocardiography (TTE), electrocardiography (ECG), coronary computed tomography angiography (CTA), cardiac magnetic resonance imaging (MRI), and rheumatologic testing. Laboratory findings included measurements of cardiac troponins (cTnI and hs-cTnT) and pro-BNP levels. Results: Among 70 patients evaluated for elevated troponin levels, 13 (18.6%) were determined to have no identifiable cardiac etiology. The median age of these 13 patients was 13.0 years (range: 9–16), with 53.8% being female. The most common presenting complaints were chest pain (53.8%) and palpitations (30.8%). TTE findings were normal in 61.5% of the patients, and all patients had normal coronary CTA and cardiac MRI findings. Although initial troponin I levels were elevated in all cases, persistent positivity was observed up to 12 months. Median cTnI levels were 1.00 ng/mL (range: 0.33–7.19) at week 1 and 0.731 ng/mL (range: 0.175–4.56) at month 12. PEG precipitation testing identified macrotroponin in three patients (23.1%). No etiological explanation could be identified in 10 cases (76.9%), which were considered idiopathic. All patients had negative results for heterophile antibody and rheumatologic tests. Conclusions: When interpreting elevated troponin levels in children, biochemical interferences—especially macrotroponin—should not be overlooked. This study emphasizes the diagnostic uncertainty associated with non-cardiac troponin elevation. To better guide clinical practice and clarify false positivity rates, larger, multicenter prospective studies are needed. Full article

Background: Potent androgen receptor pathway inhibitors induce small cell neuroendocrine prostate cancer (SCNC), a highly aggressive subtype of metastatic androgen deprivation-resistant prostate cancer (ARPC) with limited treatment options and poor survival rates. Patients with metastases in the liver have a poor prognosis relative to those with bone metastases alone. The mechanisms that underlie the different behavior of ARPC in bone vs. liver may involve factors intrinsic to the tumor cell, tumor microenvironment, and/or systemic factors, and identifying these factors is critical to improved diagnosis and treatment of SCNC. Metabolic reprogramming is a fundamental strategy of tumor cells to colonize and proliferate in microenvironments distinct from the primary site. Understanding the metabolic plasticity of cancer cells may reveal novel approaches to imaging and treating metastases more effectively. Methods: Using magnetic resonance (MR) imaging and spectroscopy, we interrogated the physiological and metabolic characteristics of SCNC patient-derived xenografts (PDXs) propagated in the bone and liver, and used correlative biochemical, immunohistochemical, and transcriptomic measures to understand the biological underpinnings of the observed imaging metrics. Results: We found that the influence of the microenvironment on physiologic measures using MRI was variable among PDXs. However, the MR measure of glycolytic capacity in the liver using hyperpolarized ¹³C pyruvic acid recapitulated the enzyme activity (lactate dehydrogenase), cofactor (nicotinamide adenine dinucleotide), and stable isotope measures of fractional enrichment of lactate. While in the bone, the congruence of the glycolytic components was lost and potentially weighted by the interaction of cancer cells with osteoclasts/osteoblasts. Conclusion: While there was little impact of microenvironmental factors on metabolism, the physiological measures (cellularity and perfusion) are highly variable and necessitate the use of combined hyperpolarized ¹³C MRI and multiparametric (anatomic, diffusion-, and perfusion- weighted) ¹H MRI to better characterize pre-treatment tumor characteristics, which will be crucial to evaluate treatment response. Full article

Background and Clinical Significance: Tuberous sclerosis complex (TSC) is an autosomal dominant disorder caused by pathogenic variants in TSC1 or TSC2. Cardiac rhabdomyoma is a common prenatal finding and can be associated with severe complications, including pericardial effusion. We administered prenatal sirolimus to mitigate pericardial effusion, which led to postnatal complications. Case Presentation: A 28-year-old pregnant woman with no significant family history underwent routine fetal ultrasound at 28.1 weeks of gestation, which identified a large right ventricular mass consistent with rhabdomyoma. Further fetal brain MRI revealed cortical-subcortical tubers and subependymal nodules, leading to a clinical diagnosis of TSC. At 30.4 weeks, oral sirolimus (3 mg/day) was started due to the significant pericardial effusion. The effusion remained after treatment, requiring pericardiocentesis at 33.6 weeks. The sirolimus dosage was raised to 6 mg/day at 35.6 weeks, reaching a plasma level of 3.76 ng/mL, but there was no discernible improvement because of the continued fluid accumulation. The mother did not experience any adverse side effects from the procedure. Genetic testing confirmed a pathogenic variant in TSC2 (c.1372C>T). After birth, the neonate received a single dose of sirolimus but subsequently developed necrotizing enterocolitis (NEC), highlighting the potential adverse effects and the need for cautious consideration of treatment options. Conclusions: This case illustrates the complexities of managing prenatal tuberous sclerosis complex (TSC). While sirolimus has been explored for fetal cardiac rhabdomyoma and associated complications, its effectiveness in resolving pericardial effusion remains uncertain. Additionally, the development of NEC postnatally raises concerns about the safety of mTOR inhibitors in this context. Further studies are necessary to assess the risks and benefits of this approach in fetal therapy. Full article

