Frontiers in Cardiovascular Medicine最新文献

A 49-year-old woman with a congenital quadricuspid aortic valve presented in cardiogenic shock due to severe aortic regurgitation. She underwent transfemoral transcatheter aortic valve replacement with a 29 mm self-expanding prosthesis. The procedure was technically successful with minimal paravalvular leak and significant symptomatic improvement. However, her long-term course was complicated by medication nonadherence, valve thrombosis, thromboembolic coronary events, and progressive heart failure. This case highlights the anatomical and technical challenges of transcatheter valve therapy in non-tricuspid anatomy, including annular sizing and valve anchoring without calcification, and underscores the critical importance of post-procedural anticoagulation adherence and meticulous follow-up to prevent thrombotic complications.

With the acceleration of population aging, the prevalence of vascular calcification (VC) is on the rise, particularly among patients with hypertension, diabetes, chronic kidney disease, and age-related diseases. VC is characterized by the abnormal deposition of calcium phosphate in the vascular walls, and there are currently no effective pharmacological treatments available. This condition is a manifestation of vascular aging. The silent information regulator (SIRT) family, which includes SIRT1 to SIRT7, functions as deacetylases and plays a crucial role in cellular resistance, energy metabolism, apoptosis, and cellular aging, often referred to as longevity proteins. The SIRT family has shown potential in alleviating vascular aging by inhibiting inflammation, reducing endoplasmic reticulum stress, lowering mitochondrial oxidative stress, and promoting DNA damage repair, all of which contribute to the suppression of vascular calcification. Notably, SIRT1, SIRT2, SIRT3, SIRT6, and SIRT7 have demonstrated therapeutic potential in the treatment of vascular calcification.

Cardiovascular disease (CVD) represents a significant global health challenge, making the detection of cardiac biomarkers crucial for early diagnosis and tailored treatment strategies. This research aims to transpire a point-of-care (POC) test using a biosensor for CVDs that will be fast and pragmatic for immediate use in acute and resource-constrained environments. Traditional techniques such as enzyme-linked immunosorbent assay and polymerase chain reaction, although very precise, are time-consuming, labor intensive, and not suitable for use in urgent care; however, optical nano biosensors provide rapid, highly selective, and sensitive detection capabilities. The optical nano biosensors produce biological signals that convey light signals as analytes interact with bioreceptors. Optical nano biosensors offer various benefits, including effortless monitoring, inexpensiveness, a broad detection spectrum, and excellent sensitivity with no interference. An optical nano biosensor platform represents an effective method for point-of-care detection of cardiac biomarkers, characterized by a low detection limit. To propose a realistic reference, this study assesses a prompt POC test, which identifies important cardiac biomarkers, such as cardiac troponins (cTnI), B-type natriuretic peptide (BNP), and C-reactive protein (CRP), which together provide an all-encompassing confinement of myocardial injury, cardiac stress, and inflammation. Subsequently, the test was performed using a random patient population; the accuracy of the test was established to be high in terms of both sensitivity (95.2% for cTnI, 91.8% for BNP, and 89% for CRP) and specificity and had a close correlation with laboratory tests. It provided results in 15 min, which makes it effectively useful when used in emergency and primary care, where quick decisions are required to be taken. The low cost and rapidity of the test increase its applicability notably; this multiplexing allows clinicians to identify individuals at high risk for different CVD events. This work highlights the possibility of incorporating biosensor technology into diagnostic systems at the POC level to enhance patient prognosis by facilitating early interventions and establishes a basis for improving biomarker detection.

