Reviews in cardiovascular medicine最新文献

Pulmonary hypertension (PH) is characterized by an abnormally high pressure within the pulmonary arteries, which can be attributed to various factors. Severe diseases affecting pulmonary vessels may result in heart failure and potentially lead to death; these conditions are linked to significant mortality and unfavorable outcomes. Approximately 1% of adults worldwide have PH, and this condition may affect up to 10% of people older than 65 years. Currently, the mechanisms involved in the development of PH are not fully known and are thought to result from multiple coordinated factors. This lack of understanding remains a bottleneck in clinical practice. Numerous studies have confirmed that pulmonary artery endothelial cell (PAEC) dysfunction plays an important role in occlusive pulmonary vascular remodeling and the pathogenesis of PH. Src homology region 2 domain-containing phosphatase-1 (SHP-1) is a regulatory molecule that negatively modulates various cellular mediators and growth factors, primarily playing a negative regulatory role in signal transduction pathways. This review mainly presents an in-depth exploration of the key signaling pathways through which SHP-1 regulates the expression of endothelial cells (ECs), thereby influencing various physiological functions, including proliferation, migration, oxidative stress, angiogenesis, apoptosis, autophagy, the inflammatory response, and vascular permeability. Furthermore, the potential mechanisms through which endothelial SHP-1 plays a role in pulmonary vascular remodeling in PH are discussed. These findings underscore SHP-1 as an encouraging therapeutic target for preventing and managing PH.

Background: Complete atrioventricular block (CAVB) following transcatheter aortic valve replacement (TAVR) is primarily attributed to mechanical compression of the penetrating or branching portions of the His bundle, and less commonly, the atrioventricular (AV) node. This study aimed to characterize the electrocardiographic features of stable escape rhythms (ERs) occurring during CAVB after TAVR.

Methods: This retrospective study analyzed 12-lead electrocardiograms (ECGs) obtained at three time points: before TAVR (ECG 1), after TAVR but before CAVB (ECG 2), and during CAVB (ECG 3). The ERs on ECG 3 were classified as AV junctional if the rate was 40-60 beats per minute (bpm) and, compared with ECG 2, if the QRS morphology matched in ≥10/12 leads, the QRS duration differed by <10 ms, and the frontal QRS axis differed by <30°. The ERs not meeting these criteria were considered ventricular in origin. Three patients with ERs <40 bpm but matching AV junctional morphology were included in the AV junctional group. ECG 2 was unavailable in 12 patients.

Results: Among the 58 patients included, 56.9% had no conduction abnormalities on baseline ECG 1. Following TAVR (ECG 2), left and right bundle branch blocks were observed in 69.6% and 17.4% of the patients, respectively. During CAVB (ECG 3), the ERs were presumed to originate from the AV junction in 23 patients (39.6%), from the ventricles in 28 (48.3%), and had an undetermined origin in 7 (12.1%).

Conclusions: Consistent with the anatomical regions commonly affected by the prosthetic aortic valve during TAVR, a substantial proportion of patients exhibited ERs likely originating from the AV junction, suggesting a potential role for conduction system pacing in managing CAVB in this setting of patients.

Diabetic cardiac autonomic neuropathy (DCAN) is a common and serious complication of diabetes, and its early diagnosis and treatment are important for preventing cardiovascular events. At present, its diagnosis is mainly based on multiple functional investigations, such as heart rate variability (HRV) and cardiovascular reflex test. However, these methods are cumbersome to perform, time-consuming, and readily affected by patient cooperation and operator technique, resulting in limited clinical application. More importantly, DCAN still lacks standardized early diagnostic criteria and specific biomarkers. In recent years, the integration of multi-index diagnosis such as HRV, electrocardiograms (ECGs), continuous glucose monitoring (CGM) and machine-learning algorithms has improved the accuracy of early screening and prognosis. Here, we systematically review the latest research progress in relation to the pathological mechanism, diagnosis and treatment of DCAN, with a focus on novel biomarkers, therapeutic targets, and the potential for individualized treatment. This review provides new insights into DCAN, as well as the basis for early diagnosis and precise intervention.

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is a life-saving intervention for patients with refractory cardiogenic shock or cardiac arrest. However, weaning from VA-ECMO remains challenging and significantly affects patient prognosis. This systematic review examined the multifactorial determinants underlying successful VA-ECMO weaning, highlighting the critical need for integrated evaluation of biventricular function, hemodynamic stability, and microcirculatory perfusion. Key predictive parameters encompass both macrocirculatory indices (including left and right ventricular performance) and metabolic parameters, all of which collectively inform evidence-based weaning decisions. Advanced imaging techniques and multidimensional assessment tools have emerged as promising strategies for optimizing weaning protocols. Pharmacological strategies and precise volume optimization are important for improving weaning success. However, gaps in standardized weaning protocols and bridging therapy algorithms highlight critical, unmet needs. Thus, future efforts should focus on developing dynamic predictive models that incorporate real-time hemodynamic data and on the clinical implementation of microcirculatory assessment technologies.