Blood–brain barrier (BBB) dysfunction is a hallmark of cerebral small vessel disease (cSVD). This study aimed to identify a mouse model that replicates BBB impairment and shares key cSVD risk factors. Transgenic db/db and LDLr^−/−.Leiden mice, both prone to obesity and hypertension, were compared to C57BL/6J controls. BBB leakage was assessed using DCE-MRI and sodium fluorescein (NaFl); cerebral blood flow (CBF) by MRI. Dyslipidemia and vascular inflammation were measured by plasma tests. Tight junction integrity, endothelial dysfunction (glucose transporter 1, GLUT-1) and neuroinflammation were evaluated with immunohistochemistry and PCR. Both transgenic models developed an obese phenotype with hyperinsulinemia, but only LDLr^−/−.Leiden mice showed human-like dyslipidemia. When fed a high-fat diet (HFD) or HFD plus cholesterol, LDLr^−/−.Leiden mice showed reduced CBF, endothelial dysfunction (lowered GLUT-1), elevated vascular inflammation (ICAM-1, VCAM-1, S-selectin), and BBB leakage, as evidenced by DCE-MRI and NaFl, together with reduced ZO-1 and claudin-5 expression. Contrastingly, db/db mice showed endothelial dysfunction without BBB leakage. Neuroinflammation (IBA-1, GFAP) was observed only in LDLr^−/−.Leiden groups, consistent with BBB disruption. These findings indicate that LDLr^−/−.Leiden mice, but not db/db mice, are a promising translational model for studying BBB dysfunction in cSVD, offering insights into disease mechanisms and a platform for therapeutic development. Full article

Background/Objectives: Congenital cytomegalovirus (cCMV) infection is the most common non-genetic cause of sensorineural hearing loss (SNHL) in children. In cases of severe-to-profound SNHL, cochlear implantation (CI) is a widely used intervention, but outcomes remain variable due to possible neurodevelopmental comorbidities. This study aimed to evaluate the long-term auditory and language outcomes in children with cCMV after CI and to explore clinical and radiological predictors of post-CI performance. Methods: Fifty-three children with cCMV and bilateral severe-to-profound SNHL who underwent CI at five tertiary referral centers in Italy were included in the study. Auditory and language outcomes were assessed pre- and post-implantation using the Categories of Auditory Performance II (CAP-II) scale, the Nottingham 3-Level Classification, and the Bates Language Development Scale. Brain MRI abnormalities were classified according to the Alarcón classification. Correlations were explored between outcome scores and symptomatic status at birth, MRI findings, and neurodevelopmental comorbidities. Results: At birth, 40 children (75.5%) were symptomatic and 13 (24.5%) asymptomatic. Neurodevelopmental comorbidities were present in 19 children (35.8%). MRI was normal in 15 (28.3%), mildly abnormal in 26 (49%), and moderately to severely abnormal in 12 (22.6%). Auditory and language outcomes improved significantly post-CI (p < 0.001), though the outcomes varied widely. Twenty-five children (47%) reached CAP level ≥ 6, and thirteen (23%) reached Bates Level 6. Symptomatic status at birth correlated weakly with worse CAP (ρ = −0.291, p = 0.038) and Bates (ρ = −0.310, p = 0.028) scores. Higher Alarcón scores were significantly associated with neurodevelopmental comorbidities, though not directly with post-CI auditory and language outcomes. Finally, the presence of neurodevelopmental disabilities was generally associated with lower results, even if without statistical significance. Conclusions: CI provides substantial auditory and language benefit in children with cCMV, even in cases of severe neurodevelopmental comorbidities. MRI and developmental assessments, as well as perinatal history for clinical signs and symptoms, are helpful in guiding expectations and personalizing post-implantation support. Full article

