Reviews in cardiovascular medicine最新文献

Atherosclerosis, a leading cause of global mortality, is a chronic inflammatory disease driven by a vicious cycle of endothelial dysfunction, dysregulated lipid metabolism, and persistent inflammation. This review examines the mechanisms through which diverse triggers initiate the cycle. We discuss key cellular and molecular events, such as the detrimental phenotypic switching of vascular smooth muscle cells. We also describe the processes through which various upstream signals converge on core inflammatory hubs, such as the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) pathway and the nucleotide-binding oligomerization domain, leucine-rich repeat-containing family, pyrin domain-containing-3 (NLRP3) inflammasome. By integrating these established mechanisms with recent findings on novel regulators, including the chemokine hemofiltrate CC chemokine 1 (HCC-1) and cell surface glycoRNA, this review identifies several potential new biomarkers. Overall, this review aimed to provide a comprehensive understanding of the pathogenesis of atherosclerosis, informing future research and the development of targeted interventions.

Background: Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents a heterogeneous clinical entity with an unclear pathophysiological basis. Fibrinogen is a key coagulation factor and inflammatory marker that has been associated with atherosclerotic burden in myocardial infarction (MI). However, the role of fibrinogen in MINOCA remains to be established. Therefore, this study aimed to investigate the association between plasma fibrinogen levels and the occurrence of MINOCA, and to evaluate the potential value of fibrinogen assessment in clinical characterization and early identification.

Methods: This retrospective study initially screened 1759 patients diagnosed with acute myocardial infarction (AMI) who underwent coronary angiography. A total of 287 patients were analyzed after applying the inclusion and exclusion criteria: 87 with MINOCA and 200 with the MI alongside obstructive coronary artery disease (MI-CAD). A logistic regression analysis was used to assess the association between fibrinogen levels and MINOCA, with subgroup and interaction analyses performed. Receiver operating characteristic (ROC) and restricted cubic spline (RCS) analyses were conducted as supplementary evaluations.

Results: Fibrinogen levels were significantly lower in the MINOCA group compared to the MI-CAD group (p = 0.005). Lower fibrinogen levels were independently associated with increased odds of MINOCA in the multivariate analysis (odds ratio (OR): 0.654, 95% confidence interval (CI): 0.483-0.885; p = 0.006). Quartile analysis revealed a significant inverse trend between fibrinogen levels and risk of MINOCA (p for trend = 0.006), which was further confirmed by a consistent dose-response relationship in the spline analysis (p for overall = 0.035; p for nonlinear = 0.590). The association remained robust across several subgroups. Fibrinogen alone showed a limited discriminative ability (area under the curve (AUC) = 0.605, 95% CI: 0.534-0.675; p = 0.005).

Conclusions: Lower plasma fibrinogen levels were independently associated with the occurrence of MINOCA, suggesting a potential role in its pathophysiology and the early identification of this condition. Fibrinogen alone has limited discriminative utility; however, fibrinogen may contribute to multi-marker approaches for determining and managing MINOCA patients.

Sarcoidosis is a rare inflammatory disorder of unknown etiology, characterized by the formation of non-caseating granulomas in affected organs. Additionally, sarcoidosis typically involves multiple systems, with the lungs and thoracic lymph nodes being most commonly affected. While many cases are self-limited and resolve spontaneously, cardiac involvement, although relatively uncommon, can be particularly severe. Indeed, cardiac sarcoidosis may lead to life-threatening arrhythmias, severe heart failure, or sudden cardiac death, significantly impacting prognosis. Meanwhile, the heterogeneity of presentation and disease course can make diagnosis and treatment challenging. An endomyocardial biopsy (EMB) is considered the gold standard for diagnosing cardiac sarcoidosis (CS); despite its high specificity, the sensitivity of this technique is low owing to the often focal and patchy cardiac involvement in sarcoidosis. New imaging techniques, such as fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) and cardiac magnetic resonance (CMR) imaging, can provide valuable information for the accurate diagnosis of CS and can be useful for evaluating treatment response and prognosis. Immunosuppressive treatments, particularly corticosteroids, are considered the cornerstone of therapy for CS. However, randomized clinical trials are lacking, and treatment decisions are based on cohort studies and consensus opinions. Moreover, the optimal strategy for determining when to initiate, how long to continue, and what dosage to use for immunosuppressive therapy remains uncertain.

Heart failure with preserved ejection fraction (HFpEF) has progressively emerged as the predominant form of heart failure. Thus, studies on the underlying mechanisms of HFpEF have shifted from pathophysiological to molecular factors. Meanwhile, previous studies have primarily focused on inflammation, oxidative stress, metabolic dysregulation, and impaired cardiac compliance (manifesting as ventricular hypertrophy and interstitial fibrosis). In addition to conventional guideline-directed medical therapies, novel therapeutic strategies targeting these aforementioned pathogenic pathways have been investigated. This review aimed to summarize recent progress in HFpEF pathogenesis and emerging treatment approaches, offering insights for developing novel diagnostic and management strategies.

Despite the relatively low incidence of Brugada syndrome (BrS) globally, the risk of sudden cardiac death remains alarmingly high, reaching rates of up to 28%. According to current clinical guidelines, implantable cardioverter defibrillators (ICDs) are recommended for high-risk patients. Meanwhile, pharmacological interventions must be used as a backup owing to the limited access to ICDs by eligible patients. Cilostazol, an adenosine uptake inhibitor and phosphodiesterase III inhibitor, has been suggested to reduce the risk of ventricular arrhythmias in BrS patients by stabilizing the action potential dome and lowering the epicardial-to-endocardial repolarization gradient, consequently decreasing the probability of phase II re-entry. However, the effectiveness of cilostazol in this situation has been questioned due to the existence of contradictory results from different case reports. Thus, this literature review aims to synthesize current evidence regarding the potential of cilostazol to lower the risk of ventricular arrhythmias in patients with BrS.

