Mitral regurgitation (MR) induces progressive atrial remodelling and dysfunction, yet conventional metrics may underestimate early mechanical impairment. This systematic review synthesised evidence on left atrial strain (LAS) across MR phenotypes, its prognostic utility and its response to intervention.

Systematic review conducted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.

MEDLINE, PubMed, Embase, CENTRAL and Web of Science were searched from 1 January 2010 to 10 July 2026.

Studies of adult patients with MR of any aetiology or severity using speckle-tracking echocardiography to report quantitative LAS. Case reports, reviews, conference abstracts without full text and non-English publications were excluded.

Two reviewers independently extracted data and assessed the risk of bias using the Risk of Bias in Non-Randomised Studies of Exposures tool, with a third reviewer resolving disagreements. Substantial heterogeneity precluded quantitative meta-analysis.

Left atrial reservoir strain (LASr) was universally reduced in patients with MR compared with controls across all aetiologies. Secondary MR demonstrated more severe impairment than primary MR, reflecting combined volume and pressure overload. Progressive LAS deterioration accompanied increasing MR severity, with LASr independently predicting surgical necessity and outperforming left ventricular global longitudinal strain as a severity marker. Multiple prognostic thresholds demonstrated independent predictive value for adverse outcomes: LASr <35% predicted cardiovascular events, while LASr ≤15% in secondary MR independently predicted mortality. Postintervention LAS responses demonstrated substantial heterogeneity; patients achieving ≥15% LASr improvement experienced significantly lower all-cause mortality and heart failure hospitalisation, establishing LAS recovery as a surrogate marker of successful reverse remodelling.

LASr is a sensitive, consistent marker of atrial dysfunction in MR, identifying mechanical impairment prior to irreversible remodelling. As most supporting evidence is retrospective and single-centre, further prospective validation will help establish standardised thresholds for clinical use.

CRD420251126721.

Regular physical activity offers numerous benefits to children's health and well-being and is essential for reducing cardiovascular risk in children with cardiovascular disease. Despite increasing evidence supporting its benefits, many young patients remain insufficiently active because of concerns regarding exercise related risks, limited expertise. This clinical consensus statement provides practical guidance for the prescription of exercise and physical activity in children and adolescents aged 6 to 17 years with cardiovascular disease. The document aims to bridge the gap between evidence supporting the benefits of physical activity and its implementation in daily clinical practice, promoting safe participation in sport and exercise across a broad spectrum of cardiovascular conditions. This consensus statement outlines an individualised, patient-centred approach to exercise prescription based on clinical assessment, cardiovascular risk stratification, and the FITT principle: frequency, intensity, time, and type. Specific recommendations are provided for congenital and acquired heart disease, cardiomyopathies, arrhythmias, pulmonary hypertension, cardio-oncology patients, and children with physical disabilities or syndromes. The document emphasises the importance of multidisciplinary care, periodic follow up, exercise testing when indicated, and tailored programs adapted to the child's clinical condition, developmental stage, and personal preferences. The overarching goal is to encourage safe and enjoyable participation in physical activity, improve quality of life and functional capacity, and foster lifelong healthy behaviours in children with cardiovascular disease.

Sudden cardiac death (SCD) remains a major cause of mortality in nonischemic cardiomyopathy (NICM) despite advances in heart failure therapy and implantable cardioverter-defibrillator (ICD) technology. Risk stratification remains challenging because left ventricular (LV) ejection fraction (LVEF) alone incompletely captures arrhythmic substrate, missing many patients at risk while leading others to receive ICDs without subsequent appropriate therapy. Cardiac magnetic resonance (CMR), particularly late gadolinium enhancement (LGE), has emerged as a central tool for identifying myocardial fibrosis and refining arrhythmic risk across NICM phenotypes. However, CMR imaging alone does not fully define arrhythmogenicity, especially in diseases with layered, septal, or intramural scar. We present a case-based framework illustrating how multimodality imaging integrates into SCD risk stratification across hypertrophic cardiomyopathy, cardiac sarcoidosis, genetic arrhythmogenic cardiomyopathy, and cardiac amyloidosis. These cases demonstrate several core principles. First, CMR can identify arrhythmogenic substrate and often refines risk beyond conventional clinical markers. Second, multimodality imaging can provide additive information, but findings must be interpreted within disease-specific context, as the prognostic implications differ across phenotypes. Third, invasive electrophysiologic evaluation, including programmed stimulation and electroanatomic mapping, can further stratify arrhythmic risk when imaging findings are incomplete or discordant with the clinical presentation. Finally, genetic testing complements imaging and invasive assessment by refining disease classification and, in selected cases, contributes to arrhythmic risk assessment by considering variant classification and wholistic clinical phenotype. Together, these observations support a substrate-based rather than function-based approach to SCD risk stratification in NICM. Multimodality imaging is foundational, but optimal assessment requires integration of imaging, electrophysiology, genetics, and clinical phenotype. Future progress will depend on longitudinal risk modeling, improved characterization of electrically active substrate, and incorporation of patient-specific tools into primary prevention ICD decision-making.

