The Fugl-Meyer Assessment of Lower Extremity (FMA-LE), Berg Balance Scale (BBS), and Brunnstrom lower-limb stage summarize lower-limb motor and balance function after stroke but do not directly reflect the electrical activity of distal muscles during a specific task. The tibialis anterior (TA) is a primary superficial agonist during active ankle dorsiflexion, and its surface electromyography (sEMG) may provide muscle-specific and task-specific complementary information relevant to foot drop and voluntary distal ankle-foot control.

To examine the relationships of TA sEMG measures obtained during active ankle dorsiflexion with lower-limb motor function, balance, and stage of motor recovery in inpatients with ischemic or hemorrhagic stroke within 1 year of onset, and to explore whether short-term improvements in clinical scales were accompanied by corresponding changes in sEMG measures.

This single-center observational study included 118 participants with supratentorial or infratentorial index stroke lesions. Bilateral TA and gastrocnemius sEMG was recorded during a standardized seated active ankle dorsiflexion task. The primary measures were paretic-side TA average rectified value (ARV) and the TA paretic/non-paretic ratio. Baseline sEMG analyses included 110 participants, clinical longitudinal analyses included 88, and sEMG longitudinal analyses included 81. Spearman correlation, multivariable linear regression, and paired Wilcoxon signed-rank tests were used, with adjustment for multiple comparisons.

At baseline, paretic-side TA ARV was lower than non-paretic-side TA ARV. Paretic-side TA ARV showed moderate positive correlations with the FMA-LE, BBS, and Brunnstrom lower-limb stage (ρ = 0.556, 0.492, and 0.496, respectively), as did the TA paretic/non-paretic ratio (ρ = 0.566, 0.440, and 0.417, respectively; all adjusted q < 0.001). Both TA measures remained associated with the FMA-LE and BBS after adjustment for age, sex, stroke type, time from stroke onset to baseline assessment, and paretic side. The FMA-LE, BBS, and Brunnstrom lower-limb stage improved during inpatient rehabilitation, whereas no sEMG measure showed a significant longitudinal change after FDR correction.

TA sEMG during active ankle dorsiflexion was associated with concurrent lower-limb motor and balance function and may provide muscle-specific and task-specific information complementary to routine clinical scales. Its longitudinal responsiveness and value in clinical practice require further investigation.

https://itmctr.ccebtcm.org.cn/mgt/search, identifier ITMCTR2026000773.

The paradigm of atherosclerosis has evolved from a passive lipid storage disease to a dynamic immuno-inflammatory disorder, yet the precise immune checkpoints governing its progression remain a therapeutic frontier. This review dissects the yin-yang regulation exerted by CD4⁺ T-cell subsets, with a particular focus on the pro-inflammatory T helper 17 cells (Th17) and the immunosuppressive regulatory T cells (Tregs). We posit that the net balance of the Th17/Treg axis, rather than the isolated activity of either subset, represents an important immunomodulatory determinant that influences plaque fate-operating in concert with other established contributors to atherosclerotic progression, including hemodynamic forces, lipid burden, plaque macrophage content, and coagulation pathways. By integrating recent advances in the metabolic and transcriptional control of this equilibrium, we highlight how its disruption fuels the chronic vascular inflammation central to atherosclerosis. Moreover, we critically evaluate the translational promise of strategically recalibrating this axis, examining next-generation immunotherapies that target lineage-specific pathways to restore homeostasis. This review not only consolidates mechanistic insights but also underscores the urgent clinical potential of harnessing the Th17/Treg balance as a viable strategy to attenuate atherosclerotic disease burden.

Globally, cardiovascular disease has consistently been the leading cause of death. Its pathogenesis is complex and involves interactions among multiple factors, with inflammatory mechanisms garnering increasing attention. Pyroptosis-pro-inflammatory programmed cell death-is categorized into classical, non-classical, and other pathways. Among these, the inflammasome-induced classical pathway has been rigorously studied. Recent findings show that pyroptosis is essential for the development and course of cardiovascular conditions, especially atherosclerosis, myocardial infarction, and heart failure. This review analyzes current evidence on the molecular underpinnings and clinical significance of NLRP3-induced pyroptosis in cardiovascular disease. This review addresses a critical gap in current anti-inflammatory therapies for cardiovascular disease by bridging molecular insights with translational innovations. It advocates for mechanism-driven clinical trials and the use of pyroptosis-modulating techniques to develop next-generation therapies, aiming to provide a theoretical framework for subsequent studies and treatment approaches.

Cardiac biomarkers offer potential for early diagnosis and prognosis; however, their utility in burn care is not well established. This systematic review aimed to evaluate the current evidence regarding the diagnostic and prognostic values of cardiac biomarkers in patients with acute burn injuries.

A systematic search of PubMed and Google Scholar (July 2015-September 2025) was conducted according to the PRISMA guidelines. We included prospective and retrospective observational studies that evaluated troponin (I or T), B-type natriuretic peptide (BNP), or N-terminal pro-BNP (NT-proBNP) in patients with acute burns and reported clinical outcomes. Case reports, reviews, and studies of patients with pre-existing cardiovascular diseases were excluded.

