Search Results (1,015)

Background: Pulmonary hypertension (PH) is associated with increased pulmonary arterial pressure and impairment of right ventricular (RV) function. Reliable characterization of RV performance is important for prognosis, risk assessment, and therapeutic planning. Cardiac magnetic resonance (CMR) is considered the reference technique for quantifying RV volumes and function, but its expense and limited availability can restrict routine implementation. Echocardiography is more widely accessible; however, the extent to which individual echocardiographic indices correspond with CMR-derived RV ejection fraction (RVEF) remains incompletely defined. Objective: Our objective was to determine the correlation of RV fractional area change (RV-FAC), RV free-wall longitudinal strain (RV-FWLS), and RV global longitudinal strain (RV-GLS) with CMR-derived RVEF in individuals with PH. Methods: PubMed, Embase, ClinicalTrials.gov, Scopus, and the Cochrane Library were searched, yielding 404 records; six studies fulfilled the eligibility criteria. Studies were eligible when they enrolled patients with PH and provided extractable correlations between at least one prespecified echocardiographic measure and CMR-derived RVEF. Correlation coefficients were converted with Fisher’s z transformation, combined using common-effect and random-effects approaches, and then transformed back to correlation coefficients. Pooled mean RV-FAC was evaluated as a separate outcome. Between-study heterogeneity was quantified with I² and τ², with random-effects estimates emphasized for interpretation. Results: Each evaluated echocardiographic measure was positively correlated with CMR-derived RVEF. RV-FWLS had the largest pooled correlation and the greatest consistency (r = 0.79, 95% CI: 0.73–0.83; I² = 0.0%). The pooled correlation for RV-GLS was 0.75 (95% CI: 0.60–0.85; I² = 80.3%), while that for RV-FAC was 0.72 (95% CI: 0.61–0.80; I² = 61.8%). The random-effects pooled mean RV-FAC was 31.10% (95% CI: 26.77–35.43), with substantial heterogeneity (I² = 90.9%). Conclusions: RV-FWLS showed the highest numerical and most consistent association with CMR-derived RVEF, suggesting that it may serve as a useful non-invasive adjunct for RV assessment in PH, especially where CMR is not readily available. Larger studies using harmonized acquisition and analysis methods are required for confirmation. Full article

Background/Objectives: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is an established heart failure biomarker, but its associations with cardiac magnetic resonance (CMR) parameters in patients with reduced ejection fraction remain unclear. This study examined the associations between serum NT-proBNP concentrations and CMR-derived functional, structural, and tissue characterization parameters in patients with HFrEF and evaluated which imaging parameters remained associated with NT-proBNP after multivariable adjustment. Methods: This retrospective single-center study included 92 consecutive patients with HFrEF who underwent CMR and NT-proBNP measurement within a 24 h window, with a median absolute interval of 6 h (range, 1–15 h) between the two assessments. CMR analysis included left ventricular ejection fraction (LVEF), left ventricular and left atrial (LA) cavity diameters, myocardial mass, extracellular volume fraction (ECV), the late gadolinium enhancement (LGE) burden, and the T2 signal intensity (T2-SI) ratio. Spearman correlation, univariate linear regression, and multivariable linear regression analyses were performed using log-transformed NT-proBNP values. Results: Log NT-proBNP demonstrated significant correlations with LVEF (r_s = −0.359, p < 0.001), T2-SI ratio (r_s = −0.332, p = 0.001), ECV (r_s = 0.383, p < 0.001), and LA diameter (r_s = 0.347, p < 0.001). No statistically significant correlations were observed between log-transformed NT-proBNP and LGE burden, LV cavity diameter, myocardial mass, LV wall thickness, age, or the recorded comorbidities. In multivariable analysis, LVEF, T2-SI ratio, and LA diameter remained associated with NT-proBNP after adjustment for the available covariates. Conclusions: Lower LVEF, a lower T2-SI ratio, and a larger LA diameter were associated with higher NT-proBNP levels in patients with HFrEF. The T2-SI ratio and LA diameter should be considered exploratory imaging markers requiring prospective validation. Full article