The risk of recurrent cardiovascular events remains high in acute myocardial infarction (AMI) patients even after revascularization. Coronary residual inflammation plays a promoting role in this process. This study aimed to address the clinical impact of pancoronary inflammation at long-term follow-up in AMI patients.

Between January 2017 and December 2021, 1312 AMI patients underwent three-vessel optical coherence tomography (OCT) imaging following successful percutaneous coronary intervention. Patients were stratified by the median number (3) of inflammatory plaques (defined as macrophage-containing non-culprit lesions) into low-inflammation (≤3 lesions) and high-inflammation (>3 lesions) groups. The primary endpoint was major adverse cardiovascular events (MACE), defined as a composite of cardiac mortality, non-fatal MI, and unplanned revascularization, assessed over a 5-year follow-up period.

The number of inflammatory plaques (i.e. pancoronary inflammation) had a significant correlation with hs-CRP level (i.e. systemic inflammation) (r = 0.109; P < 0.001). OCT features of plaque vulnerability were significantly more common in patients with high pancoronary inflammation level, compared to those with low pancoronary inflammation level. During a median 4.1-year follow-up, non-culprit lesion-related MACEs occurred more frequently in patients with more inflammatory plaques (8.1% versus 3.1% [hazard ratio, 2.71 (95% CI, 1.52-4.84)]), primarily attributable to increased risk of unplanned coronary revascularization. In multivariable models, higher pancoronary inflammation, rather than higher systemic inflammation, was the independent predictor of non-culprit lesion-related MACEs.

The high pancoronary inflammation was found to be associated with more vulnerable plaque characteristics and increased risk of long-term adverse cardiovascular events in AMI patients.

To investigate the associations of objectively measured cardiorespiratory fitness (CRF) with glaucoma-related functional, structural, and patient-reported outcomes and to compare its explanatory contribution with cumulative cardiovascular (CV) risk in patients with primary open-angle glaucoma (POAG).

Cross-sectional baseline analysis of the multicenter HIT-GLAUCOMA trial (NCT06058598).

One hundred ten patients with mild-to-moderate POAG.

CRF was assessed by symptom-limited cardiopulmonary exercise testing and expressed as peak oxygen uptake (VO₂peak). Cumulative CV risk was estimated using the Systematic COronary Risk Evaluation 2 (SCORE2). Missing data were addressed using multiple imputation. Multivariable linear regression models with restricted cubic splines were used to evaluate associations. Relative explanatory contributions of CRF and SCORE2 were explored using adequacy indices derived from model R² values.

Visual field mean deviation (MD), global retinal nerve fiber layer (RNFL) thickness, Glaucoma Activity Limitation Questionnaire (GAL-9), and National Eye Institute Visual Function Questionnaire-25 (NEI-VFQ-25).

No statistically significant associations were observed between CRF or SCORE2, and glaucoma-related outcomes. Nevertheless, higher CRF showed directionally more favorable estimates for visual field performance, glaucoma activity limitation, and vision-related quality of life. Higher SCORE2 showed a directionally less favorable estimate for global RNFL thickness, whereas apparent non-linear patterns for patient-reported outcomes should be interpreted cautiously. Exploratory adequacy analyses suggested differential explanatory contributions. CRF retained 95% of the explanatory information for visual field MD compared with 60% for SCORE2, whereas SCORE2 retained more explanatory information for RNFL thickness (97% vs. 86%) and NEI-VFQ-25 scores (86% vs. 40%). Given the modest sample size and the absence of statistically significant primary associations, these adequacy findings should be considered exploratory rather than confirmatory.

The observed directional patterns and exploratory adequacy analyses suggest that CRF and cumulative CV risk may reflect different dimensions of CV health across glaucoma-related outcomes. However, these findings are hypothesis-generating and require confirmation in larger, adequately powered longitudinal and interventional studies.

The interaction between Astragaloside IV (AS-IV) and the gut microbiota is known to help prevent cardiovascular disease, however, its underlying mechanism through which AS-IV modulates the balance of intestinal flora to ameliorate heart failure (HF) remains unclear.

A rat HF model was created using coronary artery ligation to study AS-IV's cardioprotective effects, while an AngII-activated H9c2 hypertrophy model assessed AS-IV's impact on cellular hypertrophy. AS-IV's therapeutic effects were evaluated through histopathology, 16S rRNA sequencing, SCFA-targeted omics, and HDAC molecular assays.

AS-IV markedly enhanced cardiac function in HF rats. AS-IV treatment ameliorated gut microbiota dysbiosis in HF rats. AS-IV also altered short-chain fatty acid (SCFA) levels, leading to an increase in hexanoic, heptanoic, octanoic, decanoic, valeric, pentanoic, acetic, propionic, nonanoic, isobutyric, and isovaleric acids. Additionally, AS-IV concurrently suppressed the overexpression of HDAC1, HDAC2, and HDAC3 in both HF rats and H9c2 cells, alleviated myocardial fibrosis, and reduced cardiomyocyte hypertrophy.

