Frontiers in Cardiovascular Medicine最新文献

Dysglycemia, lipid metabolism, and cardiovascular disease (CVD) progression in type 2 diabetes (T2D) are closely interconnected, yet the non-linear lipid remodeling processes underlying atherogenic dyslipidemia remain insufficiently defined. This study aimed to identify HbA1c thresholds associated with accelerated lipid-driven atherogenesis, quantify the mediating role of the triglyceride-to-HDL cholesterol ratio (TG/HDL-C)-a surrogate of insulin-resistance-related lipid metabolism-and assess the incremental predictive value of the Atherogenic Index of Plasma (AIP) within the clinically ambiguous "glycemic gray zone." A total of 271 adults with T2D not receiving lipid-lowering therapy were retrospectively grouped by HbA1c: good (<7.0%), moderate (7.0%-8.49%), and poor (≥8.5%) control. Atherogenic lipid burden was evaluated using AIP, Castelli indices, TG/HDL-C, non-HDL cholesterol, and remnant cholesterol. Restricted cubic splines were used to explore non-linear HbA1c-lipid relationships; mediation analysis estimated the TG/HDL-C contribution to the HbA1c-AIP pathway; and Net Reclassification Improvement (NRI) tested the added predictive value of AIP over conventional lipid markers. All atherogenic indices worsened with deteriorating glycemia (p < 0.001). Non-linear inflection points were observed at HbA1c 8.0% for TG/HDL-C and 8.5% for AIP (p_non-linearity < 0.01). TG/HDL-C mediated 56.9% of the HbA1c effect on AIP, indicating its central role in linking hyperglycemia to lipid remodeling. Adding AIP improved cardiovascular risk reclassification, particularly in the 8.0%-8.5% transition range (categorical NRI = 0.384; 95% CI: 0.184-0.584). These findings identify 8.0%-8.5% as a metabolically vulnerable HbA1c threshold marked by accelerated atherogenic dyslipidemia. AIP functions as a sensitive lipid-based marker for cardiometabolic risk detection within this gray zone, while TG/HDL-C acts as a key mechanistic mediator, supporting the integration of atherogenic lipid indices into individualized risk assessment and precision lipid management strategies in T2D.

The prevalence of insulin resistance (IR) with associated hyperinsulinemia (HI) is increasing worldwide, as is the prevalence of heart failure with preserved left ventricular ejection fraction (HFpEF). This narrative review aims to explore the epidemiological and pathophysiological relationship between IR/HI and HFpEF, the possible mechanisms by which IR/HI could underlie HFpEF development and worsening, and the actual and future therapeutic implications of this interplay. The prevalence of IR in patients with HF is not negligible, and we will go through the existing literature highlighting this epidemiological association and the longitudinal data supporting a causative link. We will give a brief overview of molecular and physiological mechanisms connecting IR and HFpEF, such as the alteration of vascular homeostasis resulting in endothelial dysfunction and arterial hypertension, myocardial and vascular wall cell growth resulting in microvascular and macrovascular alterations of coronary circulation, and concentric remodeling of the left ventricle resulting in increased stiffness and diastolic dysfunction. We will review the concept of "diabetic cardiomyopathy" as a study model of these correlations. Finally, we will go through existing antidiabetic drugs with a current or potential future role in the treatment of HFpEF and summarize evidence on lifestyle and rehabilitative interventions in the field. Many of the cardiovascular abnormalities caused by IR/HI may be a contributing factor to the development and worsening of HFpEF. Further research is warranted to explore whether early diagnosis and specific treatment of IR/HI in at-risk populations may prevent HFpEF or delay its progression.

Background: Patients with heart valve disease (VHD) combined with pulmonary hypertension (PH) have a higher risk for hospital-acquired pneumonia. We aimed to analyze the risk factors and construct a valid nomogram model for predicting hospital-acquired pneumonia among those patients.

Methods: Patients with VHD combined with PH who underwent heart valve replacement were collected. The perioperative risk factors for hospital-acquired pneumonia were analyzed by univariable and logistic regression, and then a nomogram prediction model was constructed and validated.

Results: A total of 377 patients were included, and 81 cases developed postoperative hospital-acquired pneumonia, with an incidence of 21.49%. The results of multifactorial analysis showed that preoperative anemia, ASA score >grade III, duration of surgery ≥313 min, duration of endotracheal intubation ≥3 d, duration of indwelling gastric tube ≥1 d, and bioprosthetic valve usage were the risk factors for the occurrence of postoperative hospital-acquired pneumonia (P < 0.05). The model validation results showed that patients judged to be at high risk of hospital-acquired pneumonia are consistent with the actual situation, indicating that the model has good predictive efficacy.