Four-dimensional (4D) flow cardiac magnetic resonance (CMR) is an advanced imaging modality that enables comprehensive qualitative and quantitative assessment of blood flow in the three spatial dimensions plus time. This technique is more accurate, reproducible, and easier to interpret visually than conventional two-dimensional phase-contrast techniques. In this narrative review, we synthesize our clinical experience-including practical insights from representative cases from routine practice-with published research to describe the technical foundations, clinical applications, advantages, and limitations of this technique. We discuss the technical aspects, including spatial and temporal resolution, velocity encoding, contrast administration, workflow requirements, and post-processing software, and their influence on diagnostic performance. Thus, 4D-flow CMR imaging can accurately assess cardiac shunts through advanced visualization of pathlines and streamlines, providing direct quantification of pulmonary flow: systemic flow ratios, blood flow volumes, and complex hemodynamic patterns in congenital heart disease (CHD). Moreover, 4D-flow CMR imaging provides robust characterization of valvular and aortic disease through dynamic flow analysis and quantitative hemodynamic metrics. Overall, 4D flow CMR imaging is a powerful, noninvasive diagnostic tool that can greatly enhance clinical decision-making. The growing body of evidence supports the use of 4D-flow CMR imaging in routine clinical practice, particularly for evaluating CHD and valvular and aortic disorders.

Cardiovascular diseases (CVDs) represent the primary cause of death worldwide, thereby demanding effective preventive measures. Incidental physical activity (IPA), which encompasses non-exercise movements naturally integrated into daily routines, offers a practical and promising strategy for reducing CVD risk. Research, particularly from the UK Biobank, has consistently highlighted the cardiovascular advantages of IPA across diverse populations. However, systematic guidelines for integrating IPA into cardiovascular care are limited. Thus, this review aims to provide a comprehensive synthesis of IPA, including a definition, classification by intensity, current evidence linking IPA to cardiovascular health, and the underlying mechanisms involved. Present research underscores the extensive benefits of IPA, particularly the pronounced effectiveness of vigorous IPA (VIPA). However, approaching these findings with caution is essential, especially considering the limited representation of individuals predisposed to exercise-induced sudden cardiac events in middle-aged and older cohorts. Therefore, while the advantages of IPA are clear, further investigation is warranted to understand the implications of IPA for all populations. In conclusion, we recommend integrating IPA as a complementary strategy alongside structured exercise in clinical practice. However, emphasizing risk mitigation strategies for VIPA is crucial, particularly for at-risk individuals. This review aims to provide practical guidance on the effective implementation of IPA in cardiovascular health management.

Background: Growth differentiation factor-15 (GDF-15) has emerged as a novel biomarker for coronary artery disease (CAD). Although the hypercoagulable state is recognized as a biological mechanism that triggers cardiac events in CAD, the relationship between GDF-15 and coagulation parameters in patients with CAD remains unclear. Thus, this study aimed to investigate the potential relationship between GDF-15 and coagulation parameters in male Chinese patients with CAD.

Methods: In total, 892 subjects were enrolled between January 2020 and December 2020, including 592 with CAD and 300 controls. The serum levels of GDF-15, blood cell count, glucose, serum lipids, and coagulation parameters were measured. Kruskal-Wallis or one-way ANOVA with post hoc tests (Holm-Sidak and Dunn's tests), as well as univariate/multivariate linear regression analyses, were used to determine the correlation between GDF-15 and coagulation parameters in male patients with CAD.

Results: Compared to controls, patients with acute myocardial infarction (AMI) and stable angina (SA) showed significantly higher levels of GDF-15 (p < 0.05). Multivariate linear regression revealed that GDF-15 levels were positively associated with activated partial thromboplastin time (APTT) in patients with CAD (β = 0.109, p = 0.024), and inversely associated with antithrombin III (AT3) (β = -0.113, p = 0.028) in an adjusted multivariate regression model. Meanwhile, in a multivariate regression model adjusted for other variables, the GDF-15 levels in patients with SA were inversely associated with AT3 (β = -0.191, p = 0.036). After adjusting for confounders, the GDF-15 levels were positively associated with APTT (β = 0.174, p = 0.002) and inversely associated with monocyte count (β = -0.159, p = 0.025) in patients with AMI.

Conclusions: Elevated levels of GDF-15 in male CAD patients are associated with altered coagulation parameters, suggesting that GDF-15 may serve as a compensatory marker for coagulation parameter instability. These results underscore the potential clinical value of GDF-15 as a novel biomarker for assessing the coagulation status in patients with CAD, especially in the acute coronary syndrome (ACS) subgroup.