AS-IV exerts its therapeutic effects against HF through a multifaceted mechanism involving the amelioration of gut dysbiosis, enrichment of SCFA-producing bacteria, restoration of SCFA levels, and suppression of HDAC1/2/3 expression.

Pathological arterial remodeling heavily depends on the aberrant proliferation and migration of vascular smooth muscle cells (VSMCs). This study explores how γ-Glutamylcysteine (γ-GC) regulates VSMC signaling to mitigate hypertensive structural damage.

Spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats received intraperitoneal injections of γ-GC (100 mg/kg) every two days for 4 weeks. Blood pressure and arterial remodeling were evaluated. Primary aortic VSMCs were cultured for cellular mechanism analysis. To verify Nrf2 pathway requirement, the Nrf2 inhibitor ML385 was applied in vitro and via osmotic pumps in vivo.

γ-GC lowered systemic blood pressure and prevented arterial medial thickening in SHR, while normotensive controls remained unaffected. In SHR-VSMCs, γ-GC inhibited cell migration, proliferation, and phenotypic switching, and alleviated cellular oxidative stress. RNA-seq revealed significant enrichment of the Nrf2 signaling pathway. Mechanistically, γ-GC induced Keap1 S-glutathionylation, which disrupted the Keap1 and Nrf2 interaction and promoted Nrf2 nuclear translocation. Notably, Nrf2 inhibition with ML385 abolished the protective effects of γ-GC in vivo and in vitro.

γ-GC attenuates hypertensive arterial remodeling by modulating intracellular signaling, specifically through Keap1 S-glutathionylation-dependent Nrf2 activation. The Keap1/Nrf2 signaling axis is required for γ-GC to restore VSMC function, suggesting a targeted molecular mechanism for cardiovascular protection.

BackgroundArtificial intelligence (AI) is quickly changing the field of biosensing technologies to the point of early, real-time, and individualized disease detection and overcoming significant drawbacks of traditional biosensors, including noise interference, signal drift, and inability to process non-linear biological data.ObjectiveThis review examines the latest developments in AI-driven biosensing systems and assess their impact on diagnostic performance and clinical relevance.MethodsThis critical review focuses on recently published works (2021-2025) on AI-integrated biosensing platforms, such as optical, electrochemical, wearable, and nanomaterial-based platforms, and machine learning, deep learning, edge AI, multimodal data fusion, and federated learning. Results: CNNs and LSTMs, Transformers and ensemble learning are advanced AI models with better sensitivity, specificity, automatic extraction of features, and prediction accuracy of critical diseases like cancer, cardiovascular, infectious, neurological, and metabolic diseases. Explainable Artificial Intelligence (XAI), nano-enabled biosensors, digital twins, and the Internet of Medical Things (IoMT) are examples of emerging technologies and ideas that are improving real-time, dependable, customized, and privacy-preserving diagnostic systems.ConclusionThe change to proactive and predictive healthcare is being facilitated by AI-enhanced biosensing. It has a good chance in early diagnosis, better treatment planning as well as the decrease in healthcare expenses. Nevertheless, there are still challenges such as lack of data, generalization of models, regulatory authorization, and moral issues.

Transthyretin amyloid cardiomyopathy (ATTR-CM) is an increasingly recognized cause of heart failure. Three disease-modifying agents are now approved for treatment in Germany: the transthyretin (TTR) stabilizers tafamidis and acoramidis, and the TTR gene silencer vutrisiran. In the absence of head-to-head trials, practical guidance for individual treatment decisions is lacking.

A multidisciplinary expert panel appointed by the German Society of Amyloid Diseases (DGAK) and the German Cardiac Society (DGK) performed a comprehensive review of pivotal randomized controlled trials, open-label extension studies, real-world data, and the approved German summaries of product characteristics to develop evidence-based consensus recommendations.

All three agents have demonstrated significant reductions in all-cause mortality and cardiovascular hospitalizations in phase 3 trials with comparable efficacy and tolerability profiles. Due to the absence of direct comparative studies, the panel concludes that tafamidis, acoramidis, and vutrisiran, based on the current scientific data, are considered similarly effective for most patients with confirmed ATTR-CM. An exception applies to patients with hereditary ATTR-CM and a mixed phenotype (concurrent cardiomyopathy and polyneuropathy), for whom vutrisiran is recommended as first-line therapy. Combination therapy is safe but, lacking randomized data regarding efficacy, cannot be recommended at present. Treatment decisions should incorporate patient preferences, comorbidities, mode of administration, and local regulatory frameworks. Regular monitoring using clinical parameters, biomarkers including TTR serum levels, and cardiac imaging is recommended.

This consensus provides a practical framework for the specific treatment of ATTR-CM in Germany, aiming for early treatment initiation. Local standards and shared decision-making remain essential for the establishment of ATTR-CM therapy in an individual patient.