Congenital heart defects (CHDs), a life-threatening congenital pathology, are reported in approximately one out of every 100 live births, with the severity ranging from mild to fatal. The prevalence of CHDs has significantly increased over the last few decades, most likely due to evolved diagnostics and increased accessibility to healthcare worldwide. The ratio of severe CHDs, which require urgent surgery, to mild forms, which may not require surgery, is between 1:4 and 1:3. Therefore, every fourth or fifth newborn with a CHD needs immediate and effective surgical treatment. Furthermore, one in 10 diagnoses involves multiple CHDs, which require complex surgical treatment and elevate the risk of peri- and post-operative mortality. In this review, we focus on ventricular septal defects (VSDs) that constitute a significant proportion of CHDs. We briefly discuss the historical background and current strategies for VSD treatment, including open-heart surgery, transcatheter surgery, and mini-invasive hybrid surgery. The hybrid method is then comprehensively discussed, considering its success and complication rates compared to the other two approaches, its implementation, typical delivery approaches, and the most common types of occluders; we accompany this discussion with our own clinical experiences. The advantages and limitations of the hybrid approach are also discussed. We conclude that the prospects for wider use of the hybrid approach for VSD correction are favorable due to its mini-invasiveness, high safety and effectiveness, and because cardiopulmonary bypass is not needed in this approach.

Atherosclerosis, driven primarily by cumulative exposure to low-density lipoprotein cholesterol (LDL-C), is the major cause of atherosclerotic cardiovascular disease (ASCVD). This narrative review examines the pathogenesis of atherosclerosis, linking risk factors, inflammatory pathways, and lipid abnormalities to the formation and progression of atheromatous plaques. Plaque characteristics such as volume, lipid content, fibrous cap thickness, and minimum lumen area are closely associated with cardiovascular outcomes, particularly the risk of major adverse cardiac events (MACEs). Intensive LDL-C lowering through statins, ezetimibe, PCSK9 inhibitors, and emerging agents like bempedoic acid has demonstrated clear benefits in regressing plaques, stabilizing their morphology, and significantly reducing cardiovascular risks. Despite guideline recommendations advocating intensive lipid-lowering strategies, real-world practice reveals considerable gaps, with many high- and very-high-risk patients failing to achieve LDL-C targets. Contributing factors include poor adherence, underuse of combination therapies, and treatment inertia. Early detection and preemptive management of subclinical atherosclerosis, particularly among younger individuals, are gaining attention as strategies to intercept the progression of disease before clinical events occur. Moreover, elevated lipoprotein(a) levels are increasingly recognized as an independent causal factor for ASCVD, and ongoing trials are evaluating specific Lp(a)-lowering therapies. Overall, optimizing lipid management through intensive, early intervention, patient adherence, and personalized treatment approaches holds the key to reducing the global burden of ASCVD. Addressing residual risks and refining early detection strategies will further advance the prevention and management of this chronic, progressive vascular disease.

Objective: To evaluate immune microenvironment markers for predicting sepsis-induced myocardial dysfunction (SIMD) and establish three predictive models-nomogram, decision tree, and gradient boosting machine (GBM)-to compare their efficacy in assessing SIMD risk.

Method: A retrospective analysis was conducted on the clinical data of 165 patients with sepsis who were admitted between January 2022 and February 2025. Patients were divided into SIMD and non-SIMD groups according to the occurrence of SIMD. Risk factors influencing the occurrence of SIMD in patients with sepsis were screened using univariate and multivariate logistic regression analyses. Nomogram, decision tree, and GBM models were constructed based on the results of the multivariate logistic regression analysis. The area under the receiver operating characteristic curve (AUC) was used to evaluate the discrimination of each model. The accuracy, sensitivity, specificity, and F1 scores of the three models were calculated.

Result: : Among the 165 patients with sepsis included in the study, 75 were in the SIMD group, accounting for 45.45% (75/165). Univariate analysis showed significant differences between the two groups in APACHE II score, white blood cell count, N-terminal pro-brain natriuretic peptide (NT-proBNP), soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), and high mobility group box 1 (HMGB1) levels (P < 0.05). Logistic regression analysis revealed that a high APACHE II score (OR = 1.480, 95% CI: 1.127-1.945), high NT-proBNP level (OR = 1.013, 95% CI: 1.005-1.021), high sTREM-1 level (OR = 1.116, 95% CI: 1.034-1.205), and high HMGB1 level (OR = 1.006, 95% CI: 1.002-1.011) were risk factors for SIMD in patients with sepsis (P < 0.05). All three prediction models demonstrated excellent performance in the training set: nomogram (AUC = 0.843), decision tree (AUC = 0.815), and GBM (AUC = 0.885). No significant differences were observed in the AUC values among the models (all P > 0.05).