Background: Surgical repair of partial and transitional atrioventricular septal defects (AVSDs) aims to achieve optimal outcomes with minimal need for reintervention. This study aimed to evaluate the mid-term outcomes of AVSD repair in both pediatric and adult populations.

Methods: We retrospectively reviewed all patients who underwent surgical repair for partial or transitional AVSDs at our center between January 2019 and December 2022. Key outcomes, including mortality, reoperation, and atrioventricular valve (AVV) repair strategies, were assessed during follow-up.

Results: A total of 136 patients were included (partial AVSD, n = 100; transitional AVSD, n = 36), with a median follow-up of 50.5 months. The median hospital stay was 14 days. No early or late deaths occurred. Reoperation was required in four patients (2.9%); all reoperations included left atrioventricular valve (LAVV) reoperation. However, reoperation rates did not differ significantly between AVSD subtypes (p = 1.000) or age groups (p = 0.177). The incidence of moderate or greater LAVV regurgitation showed no significant difference between patients with and without ring annuloplasty, either postoperatively or at the final follow-up (both p = 1.000).

Conclusions: Surgical repair of partial and transitional AVSDs results in excellent mid-term survival and a low reoperation rate across both pediatric and adult patients. Continued refinement of AVV repair strategies remains essential to reduce the risk of LAVV reintervention and prevent left ventricular outflow tract obstruction. Long-term follow-up is warranted to improve the evaluation of the durability of techniques such as suture annuloplasty and ring annuloplasty.

Background: This study aimed to evaluate the clinical efficacy of in-line mechanical insufflation-exsufflation (IL-MIE) in airway secretion management in patients receiving invasive mechanical ventilation after cardiopulmonary bypass (CPB).

Methods: A total of 56 patients who underwent CPB and required invasive mechanical ventilation in the Cardiac Surgery Intensive Care Unit of Beijing Anzhen Hospital, Capital Medical University, between July 2015 and July 2020, were enrolled and divided into an IL-MIE group (n = 28) and a conventional suction (CS) group (n = 28). The IL-MIE group received automated secretion clearance every 30 min for 8 h, supplemented with CS as needed, whereas the CS group received standard CS treatment. General patient data, respiratory and hemodynamic parameters, ventilator settings, CS frequency, mechanical ventilation duration, and intensive care unit (ICU) length of stay were recorded during the 8 h intervention.

Results: At 4 h and 8 h, the IL-MIE group exhibited significantly higher arterial oxygen partial pressure, oxygenation index, and static compliance and low plateau pressure (p < 0.05). Heart rate was significantly lower in the IL-MIE group at 4 h ((99.21 ± 13.87) vs. (89.32 ± 10.66); p < 0.01) and 8 h ((96.71 ± 14.47) vs. (89.61 ± 9.34); p = 0.033). The IL-MIE group required fewer CS interventions (0 (0, 1) vs. 4 (3, 4); p < 0.01) and had a shorter duration of mechanical ventilation (20 (16.75, 22) vs. 24 (18.75, 26.5); p = 0.029) than those in the CS group.

Conclusions: By mimicking physiological airway clearance, IL-MIE significantly improves oxygenation and lung compliance, reduces the duration of mechanical ventilation, and maintains hemodynamic stability during respiratory management in patients after CPB.

The complex anatomy of coronary bifurcation lesions (CBLs) remains a major challenge in percutaneous coronary interventions (PCIs). Currently, the single-stent strategy offers procedural simplicity; however, this strategy carries a higher risk of side-branch occlusion. Conversely, the two-stent technique improves branch coverage but is associated with increased risks of metal carina formation and late stent thrombosis. This article reviews the technical key points and indications of the provisional stent, T-stent, Crush, and Culotte techniques. Moreover, this article focuses on discussing the core challenges of different methods according to anatomical characteristics, post-dilatation stent morphology, and procedural variability of lesions during PCI. Furthermore, corresponding optimization strategies were explored to guide individualized treatment of CBLs using the Visual Risk Prediction of Side-branch Occlusion in Coronary Bifurcation Intervention (V-RESOLVE) score, functional assessments, and intracoronary imaging combined with the DEFINITION criteria.

Emerging evidence has implicated the gut microbiota in the pathogenesis and progression of numerous cardiovascular diseases. Atherosclerosis is a major pathological process that leads to many severe cardiovascular complications. Meanwhile, atherosclerosis patients may experience local and systemic inflammatory responses, with structural changes in the intestinal microbiota and increased mucosal permeability. Currently, the role of gut microbiota-derived metabolites in atherosclerosis pathology is of great concern. Relevant findings have highlighted the potential direct or indirect impacts of gut microbiota on the metabolic health of the host via the production of various metabolites. Thus, this review places an emphasis on bile acids (BAs), metabolites derived from and regulated by the gut microbiota. BAs can delay the pathological processes associated with atherosclerosis, underscoring the significance of these metabolites as an early marker for disease progression risk. In addition, we explore the potential of BA-related gut metabolites as novel therapeutic targets for atherosclerosis, and propose several promising directions for future research.