Background: Magnetic resonance imaging (MRI) allows for the assessment of myocardial strain and identification of heart failure (HF) patients with reduced (HFrEF), mildly reduced (HFmrEF), or preserved (HFpEF) left ventricular ejection fraction (LVEF). The cardiovascular angiographic analysis system magnetic resonance (Caas MR) strain (Pie Medical Imaging) has recently been implemented in the IntelliSpace Portal Suite (Philips Healthcare) to assess the global longitudinal strain (GLS), global circumferential strain (GCS), and global radial strain (GRS). However, standard values for this software across different HF entities, as well as normal values, have yet to be established. Thus, this study aimed to establish reference values for the GLS, GCS, and GRS using the Caas MR strain in healthy individuals and HF patients, to assess the ability of these parameters to differentiate between HF subtypes, and to compare CAAS-derived strain values with those obtained using CVI42 software.

Methods: Using a 1.5 T Philips Achieva scanner, we analyzed 19 healthy volunteers and 56 HF patients (HFpEF, n = 19; HFmrEF, n = 20; and HFrEF, n = 17) using the feature tracking post-processing software Caas MR Strain. GLS, GCS, and GRS were quantified using 4-chamber-view, 2-chamber-view, and short-axis (SAX) cine images. All volunteers and patients were evaluated by CVI42 to analyze inter-vendor reliability with a validated software.

Results: Mean GLS, GCS, and GRS by Caas MR Strain were significantly different for healthy volunteers compared to HF patients (GLS -15.8 ± 1.9% vs. -11.7 ± 3.0%, p < 0.001; GCS -17.0 ± 2.6% vs. -11.4 ± 3.3%, p < 0.001; GRS 27.3 ± 6.2% vs. 14.5 ± 5.5%, p < 0.001). The upper limit of the 99% confidence interval for healthy volunteers was -14.6% for GLS, -15.3% for GCS and the lower limit of the 99% CI for GRS was 23.1%. GLS, GRS, and GCS by Caas MR Strain were significantly different among HF entities (p < 0.001). Intervendor comparison showed very good agreement for GLS and GRS between Caas MR Strain and CVI42 (GLS r = 0.86, p < 0.001; GCS r = 0.83, p < 0.001; GRS r = 0.76, p < 0.001).

Conclusion: Magnetic resonance imaging assessment of left ventricular myocardial strain using Caas MR Strain software reliably identifies HF patients. Discrimination between the different HF entities is potentially feasible by GLS, GCS, and GRS. Intervendor agreement was most robust for GLS and GCS, but less robust for GRS. For practical clinical use, we propose cut-off values for GLS above -15%, GCS above -15%, and GRS below 23% to define pathological findings.

Tricuspid regurgitation (TR) is a critical factor in the progression of right heart failure. Although conventional open surgery remains the definitive treatment, the application of this technique is significantly limited in older and high-risk patients due to frequent comorbidities, including impaired right ventricular functional reserve, pulmonary hypertension, and multi-organ dysfunction, which lead to substantially increased surgical risks. Transcatheter tricuspid valve intervention (TTVI), which achieves anatomical correction through minimally invasive approaches, has emerged as an effective alternative strategy for patients deemed ineligible for surgery. During these procedures, anesthesiologists face three core challenges: susceptibility to acute changes in the preload of the right ventricle, a high risk of circulatory collapse (particularly in functional TR with right ventricular decompensation), and the precise integration of intraoperative transesophageal echocardiography (TEE) with hemodynamic monitoring. Consequently, anesthesiologists who become experts in the pathological staging of TR, key points of image-guided device implantation, and warning indicators of circulatory collapse can help maintain perioperative stability. Moreover, gaining a thorough understanding of the pathological progression of tricuspid valve disease, improving the assessment of right heart function, and optimizing the TTVI process and management capabilities are crucial for improving patient outcomes. Thus, establishing a perioperative anesthetic strategy focused on right heart protection may reduce cardiovascular-related complications and all-cause mortality.

Myocardial fibrosis represents the initial stage of cardiac failure and is characterized by the accumulation of extracellular matrix proteins. The fibrogenic niche provides a unique microenvironment for myocardial fibrosis and consists primarily of extracellular matrix proteins, various types of cardiac resident cells, inflammatory cells, extracellular vesicles, and soluble factors. Meanwhile, the composition and contents of this microenvironment undergo dynamic changes during the repair of damaged tissues. Several studies have demonstrated that the fibrogenic niche plays a key role in the activation of fibroblasts, the development of inflammation, and the onset of microvascular dysfunction. Studying the fibrogenic niche has emerged as a new method to clarify the mechanisms involved in myocardial fibrosis, and can potentially facilitate the early diagnosis and individualized medical treatment for the disease.