Conclusion: The immune markers, sTREM-1 and HMGB1, were associated with SIMD. Elevated APACHE II score and NT-proBNP, sTREM-1, and HMGB1 levels are risk factors for SIMD in patients with sepsis. Predictive models based on these factors demonstrate strong performance and effectively identify high-risk individuals, aiding in early clinical intervention.

Purpose: The ratio of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol (NHHR) has recently been identified as a novel lipid marker for assessing the risk of atherosclerosis-related diseases. However, the relationship between NHHR and the risk of retinal vein occlusion (RVO) has not yet been thoroughly investigated. The objective of this study was to investigate the correlation between NHHR and patients with RVO.

Methods: This retrospective study examined 54 patients diagnosed with RVO and 57 age- and gender-matched control subjects. Comprehensive ocular examinations and hematological assessments were conducted for all participants. Logistic regression analysis was employed to evaluate the association between lipid markers and the risk of RVO. The receiver operating characteristic (ROC) curve was utilized to analyze and determine the predictive value and optimal threshold of the NHHR, triglyceride-glucose (TyG) index, and other conventional lipid parameters for RVO.

Results: Compared to the control group, patients with RVO exhibited significantly higher levels of triglyceride (TG), TyG index, and NHHR (P = 0.0004, P = 0.0006, and P < 0.0001, respectively). Additionally, the high-density lipoprotein cholesterol (HDL-C) index was significantly lower in the RVO group compared to the control group (P < 0.0001). Univariate analysis indicated that NHHR (OR: 3.41, P < 0.001), TyG index (OR: 3.32, P = 0.001) and TG (OR: 2.64, P = 0.003) were significantly associated with RVO. Multivariate analysis revealed that NHHR was remarkably associated with RVO (OR: 2.09, P = 0.037). After further adjustment for hypertension, TG, and the TyG index, this association remained statistically significant (OR: 3.13, P = 0.003). The areas under the ROC curve for TyG index, TG, HDL-C, and NHHR were 0.679, 0.692, 0.739, and 0.752, respectively. Notably, the AUC value for NHHR demonstrated a moderate sensitivity (50.88%) and high specificity (87.04%), indicating its potential as a promising biomarker for the diagnosis and prognosis of RVO.

Conclusion: The NHHR was significantly elevated in patients with RVO, suggesting that this novel lipid marker may play a crucial role in the risk of developing RVO.

High-density lipoprotein (HDL) has earned its reputation as "good" cholesterol in cardiovascular health, primarily because of its strong inverse association with cardiovascular disease. A potential mechanism for this association is its ability to promote cholesterol efflux capacity (CEC) and consequently reduce the buildup of cholesterol in arterial plaque. However, recent research underscores the importance of not only maintaining high HDL cholesterol (HDL-C) levels but also ensuring the functionality and quality of HDL particles. HDL particles exhibit various other atheroprotective activities, including anti-inflammatory, antioxidant, and vasodilatory properties. Collectively, these functions are thought to contribute to reducing cardiovascular risk beyond mere cholesterol transport. Both acute and chronic inflammation can induce structural and functional changes in HDL, potentially rendering the particles pro-inflammatory. Factors that increase inflammation, such as lifestyle choices, autoimmune diseases, and oxidative stress, can adversely affect HDL functionality. Dysfunctional HDL, such as electronegative HDL H5 or HDL isolated from patients with cardiovascular disease (CVD), may lose its protective properties and even contribute to CVD progression by promoting inflammation, oxidative stress, and endothelial damage. Recent studies indicate that the CEC of HDL particles may serve as a more critical determinant of atheroprotection than the absolute concentration of HDL-C. This review emphasizes the need to focus on both quantity and quality of HDL to reduce cardiovascular risk more effectively. Understanding the mechanisms behind HDL's protective effects provide valuable insights into heart health and potential therapeutic strategies.