Seven original studies were included in this systematic review. The findings consistently demonstrated that elevated troponin levels were associated with larger burn sizes, sepsis, and increased mortality, reflecting systemic stress rather than primary ischemic events. BNP and NT-proBNP levels are strong independent predictors of mortality, sepsis, and toxic myocarditis. Notably, BNP demonstrated superior sensitivity to troponin for the early detection of myocarditis in patients with moderate-to-severe burns.

Cardiac biomarkers are valuable prognostic indicators in acute burn injuries, strongly associated with mortality and major complications. The integration of these factors into clinical practice could significantly enhance early risk stratification.

Bioprosthetic heart valves (BHVs) are widely used to treat aortic valve disease, and their demand is rising. However, BHV lifespan remains limited by degeneration, with patients often requiring surgical or transcatheter reintervention within a decade. BHVs lack intrinsic remodeling capabilities, and the mechanisms contributing to their failure remain poorly understood. In this review, we summarize current knowledge of BHV degeneration by integrating findings from native aortic valve disease with studies of explanted bioprosthetic valves. We discuss the structural hallmarks of degeneration, including collagen remodeling, calcification, and inflammatory cell accumulation, and examine evidence that circulating blood-derived factors infiltrate BHV tissue and contribute to degeneration progression. Particular emphasis is placed on macrophages, which are consistently identified in explanted BHVs and may promote extracellular matrix (ECM) degradation. We also highlight extracellular vesicles (EVs) as potential mediators of cardiovascular calcification and propose that macrophage-derived EVs may promote ECM remodeling beyond sites of direct cellular accumulation. In addition, we review experimental approaches, including histological imaging, in vitro cell culture models, and proteomic analyses, that may help define molecular pathways underlying degeneration. Together, we hypothesize a model of BHV degeneration driven by interactions among host immune cells, circulating factors, and bioprosthetic tissue. Improved understanding of these mechanisms may facilitate the development of therapeutic strategies to improve BHV durability and long-term clinical outcomes.

Myocardial fibrosis is a common pathophysiological process observed in various cardiac diseases and cardiac aging, characterized by excessive accumulation of extracellular matrix proteins in the cardiac interstitium. This process is highly heterogeneous and dynamic, depending on the underlying cardiac pathology and disease stage, and represents a key pathological basis for the development and progression of heart failure. Thrombospondin-2 (TSP-2), a critical extracellular matrix regulatory protein, exhibits complex dual roles in different disease contexts and stages, exerting both cardioprotective and potentially pathological effects. Recent studies have demonstrated that TSP-2 is involved in the pathogenesis of heart failure and may regulate myocardial fibrosis through modulation of extracellular matrix remodeling and related signaling pathways. This review summarizes the regulatory roles of TSP-2 in myocardial fibrosis under various cardiac disease conditions and discusses its potential molecular mechanisms. By integrating current studies, this review provides new insights into the regulatory network of myocardial fibrosis and highlights the potential of TSP-2 as a therapeutic target. However, further mechanistic and translational studies are required to validate the precise role and clinical applicability of TSP-2 in cardiac fibrosis.

Aortic aneurysm and dissection (AAD) are life-threatening vascular diseases associated with progressive aortic wall degeneration and a high risk of rupture. Despite advances in surgical and endovascular techniques, effective disease-modifying pharmacological therapies remain limited. Mitochondria are central regulators of cellular energy metabolism, redox homeostasis, and apoptosis, and their functional integrity is essential for maintaining vascular homeostasis and aortic wall stability. Increasing evidence indicates that mitochondrial dysfunction plays a pivotal role in the initiation and progression of AAD. In this review, we summarize the major mechanisms by which mitochondrial abnormalities contribute to AAD pathogenesis, including impaired mitochondrial energy metabolism, defective mitochondrial biogenesis, excessive mitochondrial oxidative stress, and imbalanced mitochondrial dynamics. These interconnected processes promote vascular smooth muscle cell (VSMC) phenotypic switching, apoptosis, and senescence, alongside extracellular matrix degradation and inflammatory activation, ultimately culminating in the structural weakening of the aortic wall. We also discuss emerging mitochondria-targeted therapeutic strategies, including interventions aimed at restoring metabolic homeostasis, enhancing mitochondrial biogenesis, suppressing oxidative stress, and regulating mitochondrial fission-fusion balance. Although the clinical translation of these approaches remains hindered by inadequate target specificity and potential off-target effects, ameliorating mitochondrial dysfunction represents a promising strategy for developing non-surgical treatments for AAD. A deeper understanding of mitochondrial regulatory networks may provide new mechanistic insights and therapeutic opportunities for preventing AAD progression.

