Frontiers in Cardiovascular Medicine最新文献

Background: Lipoprotein(a)-targeted therapies are emerging approaches for lowering lipoprotein(a) [lp(a)].

Objective: We conducted a systematic review and network meta-analysis to evaluate the efficacy and safety of lipoprotein(a)-targeted therapies in patients.

Methods: We searched PubMed, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) up to May 6, 2025, for randomized controlled trials (RCTs) with intervention duration of at least 12 weeks. The primary outcomes were percentage and absolute changes in Lp(a). Secondary outcomes included changes in low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apoB), and safety outcomes including adverse events (AEs), serious adverse events (SAEs), and injection-site reactions. A frequentist framework network meta- analysis was performed.

Results: Nine studies involving 1,432 participants were included. All six Lp(a)-targeted therapies significantly reduced Lp(a) levels. Compared with placebo, Olpasiran was the most effective therapy for both percentage [mean difference: -92.06, 95% (-109.80; -74.32), P-score: 0.94] and absolute reductions [-250.70 (-262.04; -239.36), P-score: 0.99], followed by Zerlasiran [-78.33 (-92.18; -64.48), P-score: 0.70], [-205.63 (-217.24; -194.03), P-score: 0.76]. In between-drug comparisons, Olpasiran was superior to Pelacarsen. Both Olpasiran and Zerlasiran were associated with improved LDL-C and apoB concentrations. Zerlasiran, Lepodisiran, and Pelacarsen were found to increase the risk of injection-site reactions.

Conclusions: Lp(a)-targeted therapies achieved substantial reductions in Lp(a). Olpasiran was the most effective agent in lowering Lp(a) levels. These therapies also improved LDL-C and apoB. The majority of Lp(a)-targeted therapies demonstrate generally favorable safety profiles; However, injection-site reactions, particularly with Zerlasiran, warrant careful consideration.

Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251069288, PROSPERO CRD420251069288.

Background: Cutibacterium acnes is an easily overlooked pathogen in infective endocarditis (IE) due to its slow growth, propensity for biofilm formation, and high rate of culture-negative results. When complicated by structural heart disease such as a ruptured sinus of Valsalva aneurysm (RSVA), its indolent course can lead to severe hemodynamic compromise.

Case summary: A 35-year-old male with a known ventricular septal defect (VSD) and unruptured aortic sinus aneurysm presented with persistent fever and progressive heart failure (NYHA class IV). Echocardiography revealed a ruptured right coronary sinus of Valsalva aneurysm (RCSVA) into the right ventricular outflow tract (RVOT) with a large vegetation. Blood cultures were negative. After 6 days of ineffective empirical antibiotic therapy, emergency surgery was performed to resect the aneurysm and vegetation and repair the cardiac structures. Intraoperatively, a vegetation sample was collected for metagenomic next-generation sequencing (mNGS). Postoperatively, mNGS identified Cutibacterium acnes with high sequence reads (1,284) and coverage (47.62%), enabling a definitive diagnosis. Pathology confirmed microcolonies and necrotic inflammation. The antibiotic regimen was switched to a regimen with potential activity against biofilms with oral doxycycline and intravenous clindamycin for 6 weeks. The patient's inflammatory markers normalized, and cardiac function recovered to NYHA class I, with no recurrence at 12-month follow-up.

Conclusion: This case highlights the diagnostic synergy of intraoperative histopathology and mNGS for pathogen identification, underscores the rationale for biofilm-conscious adjuvant therapy, and reaffirms the crucial role of early surgical debridement and repair in achieving cure.

Background: Myocarditis is a common feature of acute Kawasaki disease (KD) and a major contributor to myocardial contractile dysfunction, which can be alleviated by timely intravenous immunoglobulin (IVIG) treatment. However, the effects of KD on myocardial systolic function and the impact of IVIG on myocardial recovery are not well understood in animal models. This study aims to explore whether left ventricular systolic dysfunction occurs in a KD mouse model and to evaluate the potential benefits of IVIG in mitigating myocardial contractile impairment using high-resolution speckle-tracking imaging (STI).

Methods: We utilized a Lactobacillus casei cell-wall extract (LCWE)-induced murine model of KD vasculitis to assess the effects of IVIG treatment on myocardial dysfunction. Histological analyses and speckle-tracking strain imaging were performed to evaluate myocardial function during the progression of KD-induced vasculitis and myocarditis.

Results: IVIG treatment significantly prevented both myocarditis and vasculitis. Conventional echocardiographic analyses showed differences in ejection fraction between the KD and control groups 14 days after LCWE injection, regardless of IVIG treatment. Notably, both the KD and KD + IVIG groups exhibited reduced longitudinal strain (LS) as early as 3 days post-injection compared to the control group. While LS remained decreased in the KD group throughout the disease progression, the KD + IVIG group showed a recovery to normal LS levels by day 56. At 14 and 28 days post-LCWE injection, LS in the KD group was significantly lower than in the KD + IVIG group. LS was negatively related to myocarditis scores (r = -0.94, P < 0.001).