Conclusions: The constructed six-variable nomogram prediction model has satisfying efficacy in predicting hospital-acquired pneumonia after valve replacement in patients with VHD combined with PH. It is significant for early identification and future quality improvement to reduce the risk of hospital-acquired pneumonia.

Background: The optimal revascularization approach for intermediate- and high-risk individuals with severe aortic stenosis (AS) and concomitant coronary artery disease (CAD) remains uncertain, particularly regarding the comparative short- and mid- to long-term outcomes of transcatheter aortic valve replacement with percutaneous coronary intervention (TAVR + PCI) vs. surgical aortic valve replacement with coronary artery bypass grafting (SAVR + CABG).

Methods: A systematic search of major databases was conducted up to March 2025 to identify studies comparing TAVR + PCI vs. SAVR + CABG in this population. Meta-analyses were performed using a random-effects model to estimate pooled odds ratios (ORs) and 95% confidence intervals (CIs). Evidence quality was assessed using the GRADE framework.

Results: Thirteen studies comprising 53,869 patients were analyzed. Compared with SAVR + CABG, TAVR + PCI was associated with lower 30-day risks of stroke, myocardial infarction, and acute kidney injury, but higher permanent pacemaker implantation. No differences were found in all-cause mortality, major vascular complications, or major bleeding. In mid- to long-term follow-up (≥2 years), the TAVR + PCI group exhibited increased risks of all-cause mortality, myocardial infarction, and repeat revascularization, with similar stroke rates between strategies. Certainty of evidence ranged from very low to moderate.

Conclusions: In intermediate- and high-risk patients with severe AS and concomitant CAD, TAVR + PCI appears to confer short-term safety advantages but may be associated with less favorable mid- to long-term outcomes compared with SAVR + CABG. These findings support individualized revascularization strategies that balance early procedural safety against longer-term risks and highlight the need for further randomized trials with extended follow-up.

Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251000317, PROSPERO CRD420251000317.

Cardiac magnetic resonance (CMR) tissue characterisation is central to the diagnosis and risk stratification of myocardial disease. However, for certain techniques tissue characterisation CMR is limited by reliance on contrast agents, sensitivity to motion, prolonged acquisition times, and time- and labour-intensive image reconstruction and analysis. Artificial intelligence (AI) has emerged as a promising approach to address these challenges by enhancing and accelerating multiple stages of the CMR workflow. Deep learning methods can automate LGE segmentation, improve motion correction and image reconstruction for parametric mapping, and enable contrast-free characterisation of scar by exploiting native CMR signals, including myocardial motion and native T1 mapping. AI has also accelerated emerging techniques such as cardiac magnetic resonance fingerprinting and diffusion tensor imaging. In addition, radiomics and deep learning-based feature extraction offer the potential to derive high-dimensional tissue phenotypes and risk markers beyond those identifiable by expert clinicians. Despite these advances, translation remains limited by access to large-scale, heterogeneous training data, alongside concerns over generalisability, fairness, and interpretability, as well as barriers to regulatory approval and clinical deployment. In this mini-review, we summarise recent developments in AI-enabled myocardial tissue characterisation using CMR, highlighting both the promises and challenges for clinical translation.

Among all innovations in cardiovascular medicine, the left internal thoracic artery to left anterior descending artery (LITA-LAD) graft stands as one of the most successful and enduring therapeutic paradigms. Introduced in the late 1960s, it quickly transformed the surgical treatment of ischemic heart disease, establishing new standards of durability, patency, and survival. More than fifty years later, the LITA-LAD graft remains the cornerstone of coronary artery bypass grafting (CABG) and continues to define excellence in both cardiac surgery and interventional cardiology.

Pulmonary vein pulsed-field ablation (PFA) is widely regarded as a safe procedure for patients with atrial fibrillation (AF), with sinoatrial disturbances as a rare complication. A 62-year-old female patient with paroxysmal AF underwent ablation using an 8-polar circular PFA catheter. During pulmonary vein isolation (PVI) of the right superior pulmonary vein, an intermittent increase in sinus rate was noted. Recurrent sinoatrial block was observed shortly after the procedure but resolved completely within six hours. This report presents the first documented case of transient sinoatrial node dysfunction as a complication of pulmonary vein PFA. Although the underlying mechanism-whether singular or multifactorial-remains unconfirmed, this case highlights the need for caution when utilizing the 8-polar circular PFA catheter.