Objectives: The presence of a bicuspid aortic valve (BAV) is known to alter transvalvular flow and increase shear stress on the ascending aorta, contributing to alterations in aortic geometry and the progression of BAV-related aortopathy. The purpose of the current study was to characterize aortic flow abnormalities and their associations with aortic geometry and ventricular mechanics using cardiac magnetic resonance imaging (CMR). Methods: In this prospective cross-sectional study, 56 young adults with CMR-confirmed BAV and 56 age- and sex-matched healthy volunteers underwent standardized CMR. Biventricular volumes and function, LV global longitudinal strain (LV-GLS), LV torsional mechanics, ascending aortic geometry, pulse-wave velocity, aortic distensibility, and two-dimensional phase-contrast-derived forward and backward flow parameters were quantified. Associations between myocardial mechanics and haemodynamic variables were assessed using correlation analyses and multivariable linear regression. Results: Compared with healthy controls, patients with BAV exhibited preserved LV ejection fraction but impaired LV-GLS, reduced LV torsion, increased aortic stiffness, and a significantly greater backward-flow burden despite similar net aortic flow (all p < 0.001). Higher peak backward-to-forward flow-rate ratios were associated with less negative LV-GLS (p = 0.006), whereas greater aortic regurgitant volume was also associated with impaired longitudinal deformation (p = 0.001). In multivariable analysis, LV-GLS and aortic regurgitant volume remained associated with the peak backward-to-forward flow-rate ratio within the specified model, whereas ascending-aortic dimensions were not. The final model explained 52% of the variability in backward-flow burden. Conclusions: CMR identified a subclinical ventricular-aortic phenotype in young adults with BAV characterized by altered LV mechanics, increased aortic stiffness, and greater relative backward-flow burden despite preserved conventional LV systolic function. The association between backward-flow burden and LV longitudinal mechanics suggests that these abnormalities may represent interrelated manifestations of BAV disease; however, their temporal and causal relationships cannot be established from this cross-sectional study. Full article

Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors, originally developed as glucose-lowering agents for type 2 diabetes mellitus, have been shown in large, randomized trials to improve clinical outcomes in heart failure (HF) across the ejection fraction (EF) spectrum. The imaging-derived and hemodynamic changes that accompany these benefits remain incompletely characterized, and it is not known whether the patterns of cardiac remodeling observed differ between HF with reduced ejection fraction (HFrEF, left ventricular ejection fraction [LVEF] ≤ 40%) and HF with preserved ejection fraction (HFpEF, LVEF ≥ 50%). This systematic review synthesized randomized evidence on the effects of SGLT2 inhibitors on cardiac remodeling parameters and described the patterns observed in each phenotype. Methods: PubMed/MEDLINE, Scopus and Embase were searched for randomized controlled trials (RCTs) published between February 2016 and March 2026. Eligible studies enrolled adults with chronic HF receiving an SGLT2 inhibitor, included a non-SGLT2-inhibitor comparator and assessed cardiac structure, function or loading by echocardiography, cardiac magnetic resonance (CMR) or cardiac catheterization over at least three months. Risk of bias was assessed with Cochrane RoB 2, separately for each outcome domain and targeting the effect of assignment to intervention, and certainty of evidence with GRADE, separately by phenotype and imaging modality. A structured narrative synthesis following Synthesis Without Meta-analysis (SWiM) guidance that prioritized the direction, magnitude and precision of randomized between-group treatment effects was performed. Results: Fourteen publications from thirteen unique RCTs (1232 participants) were included: four trials enrolled HFrEF (LVEF ≤ 40%), five enrolled mixed reduced and mildly reduced EF cohorts (LVEF < 50% or 35–49%), four enrolled HFpEF (LVEF ≥ 50%) and one enrolled a mixed ejection-fraction population. No trial enrolled an exclusively HFmrEF population. In reduced EF, the direction of effect on LV volumes favored SGLT2 inhibition in four of eight trials reporting volumes, but the estimates were not compatible in magnitude, and the one