Background: High-intensity interval training (HIIT) is increasingly used in cardiac rehabilitation. Its effects on cardiopulmonary function and quality of life in patients with myocardial infarction (MI) require systematic evaluation.

Methods: A systematic search was conducted in PubMed, Embase, Web of Science, Cochrane Central, and CNKI from inception to April 1, 2025. Randomized controlled trials assessing the effects of HIIT on peak heart rate (HRpeak), peak oxygen uptake (VO₂peak), respiratory exchange ratio (RER), and quality of life (QOL) in post-MI patients were included. Data were synthesized using a random-effects model. Standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated. Heterogeneity was assessed with the I² statistic, and sensitivity analyses were performed.

Results: Nine trials with 508 participants were included. HIIT did not significantly affect HRpeak (SMD = -0.20; 95% CI: -1.10 to 0.70; I² = 62.4%) or VO₂peak (SMD = 0.32; 95% CI: -0.07 to 0.71; I² = 69.1%). RER was significantly reduced in the HIIT group (SMD = -1.26; 95% CI: -1.54 to -0.98; I² = 0%). No significant improvement was observed in QOL (SMD = 0.07; 95% CI: -0.37 to 0.50; I² = 0%). Sensitivity analyses suggested that individual studies contributed to heterogeneity in HRpeak and VO₂peak outcomes.

Conclusions: HIIT may influence selected cardiopulmonary indicators in post-MI patients, particularly metabolic efficiency. Its effects on exercise capacity and quality of life remain uncertain. Further research with standardized protocols is needed.

Background: Type 2 diabetes (T2DM) and hypertension (HTN) are key risk factors for retinopathy and often coexist with coronary heart disease (CHD). While AI-based retinal imaging predicts CHD risk, links between CHD lesion complexity and retinopathy, and potential benefits of Sodium-Glucose Cotransporter-2 (SGLT2) inhibitors on retinopathy in CHD patients with T2DM, lack sufficient evidence.

Methods: This case-control study (Jan 2024-Mar 2025) enrolled 642 subjects from Beijing Tongren Hospital (affiliated with Capital Medical University). Retinal imaging data were analyzed. Propensity score matching (PSM) created baseline and optimized datasets. Univariate/multivariate logistic regression assessed if CHD increases retinopathy risk in patients with T2DM, HTN, or both. Pearson correlation evaluated associations between CHD lesion complexity (SYNTAX score) and retinal parameters. Stratified analysis assessed SGLT2 inhibitor effects on retinopathy in hypertensive-diabetic subgroups with/without CHD. The analysis of SGLT2 inhibitor efficacy was based on a retrospective cohort study of drug utilization rather than a prospective randomized intervention.

Results: Within the hypertensive-diabetic cohort, CHD patients (n = 97 SGLT2i treated vs. n = 69 controls) showed SGLT2 inhibitors reduced MRV(Venular)C risk (P < 0.001, OR = 0.584) but increased AVR1.5-2.0PD risk (P = 0.003). Post-PSM, CHD + T2DM + HTN patients had decreased MRAC vs. T2DM + HTN patients (P < 0.001, OR = 0.776). SYNTAX score positively correlated with retinal vein diameter and negatively with AVR (both P < 0.05).

Conclusion: CHD elevates retinopathy risk in patients with T2DM, HTN, or both. Coronary lesion complexity correlates with retinal microvascular changes. SGLT2 inhibitors demonstrate a potential protective effect against some aspects of retinopathy development.