Coronary microvascular dysfunction (CMD) is a syndrome characterized by myocardial ischemia resulting from structural and/or functional impairments of the coronary microvasculature, which includes pre-arterioles, arterioles, and capillaries. It has taken center stage in cardiovascular research due to its established role in triggering heart failure with preserved ejection fraction (HFpEF). The pathogenesis of CMD is closely associated with endothelial dysfunction, characterized by both structural and functional impairment of endothelial cells. This interplay between functional and structural injury underlies the significant heterogeneity in clinical phenotypes and hemodynamic characteristics across CMD subtypes, thus highlighting the necessity for a multidimensional investigation of its underlying pathological mechanisms. This review article systematically elaborates the pathophysiological features of CMD with a focus on two dimensions: microcirculatory functional regulation and vascular structural remodeling, aiming to provide a theoretical foundation for innovations in clinical diagnosis and treatment strategies.

Objective: The objective of this research was to investigate the association between non-traditional lipid parameters and optical coherence tomography (OCT)-characterized high-risk plaques in patients with acute myocardial infarction (AMI).

Methods: This retrospective study included 249 first-episode AMI patients admitted to the First Affiliated Hospital of Lanzhou University between January 2022 and December 2024. All patients underwent OCT-guided assessment of culprit lesions before revascularization. High-risk plaques were defined by more than two of the following features: lipid arc ≥90 °, fibrous cap thickness <65 μm, or plaque rupture/thrombus. Lesions with fewer than two of these criteria were classified as non-high-risk plaques. Clinical and laboratory data were collected, and a comprehensive lipid profile was calculated, including traditional indicators [e.g., non-HDL cholesterol (non-HDL-C)] and non-traditional ratios [e.g., apolipoprotein B/A1 ratio (ApoB/A1)]. Spearman correlation was used to assess relationships between lipid parameters and high-risk plaques. After excluding collinear variables, logistic regression, restricted cubic spline (RCS), and subgroup analyses were performed. Model discrimination and clinical value were evaluated using receiver operating characteristic (ROC) curves, the DeLong test, integrated discrimination improvement (IDI), net reclassification index (NRI), and decision curve analysis (DCA).

Results: Among 249 AMI patients, 137 (55.0%) exhibited OCT-characterized high-risk plaques. These patients were more often male (89.8%) and presented with STEMI (84.7%). They had elevated levels of myoglobin, LDL-C, non-HDL-C, ApoB, ApoB/A1, remnant lipoprotein cholesterol (RLP-C), non-HDL-C/HDL-C ratio (NHHR), and TC/HDL-C (all P < 0.05). OCT features included thinner fibrous caps, smaller lumen areas, larger lipid arcs, and higher incidences of rupture, erosion, thrombus, macrophage infiltration, cholesterol crystals, and calcification (all P < 0.05). Both ApoB/A1 (OR = 3.688, 95% CI: 1.211-11.230) and non-HDL-C (OR = 3.023, 95% CI: 1.238-7.378) were independently and linearly associated with high-risk plaques. No significant interactions were observed across clinical subgroups (all P for interaction > 0.05). The combined model incorporating the two markers achieved the highest discriminative performance (AUC = 0.696) and significantly improved the baseline model (DeLong test P < 0.05), with additional gains confirmed by IDI, NRI, and DCA (all P < 0.05).

Conclusion: Both the non-traditional ApoB/A1 ratio and the traditional lipid marker non-HDL-C were independently and linearly associated with OCT-characterized high-risk plaques in AMI. Their combined assessment enhanced the identification of high-risk plaques morphology.

Cardiovascular diseases (CVDs) continue to be the leading cause of mortality worldwide, highlighting the need for enhanced diagnostic tools to enable early intervention. However, the complexity of these diseases poses significant challenges to their diagnosis and management. Therefore, a deeper understanding of CVD mechanisms and the development of novel diagnostic and therapeutic strategies are of critical importance. Retinol-binding protein 4 (RBP4), a member of the lipocalin family, is mainly secreted by the liver and adipose tissue and is widely recognized for its role in transporting retinol (vitamin A). Beyond functioning as a selective retinol carrier, growing evidence suggests that RBP4 is intricately involved in the pathogenesis of CVDs and their associated risk factors. Although numerous studies have established a link between RBP4 and the onset and progression of CVDs, the underlying mechanisms remain incompletely elucidated. This review summarizes the biological characteristics and multifunctional roles of RBP4 in CVD pathophysiology, examines its potential as a biomarker for diagnosis and prognosis, and explores its implications for developing new strategies to prevent and treat cardiovascular disorders.