adequately powered trial at low risk of bias (EFFORT) was neutral; the largest volumetric estimates came from EMPA-TROPISM, which published no adjusted between-group estimate. The only prespecified, adjusted and confidence-interval-bearing volumetric estimates were those of SUGAR-DM-HF (left ventricular end-systolic volume index −6.0 mL/m², 95% CI −10.8 to −1.2; end-diastolic volume index −8.2 mL/m², 95% CI −13.7 to −2.6). The global longitudinal strain improved in the trial with blinded core-laboratory reading (EFFORT −1.44%, 95% CI −2.42 to −0.46), but effect sizes in the open-label trials without stated reader blinding were two to three times larger, and the CMR-derived strain was unchanged. In HFpEF, volumes, EF, mass and strain were unchanged throughout. The most secure finding of the review was invasive: in CAMEO-DAPA, dapagliflozin reduced pulmonary capillary wedge pressure at rest by 3.5 mmHg (95% CI −6.6 to −0.4) and at peak exercise by 5.7 mmHg (95% CI −10.8 to −0.7). NT-proBNP results were directionally inconsistent, and the trials in which NT-proBNP was a prespecified primary endpoint (Empire HF, CANDLE) were neutral. Certainty of evidence was very low for 18 of 20 evidence profiles and low for the remaining two. Conclusions: Randomized imaging and hemodynamic studies suggest phenotype-related differences in the cardiac remodeling associated with SGLT2 inhibitor therapy. In studies enrolling patients with reduced EF, treatment was associated predominantly with reverse remodeling of left ventricular volumes and modest improvements in myocardial function, whereas in preserved EF, the observed changes were mainly confined to filling pressures and diastolic function, with no consistent evidence of left ventricular volumetric remodeling. Given the limited number of studies, substantial heterogeneity, and the overall low certainty of evidence, these findings should be considered hypothesis-generating and warrant confirmation in adequately powered phenotype-specific mechanistic trials. Full article

Pulmonary hypertension (PH) is a heterogeneous clinical syndrome in which similar haemodynamic abnormalities may arise from distinct vascular, cardiac, pulmonary, thromboembolic, and molecular mechanisms. This complexity limits the ability of conventional classifications and risk scores to fully capture individual disease trajectories and treatment responses. Artificial intelligence (AI) offers a framework for integrating clinical data, electrocardiography, multimodal imaging, invasive haemodynamics, biomarkers, and multi-omics information across the PH care pathway. This review summarises current applications of machine learning and deep learning in early detection, diagnostic referral, right-ventricular and pulmonary vascular phenotyping, molecular endotyping, risk stratification, and therapeutic decision support. Available studies show promising results for AI-assisted electrocardiographic screening, automated echocardiographic and cardiac magnetic resonance analysis, computed tomography (CT)-based phenotyping, and multimodal prognostic modelling. True multi-omics integration in PH remains limited to discovery studies and has not yet yielded externally validated endotype or treatment-response classifiers. Evidence maturity is task-dependent: screening and phenotyping span several PH groups, whereas validated risk tools, molecular endotyping, and pathway-directed therapy remain predominantly PAH-based, particularly in idiopathic/heritable PAH. However, most evidence remains retrospective, derives from selected referral populations, and lacks robust external or prospective validation. No AI-based model currently supports routine drug selection or autonomous clinical decision-making. Future progress will require harmonised multicentre datasets and standardised acquisition protocols, transparent and interpretable models, and prospective studies demonstrating meaningful clinical benefit. AI should therefore be viewed as an emerging decision-support tool that may strengthen precision medicine in PH while complementing clinical expertise across diagnosis, phenotyping, risk assessment, and therapeutic stratification pathways. Full article