Cardiac rehabilitation (CR) improves outcomes in heart failure, but optimal initiation timing during acute hospitalization remains undefined. We characterized the dose-response association between door-to-cardiac rehabilitation time and in-hospital outcomes, describing how this pattern appeared to differ between death and functional measures.

Using the Japanese Registry of All Cardiac and Vascular Diseases-Diagnosis Procedure database, we identified 564 830 patients hospitalized for acute heart failure (2012-2023), categorized into non-CR (n=275 454) and CR groups by door-to-cardiac rehabilitation quartiles: quartile 1 (≤1 day), quartile 2 (2-3 days), quartile 3 (4-5 days), and quartile 4 (≥6 days). Generalized propensity score-based weighting adjusted for 32 confounders. Restricted cubic splines evaluated dose-response patterns among CR recipients. The primary outcome was in-hospital death; secondary outcomes were Barthel Index at discharge and Barthel Index improvement.

All door-to-cardiac rehabilitation quartiles showed lower in-hospital death versus non-CR (adjusted odds ratios, 0.39-0.49; all P<0.001). Barthel Index at discharge was higher in quartile 1 to quartile 3 (mean difference, +3.2 to +3.8 points), with a smaller difference in quartile 4. Spline analysis revealed nonlinear associations: The mortality nadir was observed at 6.1 days, whereas functional measures showed the most favorable associations at 3.3 days. Sensitivity analyses addressing immortal time bias yielded consistent mortality results.

CR was associated with a lower in-hospital mortality rate across all timing quartiles. The association pattern appeared to differ by outcome domain: Functional measures showed more favorable associations with earlier initiation (within 2-3 days), whereas a lower mortality rate was observed across a broader window. These findings warrant prospective evaluation.

Significant knowledge gaps persist on cardiovascular conditions that predominantly, disproportionately, or only affect women. Historically overshadowed by the focus on obstructive coronary artery disease, conditions such as myocardial infarction with nonobstructive coronary arteries, spontaneous coronary artery dissection, and Takotsubo cardiomyopathy have only recently gained research attention, despite substantial prevalence and impact among women. Similarly, coronary microvascular dysfunction and vasospastic angina, long dismissed as symptoms of psychological origin, are now recognized as common and underdiagnosed mechanisms of chest pain. Disparities in research also extend to heart failure with preserved ejection fraction, disproportionately affecting more women, and with comparable impacts on prognosis and quality of life, yet poorly understood compared with heart failure with reduced ejection fraction. Moreover, female hypertension is underestimated, underdiagnosed, and understudied. Furthermore, pregnancy-related cardiovascular complications, including preeclampsia and peripartum cardiomyopathy underscore the urgent need for research into sex-specific mechanisms and targeted preventive and therapeutic strategies, particularly in resource-limited settings. This review consolidates knowledge on cardiovascular conditions with pronounced sex differences, focusing on translational discoveries that direct current strategies, but most of all, emphasizing the need for future research to bridge the gap between mechanistic insights and clinical application. By identifying knowledge gaps, this article provides a road map for advancing sex-specific understanding and care in cardiovascular disease, ensuring progress in diagnosis, treatment, and prevention. Bridging the sex gap in cardiac research and care requires a multidisciplinary, globally inclusive approach. By integrating knowledge of biological, clinical, and sociocultural perspectives, we can move toward equitable and effective cardiovascular health for all.

Indices reflecting the discordance between QRS complex voltages on ECG and left ventricular (LV) wall thickness or LV mass index on echocardiogram (echo) have enabled identification of cardiac amyloidosis (CA) among patients with hypertrophic hearts. However, this evidence comes from studies that have excluded patients with established hypertrophic cardiomyopathy (HCM) and Anderson-Fabry disease (AFD). The aim of this study was to assess the performance of ECG/echo indices in characterizing adult patients with cardiomyopathies and hypertrophic phenotype.

This was an Italian retrospective, cross-sectional, multicenter study. Data from ECGs and echo of consecutive adult patients with confirmed CA, HCM, and AFD, and an LV wall thickness >12 mm were analyzed to calculate different ECG/echo indices.

Of the 1181 patients included (median age, 65 years; 69% men), 35.5% (n=416) had CA, 46.5% (n=594) had HCM, and 14.5% (n=171) had AFD. All ECG/echo indices were able to distinguish CA from other HCM and AFD (P<0.001). The total QRS score/LV mass index was the best performing ECG/echo index for differentiating CA from other hypertrophic phenotypes (accuracy: 83%). The total QRS/maximum LV wall thickness was the best performing index in discriminating between the 3 cardiomyopathies (cutoff values of 6.21 versus 9.81 versus 11.47 in CA, HCM, AFD, respectively; P<0.001 for all comparisons).

ECG/echo indices, particularly total QRS/maximum LV wall thickness, may serve as easily accessible first-line tools to differentiate CA from HCM and AFD. These findings may enable prompt recognition of patients with different cardiomyopathies in everyday clinical practice, both in community-based centers and tertiary care facilities, and to orient subsequent diagnostic workup.