Background: Most of the existing hyperpolarized (HP) ¹³C MRI analyses use univariate rate maps of pyruvate-to-lactate conversion (k_PL), and radiomic-style multiparametric models extracting complex, higher-order features remain unexplored. Purpose: To establish a multivariate framework based on whole abdomen/pelvis HP ¹³C-pyruvate MRI and evaluate the association between multiparametric features of metabolism (MFM) and clinical outcome measures in advanced and metastatic prostate cancer. Methods: Retrospective statistical analysis was performed on 16 participants with metastatic or local-regionally advanced prostate cancer prospectively enrolled in a tertiary center who underwent HP-pyruvate MRI of abdomen or pelvis between November 2020 and May 2023. Five patients were hormone-sensitive and eleven were castration-resistant. GMP-grade [1-¹³C]pyruvate was polarized using a 5T clinical-research DNP polarizer, and HP MRI used a set of flexible vest-transmit, array-receive coils, and echo-planar imaging sequences. Three basic metabolic maps (k_PL, pyruvate summed-over-time, and mean pyruvate time) were created by semi-automatic segmentation, from which 316 MFMs were extracted using an open-source, radiomic-compliant software package. Univariate risk classifier was constructed using a biologically meaningful feature (k_PL,median), and the multivariate classifier used a two-step feature selection process (ranking and clustering). Both were correlated with progression-free survival (PFS) and overall survival (OS) (median follow-up = 22.0 months) using Cox proportional hazards model. Results: In the univariate analysis, patients harboring tumors with lower-k_PL,median had longer PFS (11.2 vs. 0.5 months, p < 0.01) and OS (NR vs. 18.4 months, p < 0.05) than their higher-k_PL,median counterparts. Using a hypothesis-generating, age-adjusted multivariate risk classifier, the lower-risk subgroup also had longer PFS (NR vs. 2.4 months, p < 0.002) and OS (NR vs. 18.4 months, p < 0.05). By contrast, established laboratory markers, including PSA, lactate dehydrogenase, and alkaline phosphatase, were not significantly associated with PFS or OS (p > 0.05). Key limitations of this study include small sample size, retrospective study design, and referral bias. Conclusions: Risk classifiers derived from select multiparametric HP features were significantly associated with clinically meaningful outcome measures in this small, heterogeneous patient cohort, strongly supporting further investigation into their prognostic values. Full article

Background: Delay in diagnosing metastatic epidural spinal cord compression (MESCC) adversely impacts clinical outcomes. High-grade MESCC is frequently overlooked on routine staging CT scans. We aim to assess the potential of our deep learning model (DLM) in detecting high-grade MESCC and reducing diagnostic delays. Methods: This retrospective review analyzed 140 patients with surgically treated MESCC between C7 and L2 during 2015–2022. An experienced radiologist (serving as the reference standard), a consultant spine surgeon, and the DLM independently classified staging CT scans into high-grade MESCC or not. The findings were compared to original radiologist (OR) reports; inter-rater agreement was assessed. Diagnostic delay referred to the number of days elapsed from CT to diagnostic MRI scan. Results: Overall, 95/140 (67.8%) patients had preoperative CT scans. High-grade MESCC was identified in 84/95 (88.4%) of the scans by the radiologist (reference standard), but in only 32/95 (33.7%) of the preoperative scans reported by the OR. There was almost perfect agreement between the radiologist and the surgeon (kappa = 0.947, 95% CI = 0.893–1.000) (p < 0.001), and between the radiologist and the DLM (kappa = 0.891, 95% CI = 0.816–0.967) (p < 0.001). In contrast, inter-observer agreement between the OR and all other readers was slight (kappa range = 0.022–0.125). Diagnostic delay was potentially reduced by 20 ± 28 (range = 1–131) days. Conclusions: The original radiologist reports frequently missed high-grade MESCC in staging CT. Our DLM for CT diagnosis of high-grade MESCC showed almost perfect inter-rater agreement with two experienced reviewers. This study is the first to demonstrate that the DLM could help reduce diagnostic delays. Further prospective research is required to understand its precise role in improving the early diagnosis/treatment of MESCC. Full article