Background: Cardiac sarcoidosis (CS) is a potentially life-threatening manifestation of systemic granulomatous disease, characterized by a heterogeneous spectrum of arrhythmic and conduction disorders that represent the leading cause of CS-related sudden cardiac death (SCD). Clinical cardiac involvement is estimated at 5% of sarcoidosis patients, while silent myocardial infiltration is detected in 20–25% of autopsy series. Diagnosis is difficult because the disease frequently runs a subclinical course and no single test is pathognomonic. Methods: PubMed and Embase were searched to 5 August 2026 for this narrative review, incorporating peer-reviewed articles, international guidelines (HRS 2014, JCS 2016, AHA/ACC/HRS 2017, ESC 2022, AHA 2024, the 2024 European clinical consensus statement and the 2025 ESC guidelines on myocarditis and pericarditis), and registry data. Results: Atrioventricular (AV) block occurs in 23–30% of CS patients and frequently requires permanent pacing. Fatal ventricular arrhythmia rates reach 20.7% at 5 years and 31.9% at 10 years (ILLUMINATE-CS registry, n = 512). Late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) performs well diagnostically (pooled sensitivity 95%, specificity 85%) and is associated with an odds ratio of 10.74 for arrhythmic events. 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) provides complementary value for guiding immunosuppressive therapy and pre-ablation risk assessment. Implantable loop recorders enable early arrhythmia detection in patients not yet meeting implantable cardioverter-defibrillator (ICD) criteria. Conclusion: Optimal management of arrhythmias in CS requires a multimodal diagnostic approach integrating electrocardiography, advanced cardiac imaging, and continuous rhythm monitoring. Risk stratification for SCD remains the central challenge, requiring individualized decision-making that integrates left ventricular ejection fraction (LVEF), imaging biomarkers, and electrophysiological data. Future prospective studies should aim to refine predictive risk algorithms, assess the role of emerging immunomodulatory agents such as JAK/STAT inhibitors, and validate artificial intelligence (AI)-assisted tools intended to identify cardiac involvement and arrhythmic risk earlier in the disease course. Full article

Background: Myocardial infarction (MI) remains a leading cause of morbidity and mortality despite major advances in reperfusion and secondary prevention. Inflammation contributes throughout the MI continuum, from atherosclerotic plaque development and destabilization to myocardial injury, adverse ventricular remodeling, and recurrent cardiovascular events. Objective: This narrative review summarizes current evidence on inflammation across the MI continuum, focusing on inflammatory biomarkers, cardiovascular imaging, residual inflammatory risk, and emerging anti-inflammatory therapies. Methods: We reviewed current evidence on the pathophysiological and clinical relevance of inflammation in MI, with particular emphasis on circulating biomarkers, multimodality imaging, and inflammation-targeted therapeutic strategies. Results: High-sensitivity C-reactive protein remains the best-established biomarker of residual inflammatory risk, while interleukin-6, myeloperoxidase, suPAR, and GlycA provide complementary information. Advanced imaging, including coronary computed tomography-derived perivascular fat attenuation index, cardiac magnetic resonance, and positron emission tomography, may further characterize vascular and myocardial inflammation. Clinical trials support inflammation as a potentially modifiable component of cardiovascular risk; however, therapeutic benefit has been inconsistent across inflammatory targets, agents, and clinical settings. Canakinumab and low-dose colchicine have demonstrated cardiovascular benefit in selected secondary-prevention populations, although recent neutral trials highlight heterogeneity across clinical settings. Similarly, IL-6-targeted strategies have yielded mixed results, with the neutral ZEUS trial underscoring that biomarker reduction does not necessarily translate into cardiovascular benefit, while NLRP3-targeted approaches remain investigational. Conclusions: Integrating inflammatory biomarkers, multimodality imaging, and targeted therapies may improve risk stratification and support personalized secondary prevention. Further evidence is needed to define optimal patient selection and determine whether biomarker- or imaging-guided anti-inflammatory strategies improve clinical outcomes. Full article