Conclusions: Myocardial contractile dysfunction resulting from myocarditis occurs in the KD mouse model and can be improved with IVIG treatment. High-resolution STI offers a more sensitive and accurate method for assessing myocardial dysfunction and the effects of cardioprotective treatments compared to conventional echocardiography.

Background: The Triglyceride-Glucose (TyG) index, a surrogate marker of insulin resistance, is associated with increased cardiovascular risk. However, its relationship with subclinical atherosclerosis in diabetic patients with early-stage kidney injury, characterized by an elevated urinary albumin-to-creatinine ratio (ACR), remains unclear. This study examined the association between carotid intima-media thickness (IMT) and the TyG index, specifically investigating how this association is modified by albuminuria status.

Methods: This cross-sectional study included 507 patients with type 2 diabetes and preserved kidney function who had ACR values of 0-300 mg/g. Participants were stratified into quartiles based on ACR levels. IMT was measured using high-resolution B-mode ultrasonography. The relationship between the TyG index and IMT was evaluated using partial correlation and multivariate linear regression analyses, with emphasis on assessing this relationship across ACR-based strata.

Result: A weak positive correlation was observed between the TyG index and IMT overall (r = 0.12, P = 0.035), with a significant interaction effect of ACR (p = 0.008). Stratification by ACR showed that for patients with ACR ≤ 30 mg/g, each unit increase in the TyG index was associated with a 0.038 mm increase in IMT (95% CI: 0.015-0.061, p = 0.002), while for those with ACR > 30 mg/g, the increase was 0.071 mm per unit (95% CI: 0.036-0.106, p < 0.001). Furthermore, a graded pattern was observed across ACR quartiles, with the positive correlation between TyG and IMT showing graded strengthening (β values increased from 0.022 to 0.078, p for trend <0.001;). Finally, the TyG-IMT correlation exhibited age specificity, being significant in patients under 50 years (<40 years: β = 0.085, p = 0.002; 40-49 years: β = 0.051, p = 0.015) and diminishing in older age groups.

Conclusions: The association between the TyG index and IMT exhibits stage-specific and population-heterogeneous patterns. A significant, ACR-dependent positive correlation was observed, with the association being pronounced in patients with elevated ACR (>30 mg/g) and in those younger than 50 years. These findings suggest that the pro-atherogenic effect of insulin resistance is more pronounced in diabetic patients with early albuminuria or in younger individuals, underscoring the need for enhanced vascular management to reduce insulin resistance in these high-risk populations.

Background: Branch pulmonary artery (PA) stenosis is a common complication in congenital heart disease (CHD) that can result in unequal pulmonary perfusion, cyanosis, and increased ventricular workload. Although surgical repair remains an option, pulmonary artery stenting has emerged as a less invasive and effective alternative for restoring vessel patency.

Methods: This single-center retrospective study included 18 pediatric patients (median age 5.4 years, range 3 months-17 years) who underwent PA stenting for branch stenosis associated with complex CHD. Patient demographics, procedural characteristics, complications, and follow-up outcomes were analyzed.

Results: A total of 19 stents were successfully implanted; 10 in the left PA, 7 in the right PA, and one case of bilateral stenting. The mean pre-procedural oxygen saturation improved from 78.1% ± 12.5 to 91.6% ± 7.3 during follow-up. Procedural success was achieved in all cases. Five complications were recorded, including one case of stent dislodgement requiring surgical retrieval and one case of inadequate stent expansion due to over-compliant pulmonary arteries. Three deaths occurred, all attributed to underlying clinical deterioration rather than the procedure itself. No instances of vascular rupture or pericardial tamponade were observed. Most surviving patients demonstrated sustained improvement in oxygenation and progressed to definitive surgical repair or Fontan completion.

Conclusions: Pulmonary artery stenting is a safe and effective intervention for managing branch PA stenosis in complex pediatric CHD, providing significant hemodynamic and clinical benefits with an acceptable complication profile. Careful pre-procedural imaging, appropriate stent selection, and meticulous deployment technique are essential to prevent complications such as dislodgement or incomplete expansion, ensuring durable long-term outcomes.

Objective: To explore the influencing factors for the enlargement of inter-arm systolic blood pressure difference (IASBPD) between different genders.

Methods: A retrospective analysis was performed on the data of individuals who underwent body composition testing in our department and completed limb arterial blood pressure measurement, biochemical examinations, and other relevant tests at the physical examination center or outpatient clinic of our hospital between September 2019 and December 2022. The participants were divided into two groups based on whether the inter-arm systolic blood pressure difference (IASBPD) was increased: the IASBPD≥10mmHg group and the IASBPD < 10mmHg group. The influencing factors for an increased IASBPD were analyzed in the overall population as well as in different gender subgroups.