Musculoskeletal (MSK) disorders remain a major global cause of disability, with diagnostic complexity arising from their heterogeneous presentation and multifactorial pathophysiology. Recent advances across imaging modalities, molecular biomarkers, artificial intelligence applications, and point-of-care technologies are fundamentally reshaping musculoskeletal diagnostics. This review offers a novel synthesis by unifying recent innovations across multiple diagnostic imaging modalities, such as CT, MRI, and ultrasound, with emerging biochemical, genetic, and digital technologies. While existing reviews typically focus on advances within a single modality or for specific MSK conditions, this paper integrates a broad spectrum of developments to highlight how use of multimodal diagnostic strategies in combination can improve disease detection, stratification, and clinical decision-making in real-world settings. Technological developments in imaging, including photon-counting detector computed tomography, quantitative magnetic resonance imaging, and four-dimensional computed tomography, have enhanced the ability to visualize structural and dynamic musculoskeletal abnormalities with greater precision. Molecular imaging and biochemical markers such as CTX-II (C-terminal cross-linked telopeptides of type II collagen) and PINP (procollagen type I N-propeptide) provide early, objective indicators of tissue degeneration and bone turnover, while genetic and epigenetic profiling can elucidate individual patterns of susceptibility. Point-of-care ultrasound and portable diagnostic devices have expanded real-time imaging and functional assessment capabilities across diverse clinical settings. Artificial intelligence and machine learning algorithms now automate image interpretation, predict clinical outcomes, and enhance clinical decision support, complementing conventional clinical evaluations. Wearable sensors and mobile health technologies extend continuous monitoring beyond traditional healthcare environments, generating real-world data critical for dynamic disease management. However, standardization of diagnostic protocols, rigorous validation of novel methodologies, and thoughtful integration of multimodal data remain essential for translating technological advances into improved patient outcomes. Despite these advances, several key limitations constrain widespread clinical adoption. Imaging modalities lack standardized acquisition protocols and reference values, making cross-site comparison and clinical interpretation difficult. AI-driven diagnostic tools often suffer from limited external validation and transparency (“black-box” models), impacting clinicians’ trust and hindering regulatory approval. Molecular markers like CTX-II and PINP, though promising, show variability due to diurnal fluctuations and comorbid conditions, complicating their use in routine monitoring. Integration of multimodal data, especially across imaging, omics, and wearable devices, remains technically and logistically complex, requiring robust data infrastructure and informatics expertise not yet widely available in MSK clinical practice. Furthermore, reimbursement models have not caught up with many of these innovations, limiting access in resource-constrained healthcare settings. As these fields converge, musculoskeletal diagnostics methods are poised to evolve into a more precise, personalized, and patient-centered discipline, driving meaningful improvements in musculoskeletal health worldwide. Full article

Summary: COVID-19, caused by SARS-CoV-2, has been associated with a range of cardiovascular complications, including myocarditis. This review aims to systematically present the clinical manifestations, underlying pathophysiological mechanisms, diagnostic approaches, and management strategies for both COVID-19-associated myocarditis and myocarditis related to SARS-CoV-2 vaccination. We conducted a literature search using the PubMed database, covering studies published up to early 2024. Search terms included combinations of “COVID-19”, “Coronavirus”, “SARS-CoV-2”, and/or “vaccination” with “cardiac injury”, “cardiac inflammation”, “myocarditis”. The reported prevalence of COVID-19-associated myocarditis varies between 2.3% and 5.0%, though myocardial injury is more frequently observed than confirmed myocarditis. Pathophysiological mechanisms include direct viral damage, immune-mediated injury, and molecular mimicry. Clinically, patients may present with chest pain, dyspnea, and fever. Diagnostic workup includes electrocardiography (ECG), troponin measurement, echocardiography, cardiac magnetic resonance imaging (cMRI), and in selected cases, endomyocardial biopsy (EMB). The management and disposition of COVID-19-associated myocarditis varies according to severity, especially to allow targeted treatment of complications. Glucocorticoids are a mainstay of treatment in severe cases. Myocarditis following SARS-CoV-2 vaccination is rare, more frequently reported in males under 30 years, and is generally associated with a favorable prognosis. Despite this, the benefits of vaccination continue to outweigh the risks. COVID-19 is associated with an increased risk of heart failure and other cardiovascular complications, underlining the importance of long-term follow-up and preventive strategies. Further research is needed to better understand the pathogenesis and optimal management of myocarditis in the context of COVID-19, with the goal of developing evidence-based therapeutic algorithms. Full article