Late gadolinium enhancement (LGE) cardiac magnetic resonance is the reference standard for non-invasive myocardial tissue characterization. Conventional LGE analysis focuses on the presence and extent of fibrosis, yet these measures incompletely describe the spatial complexity of myocardial scar that underpins arrhythmogenesis. Entropy, derived from radiomic analysis of LGE signal-intensity distributions, has emerged as a surrogate marker of myocardial tissue heterogeneity. Mechanistically, heterogeneous fibrosis promotes electrical conduction alterations, and entropy serves as a global descriptor of this complex substrate. A growing body of evidence suggests that higher LGE entropy is associated with increased arrhythmogenicity and major adverse cardiac events. Several studies have shown that this association remains significant after adjustment for conventional clinical and imaging predictors. A smaller number of studies have gone further, demonstrating that incorporation of LGE entropy improves the discriminatory or reclassification performance of established risk-prediction models. This narrative review critically synthesizes the current evidence on LGE-derived entropy, compares methodological approaches and clinical applications, and discusses its principal limitations. After standardization and prospective validation, entropy-based phenotyping may prove useful for individualized risk stratification beyond conventional LGE metrics and guide clinical decision-making. Full article

Background/Objectives: Idiopathic Carpal Tunnel Syndrome (CTS) can be an early manifestation of systemic amyloidosis, particularly transthyretin cardiac amyloidosis (ATTR-CA). The primary purpose of this retrospective case series was to describe the presence of amyloid deposits in tenosynovial tissue and explore potential cardiac involvement in patients undergoing carpal tunnel release surgery. Methods: From a cohort of 54 patients diagnosed with bilateral idiopathic CTS with surgical indication, 12 patients were selected for tenosynovial tissue samples, which were subsequently evaluated using Congo red staining and proteomic confirmation via mass spectrometry. Before the procedure, patients underwent a clinical assessment of medical history, electrocardiogram, and cardiac scintigraphy with Technetium-99 m 3,3-diphosphono-1,2-propanodicarboxylic acid (^99mTc-DPD). Transthoracic echocardiogram and cardiac magnetic resonance were subsequently performed in all patients with positive scintigraphy, while a subset of scintigraphy-negative patients underwent an echocardiogram. Results: Congo red staining identified amyloid deposits in 3 of the 12 patients (25%). Proteomic analysis confirmed ATTR amyloidosis deposits in 2 of these patients (17%). One of these 2 patients presented Perugini grade 3 uptake on cardiac scintigraphy, suspicious for ATTR-CA. Complete concordance across histology, proteomics, and cardiac imaging was observed in only 1 patient (8.3%). Three discordances were noted: one case of tenosynovial ATTR without evident cardiac disease, one patient with a discordant Congo red result likely reflecting low amyloid burden or tissue heterogeneity, and one with imaging findings suspicious for ATTR-CA despite a negative tenosynovial biopsy. Conclusions: Tenosynovial biopsy obtained during CTS surgery can reveal early amyloid deposition, which may precede overt cardiac involvement. The variability observed across findings underscores the need for a multimodal diagnostic approach that integrates histological, proteomic, and imaging data, thereby mitigating the risk of amyloidosis misclassification. Full article

Cardiac amyloidosis (CA) is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins, most commonly immunoglobulin light chains (AL) or transthyretin (ATTR). Once considered a rare disease, CA is increasingly recognised due to improved diagnostic strategies and the availability of disease-modifying therapies. Early diagnosis is crucial, as treatment efficacy and clinical outcomes are strongly influenced by the stage of cardiac involvement. Multimodality cardiac imaging plays a central role in the diagnostic pathway, risk stratification, and evaluation of therapeutic response in CA. Echocardiography represents the first-line imaging modality and is essential for raising clinical suspicion through the identification of characteristic structural and functional abnormalities, including ventricular wall thickening, diastolic dysfunction, and distinctive strain patterns. Bone scintigraphy has revolutionised the non-invasive diagnosis of ATTR-CA, allowing accurate