Results: Participants with IASBPD≥10mmHg exhibited higher obesity-related indicators, including body mass index (BMI), waist circumference (WC), neck circumference (NC), abdominal circumference (AC), and visceral fat area (VFA) (P < 0.05). Additionally,the group with an IASBPD≥10mmHg had a higher proportion of males, elevated levels of white blood cells, monocytes, and lymphocytes, as well as a higher prevalence of hypertension and dyslipideia (P < 0.05). IASBPD was positively correlated with NC, age, and lymphocytes, and negatively correlated with Ankle-Bronchial Index (ABI). An increased ABI was a protective factor for IASBPD in the general population, while an increased NC and hypertension were risk factors for an increased IASBPD. However, an increase in NC is a risk factor for an elevated IASBPD in males, while advanced age is a risk factor for increased IASBPD in females.There are differences in IASBPD values between males and females in the quartile groups stratified by NC and age. ABI-left, right and left upper arm systolic blood pressure all exhibit certain predictive performance for the increase in IASBPD in both male and female populations. The cut-off values of NC and age for predicting the elevation of IASBPD were 37.75 (sensitivity: 66.1%, specificity: 53.5%) and 49.5 (sensitivity: 77.0%, specificity: 47.5%), respectively.

Conclusion: The incidence of increased IASBPD is higher in the male population. An increase in NC and advancing age are identified as risk factors for IASBPD elevation in the male and female populations, respectively.

Myocardial fibrosis (MF) is a maladaptive pathological response of the heart to chronic injury. Accumulating evidence indicates that MF plays a central role in the development and progression of hypertensive heart disease, ischemic cardiomyopathy, diabetic cardiomyopathy, and heart failure, and is closely associated with an increased risk of arrhythmias and sudden cardiac death. In recent years, advances in experimental and analytical approaches have improved our understanding of the molecular mechanisms underlying MF and informed the development of potential therapeutic strategies. However, many existing pharmacological interventions exhibit limited target specificity, uncertain long-term efficacy, and incompletely defined mechanisms of action in humans. In this review, we summarize the major molecular pathways involved in myocardial fibrosis and discuss current and emerging therapeutic approaches, incorporating mechanistic insights from recent single-cell and spatial transcriptomic studies to better contextualize fibrotic signaling heterogeneity and translational challenges.

Background: Younger patients with acute aortic dissection (AAD) are thought to present with distinct anatomical and hemodynamic features compared with older patients. This study evaluated the association between age, dissection extent, and false-lumen flow characteristics in AAD.

Methods and results: We retrospectively analyzed 400 consecutive patients with radiologically confirmed AAD from April 2014 to April 2024, categorizing them into a younger group (<76 years, n = 229) and an older group (≥76 years, n = 171). The distribution of Stanford type A vs. B dissections was similar between groups. However, younger patients more frequently demonstrated DeBakey type I dissection, whereas older patients more commonly had type II. Regarding false-lumen morphology, younger patients showed a higher prevalence of communicating false lumen, while non-communicating patterns predominated in the elderly. Although overall sex distribution of false-lumen types was not significantly different, younger males were more prevalent within each subtype. Preoperative malperfusion occurred more often in younger patients, whereas 30-day mortality did not differ significantly between age groups.

Conclusions: Younger AAD patients typically exhibit more extensive dissection and patent false-lumen flow, while older patients more often present with localized dissection and thrombosed false lumen. These age-related distinctions may reflect progressive aortic wall stiffening and should be considered in clinical assessment and management strategies.

Introduction: Despite standardized transfusion and chelation therapy, children with transfusion-dependent β-thalassemia (TDT) remain at high risk for cardiac dysfunction due to iron overload. Conventional ejection fraction assessment lacks sensitivity for early injury. This study evaluated multimodal indicators to develop a robust early-warning model.

Methods: A prospective cohort of 128 TDT children (3-16 years) underwent cardiac magnetic resonance (CMR) T2* imaging, echocardiography with global longitudinal strain (GLS), and measurement of circulating biomarkers including high-sensitivity cardiac troponin I (hs-cTnI), B-type natriuretic peptide (BNP), interleukin-6, and tumor necrosis factor-α. Children were classified into dysfunction and normal groups based on LVEF and GLS. Logistic regression identified predictors, and ROC analysis validated the integrated model.

Results: The dysfunction group demonstrated reduced GLS, ventricular remodeling, elevated hs-cTnI and BNP, and significantly shorter T2* values compared with controls (p < 0.001). Inflammatory cytokines were also upregulated. Multivariate analysis identified hs-cTnI, BNP, and T2* as independent predictors. The combined three-factor model achieved excellent discrimination (AUC 0.914), outperforming single markers, with preserved calibration following bootstrap validation.

Conclusion: By linking iron overload, myocardial injury, inflammation, and structural dysfunction, this study proposes a clinically feasible integrated model for early cardiac risk detection in pediatric TDT. The approach supports precision monitoring and prevention of heart failure.