identification of transthyretin-related disease in the absence of monoclonal gammopathy, which needs to be excluded via serum and urinary immunofixation. Cardiovascular magnetic resonance provides advanced tissue characterisation through late gadolinium enhancement and quantitative mapping techniques, enabling detection of early myocardial involvement and robust prognostic stratification. Emerging imaging modalities, including dual-energy (spectral) computed tomography and positron emission tomography tracers, show promise in myocardial amyloid quantification and subtype differentiation, although their role is still evolving. Integration of imaging findings with clinical and laboratory parameters allows comprehensive disease assessment, facilitating early diagnosis, guiding therapeutic decisions, and improving risk stratification. This review summarises the current role of multimodality imaging in CA, highlighting its contribution from early detection to prognostic evaluation and monitoring of treatment efficacy, with particular emphasis on the emerging role of quantitative imaging in monitoring treatment response. Full article

Background/Objectives: This study aimed to evaluate the prognostic role of the extracellular volume (ECV) assessed by cardiac magnetic resonance imaging (MRI) in relation to systolic dysfunction and unfavorable remodeling of the left ventricular (LV) at 24 weeks after myocardial infarction (MI) and revascularization. Methods: The study included 154 patients aged 56 ± 8 years who had been diagnosed with their first MI. Cardiac MRI was performed at 7–10 days and after 24 weeks, including assessment of indexed volumes, LV ejection fraction (LVEF), ECV, and patterns of ischemic and reperfusion injury. The study is registered in the international clinical trials registry with the number NCT04347434 (ClinicalTrials.gov). Results: Patients were divided into two groups after 24 weeks: group 1 (n = 24) with LVEF < 50% and group 2 (n = 130) with LVEF ≥ 50%. At 7–10 days, the scar mass in group 1 was 58.5 (39.5; 69.8) g vs. 17.1 (9.2; 29.7) g in group 2 (p < 0.001); microvascular obstruction was present in 23 cases (95.8%) vs. 55 (42.3%) (p < 0.001). After 24 weeks, inter-group differences increased (p < 0.05). Global ECV and remote myocardial ECV were significantly higher in patients with LVEF < 50% both at 7–10 days and after 24 weeks compared to those with LVEF ≥ 50% (p < 0.05). Infarct zone ECV did not differ between groups. Systolic dysfunction after 24 weeks was predicted by global ECV > 38.3% (p < 0.001) and remote myocardial ECV > 33.6% (p = 0.008). Predictors of an increase in end-diastolic volume index > 12% after 24 weeks in the subgroup of patients with initial systolic dysfunction were global ECV > 42.8% (p = 0.017) and remote myocardial ECV > 35.6% (p = 0.012). Conclusions: Global ECV and ECV of the remote myocardium, which exceed a certain level established by a cardiac MRI in the acute stage of MI, are among the predictors of LVEF < 50% and unfavorable LV remodeling in the medium term. Full article

Kounis syndrome (KS) is a largely underdiagnosed cause of acute coronary syndromes triggered by allergic or hypersensitivity reactions. The syndrome results from complex immune cell activation with the release of vasoactive and prothrombotic mediators leading to coronary vasospasm (type I KS) or thrombosis of plaque (type II KS), stent (type III KS) or coronary artery bypass graft (type IV KS). Despite increasing recognition over the past few decades, its pathophysiological mechanisms, diagnostic boundaries, and therapeutic implications remain incompletely understood. A comprehensive diagnostic approach, including signs, symptoms, biochemical findings, electrocardiography, echocardiography, coronary angiography, and multimodality imaging, as well as invasive assessment in selected cases, can be recommended, although its implementation in routine practice remains limited. Available data indicate that angiographically documented epicardial coronary spasm is observed in only a minority of patients, while normal or non-obstructive coronary arteries are frequently encountered. Emerging data from provocative testing, invasive coronary functional assessment, cardiac magnetic resonance and nuclear imaging suggests that coronary microvascular dysfunction may contribute substantially to the clinical phenotype, expanding the traditional concept of allergic epicardial vasospasm. Current evidence supports the recognition of type I KS as a distinct allergic vasomotor acute coronary syndrome within the myocardial infarction non-obstructive coronary artery (MINOCA) spectrum, deserving greater recognition in future diagnostic classifications and clinical practice guidelines. This narrative review critically appraises current evidence, integrating historical perspectives with contemporary insights into classification, pathophysiology, triggers, diagnostic strategies and therapeutic approaches, focusing on the most frequent manifestation represented by the vasospastic variant. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) is a global epidemic strongly associated with an increased risk of heart failure, independent of coronary artery disease or hypertension. This condition, historically termed diabetic cardiomyopathy (DCM) and recently redefined as “diabetic myocardial disorder,” remains frequently underdiagnosed in its subclinical stages. The objective of this non-systematic review is to synthesize current evidence on the pathophysiological mechanisms, diagnostic advancements, and evolving therapeutic strategies for diabetic myocardial involvement. Methods: A comprehensive review of contemporary literature was conducted, focusing on recent consensus statements from the ESC and AHA, large-scale epidemiological data (IDF/WHO), and pivotal clinical trials (EMPA-REG, DAPA-HF, and LEADER). We analyzed the role of multimodal imaging—specifically speckle-tracking echocardiography (STE) and multiparametric cardiac magnetic resonance (CMR)—and circulating biomarkers in early phenotyping. Results: Pathophysiological drivers include lipotoxicity, oxidative stress, and AGE-mediated fibrosis. Advanced imaging techniques, such as global longitudinal strain (GLS) and CMR T1-mapping/ECV quantification, demonstrate superior sensitivity over LVEF in detecting early subendocardial dysfunction and diffuse fibrosis. Furthermore, NT-proBNP serves as a robust prognostic marker for the HFpEF-like trajectory typical of diabetes. Clinically, the therapeutic landscape has shifted with SGLT2 inhibitors and GLP-1 receptor agonists, which provide significant cardioprotection and reduction in heart failure hospitalizations through mechanisms beyond glycemic control. Conclusions: Diabetic myocardial disorder represents a complex continuum within the cardiometabolic spectrum. Early detection through multimodal imaging and biomarkers is essential for risk stratification. Integrating novel glucose-lowering therapies with proven cardiovascular benefits is now mandatory to alter the natural history of the disease and prevent progression to overt heart failure. Full article

Background: Cardiac arrhythmias in children and adolescents may present with nonspecific symptoms such as precordial pain, palpitations, and syncope. We evaluated the clinical characteristics and rhythm findings of symptomatic pediatric patients and examined cross-sectional associations between reported symptoms and selected rhythm diagnoses, with particular attention to the diagnostic and management yield of ambulatory Holter monitoring. Because symptom timing is not always captured during diagnostic monitoring, associations between reported symptoms and detected rhythm abnormalities must be distinguished from temporal symptom–rhythm correlation and causation. Methods: We conducted an observational study of 119 children and adolescents aged 1–18 years, who were evaluated at a tertiary pediatric hospital for symptoms potentially suggestive of cardiac rhythm abnormalities. Data included demographic characteristics, clinical symptoms, personal and family history, resting electrocardiography, ambulatory Holter monitoring, and exercise testing where clinically indicated. The primary analysis was cross-sectional. Because symptom timing during ambulatory monitoring was not recorded, the study was not designed to establish temporal symptom–rhythm correlation or causality. Descriptive analyses were performed for the final 119-participant cohort. Selected symptom–rhythm associations were evaluated using the contingency table methods with odds ratios (ORs), 95% confidence intervals (CIs), and Fisher’s exact tests where appropriate. Holm’s adjustment was applied to the prespecified family of reconstructed symptom–rhythm comparisons. Results were interpreted according to both statistical evidence and effect-size precision. Results: The cohort comprised 119 participants, including 75 females (63.0%) and 44 males (37.0%). The most frequently reported symptoms were precordial pain (105/119, 88.2%), palpitations (80/119, 67.2%), and syncope or lipothymia (39/119, 32.8%). A family history of sudden cardiac death was reported by 28 participants (23.5%). Forty-two participants (35.3%) had a normal resting ECG, while 77 (64.7%) underwent ambulatory Holter monitoring. Among those undergoing Holter monitoring, 65/77 (84.4%) had rhythm abnormalities detected exclusively by ambulatory monitoring and not identified on the resting ECG. Holter findings resulted in at least one documented management change in 38/77 participants (49.4%). Management categories were not mutually exclusive and included lifestyle or activity adjustment in 21 participants, initiation of antiarrhythmic therapy in 19, medication monitoring in 19, and targeted cardiac imaging, including cardiac magnetic resonance imaging, in 5. In this cross-sectional analysis, reported syncope/lipothymia was strongly associated with the presence of complete atrioventricular block (10/39 [25.6%] versus 1/80 [1.3%]; OR 27.24, 95% CI 3.34–222.29; Fisher’s exact p < 0.001; Holm’s adjusted p approximately 0.0004). The unadjusted association between syncope/lipothymia and the WPW-labelled diagnosis did not remain statistically significant after Holm’s adjustment. No statistically significant associations were identified between syncope/lipothymia and PSVT or VT. Conclusions: In this pediatric cohort, ambulatory Holter monitoring identified rhythm abnormalities not detected on resting ECG in a substantial proportion of monitored participants and resulted in documented changes in clinical management in approximately half of those monitored. Reported syncope/lipothymia was strongly associated with the presence of complete atrioventricular block in the reconstructed cross-sectional analysis. Because symptom timing during monitoring was not recorded, these findings do not establish that the detected rhythm abnormalities caused the reported symptoms or that symptoms predict future rhythm outcomes. Further studies using prospectively defined symptom–rhythm event recording and longitudinal follow-up are needed to evaluate temporal correlation and prognosis. Full article

Atrial cardiomyopathy (ACM) is defined as any complex of structural, architectural, functional, electrophysiological, and molecular changes affecting the atria that may result in clinically significant health consequences. ACM can be caused by a variety of factors, including age-related changes, valvular or vascular disease, genetic diseases, congestive heart failure, metabolic diseases, cardiovascular disease (CVD) risk factors such as arterial hypertension (AH) or obesity, obstructive sleep apnea, and other infectious or noninfectious diseases predisposing to chronic inflammation. The diagnosis of ACM relies on several modalities, including electrocardiography, echocardiography, cardiac magnetic resonance imaging (MRI), computed tomography (CT), electroanatomical mapping (EAM), genetic studies, and biomarkers, which can detect and characterize structural, mechanical, and electrical atrial dysfunction. These changes often include structural atrial remodeling (fibrosis), abnormal structure of the atrial wall and its components, and contractile and electrical dysfunctions. When assessing aspects of ACM, structural changes in the atria such as left atrium (LA) size and fibrosis; LA architectural changes such as the expression of remodeling; changes in LA mechanics such as echocardiographic stress indices; changes in reservoir function and changes in contraction; biological factors determining changes in biomarkers; possible genetic predispositions and higher expression of certain genes encoding certain proteins; and arrhythmogenic factors associated with a higher risk of atrial fibrillation (AF) and stroke and a worse short- and long-term prognosis are very important. When considering the challenges of diagnosing ACM, it should be noted that without standardized diagnostics, most ACM diagnostic situations remain primarily research tools rather than practical clinical diagnostic methods. This review critically evaluates the evidence and translational gaps in the diagnosis of ACM, synthesizing the emerging role of advanced diagnostics and their clinical and prognostic implications as a key future tool for individual risk stratification. Full article