Reviews in cardiovascular medicine最新文献

Cardiac amyloidosis (CA) represents an increasingly recognized but historically underdiagnosed cause of restrictive cardiomyopathy and heart failure. CA is now understood to be more prevalent, particularly in older adults, as advancements in imaging and biomarker technologies have improved detection. The disease results from the misfolding of precursor proteins, primarily immunoglobulin light chains (in light chain (AL) amyloidosis) or transthyretin (in transthyretin (ATTR) amyloidosis), into insoluble fibrils that deposit in myocardial tissue. These deposits cause structural and functional cardiac impairment through both physical infiltration and cytotoxic mechanisms, leading to diastolic dysfunction, arrhythmias, and progressive heart failure. Understanding the molecular basis of amyloid formation and deposition has revealed subtype-specific mechanisms of toxicity and tissue tropism, highlighting the central role of protein instability, proteolytic cleavage, and oxidative stress in disease progression. Furthermore, increasing awareness of phenotypic variability and sex- or ethnicity-based diagnostic disparities has called for earlier recognition and differentiation of CA subtypes. Diagnostic precision is enhanced by a multimodal approach incorporating histopathology, biomarker staging, and advanced imaging techniques such as echocardiography, cardiac magnetic resonance, and nuclear scintigraphy. This review addresses our contemporary understanding of the molecular mechanisms, pathophysiologic cascade, and diagnostic evolution of AL and ATTR CA, emphasizing clinical progress. By delineating the biological mechanisms and tools for early identification, this paper aims to strengthen the framework for diagnosing and managing a disease that was once overlooked but is now at the forefront of modern cardiovascular medicine.

Heart failure (HF) represents a class of cardiovascular diseases that poses a serious threat to global health. Although current pharmacological and device-based therapies have exhibited some progress, significant challenges remain, including suboptimal treatment responses and the inability to effectively halt disease progression. Extracellular vesicles (EVs) are nanoscale membranous particles actively secreted by cells, which are capable of transporting bioactive molecules such as nucleic acids and proteins to mediate intercellular communication. Owing to the broad cellular origins and excellent biocompatibility of EVs, these particles offer extensive therapeutic potential. This review systematically elaborates on the key aspects of EVs, including the core molecular composition of these particles, as well as the biogenesis pathways and functional regulatory mechanisms involved. We further dissect the functional heterogeneity of EVs derived from cardiomyocytes, cardiac fibroblasts, endothelial cells, and immune cells in HF, highlighting the dual roles of EVs in either promoting or counteracting disease progression via cargo-dependent mechanisms. Additionally, we explore the translational applications of EVs in the diagnosis and treatment of HF, covering EV isolation, characterization, and scalable production strategies. The potential use of EVs as biomarkers, as well as the precision engineering of EVs for targeted clinical therapy, are also critically discussed.

Epicardial ablation is an increasingly important treatment for refractory ventricular tachycardia (VT), particularly in nonischemic cardiomyopathy or when the substrate is epicardial or mid-myocardial. This review provides an overview of the pathophysiology and disease-specific characteristics of VT substrates, with a particular focus on epicardial involvement and indications based on electrocardiographic, imaging, and clinical findings. We present advanced substrate-mapping strategies, including functional and high-resolution approaches, and practical examples of three-dimensional mapping using the CARTO™ (Biosense Webster, Diamond Bar, CA, USA) and EnSite™ (Abbott, Abbott Park, IL, USA) systems to overcome the known limitations of conventional mapping techniques. In the latter part of the review, we discuss the technical aspects of epicardial access, as well as the clinical challenges and strategies for challenging scenarios, such as bipolar ablation and ablation after prior cardiac surgery, supported by practical examples from our institution. We also highlight future perspectives. These insights are expected to contribute to the optimization of treatment strategies for refractory epicardial VT and to support the development of more precise and durable patient care.

Background: Inflammation has recently been identified as a critical regulator of the pathophysiology and prognosis of acute coronary syndrome (ACS). The systemic immune-inflammation index (SII), derived from platelet, neutrophil, and lymphocyte counts, has gained attention as a potential marker for predicting adverse outcomes in cardiovascular diseases. However, the prognostic value of the SII, particularly in relation to gender differences, has not been extensively studied.

Methods: Thus, we conducted a retrospective cohort study of 835 patients hospitalized for ACS at Hippokration Hospital, Thessaloniki, Greece, between 2017 and 2023. The SII was calculated using blood samples taken at admission. Logistic and Cox regression models were used to evaluate the relationship between the SII and all-cause mortality, with stratified analyses conducted according to gender. Receiver operating characteristic (ROC) analysis, Kaplan-Meier survival curves, and restricted cubic spline (RCS) modeling were also performed to assess the discriminative ability and non-linear associations of the SII with mortality.

Results: A total of 835 patients were included, with a median follow-up of 25 months. An elevated SII was independently associated with increased long-term mortality, with patients in the highest SII quartile exhibiting a 2.3-fold higher risk of death compared to those in the lowest quartile (adjusted hazard ratio (aHR) = 2.31, 95% confidence interval (CI): 1.60-3.32; p < 0.001). The optimal cut-off value for the SII was identified as 1864.19. Gender-stratified analyses revealed a stronger prognostic value in women compared to men (area under the curve (AUC) = 0.70 vs 0.58; p = 0.018). The Kaplan-Meier and Cox regression analyses confirmed significantly worse survival for patients with SII levels above this threshold (p < 0.05). The RCS modeling demonstrated a non-linear relationship between the SII and mortality, with a marked increase in risk at higher levels of the SII, especially in women.

Conclusions: The SII is a simple, easily accessible biomarker that independently predicts mortality in ACS patients, with notable gender-specific differences in the prognostic value of the SII. Nonetheless, incorporating SII into routine risk assessment could enhance risk stratification and improve personalized treatment strategies, particularly in settings with limited resources.

Background: Gut microbiota are associated with heart failure (HF); however, the causal relationship between gut microbial communities and HF of varying etiologies remains incompletely established.

Methods: This study leveraged two-sample Mendelian randomization (MR) to investigate whether genetically determined gut microbiota features causally influence HF and its related subtypes. Instrumental variables (IVs) for gut microbiota were derived from a large-scale, genome-wide association study (GWAS) of microbial traits conducted by the MiBioGen consortium, which included 18,340 individuals. Summary statistics for HF and its subtypes were extracted from the FinnGen Release 7, encompassing 19,350 all-cause HF cases and 288,996 controls. The Wald ratio and inverse-variance weighted analyses were applied to calculate the causal estimates.

Results: A total of 19 single-nucleotide polymorphisms (SNPs) corresponding to 18 gut microbial taxa were selected as IVs. A significant inverse causal association was identified between the family Peptostreptococcaceae and the risk of hypertensive heart disease (odds ratio (OR): 0.355, 95% confidence interval (CI): 0.193-0.656; p < 0.001; q = 0.018). Several additional taxa showed suggestive causal associations with HF or its precursor conditions, although these did not survive multiple-testing correction.

Conclusions: Genetically predicted enrichment of Peptostreptococcaceae is causally associated with a lower risk of hypertensive heart disease. These MR findings warrant a mechanistic dissection of Peptostreptococcaceae-mediated pathways as a potential therapeutic lever for the prevention and treatment of hypertension-mediated HF.

Hypertrophic cardiomyopathy (HCM) represents the most common inherited cardiac disease and a leading cause of heart failure, arrhythmias, and sudden cardiac death in young individuals. For decades, management of HCM has relied on symptom control with β-blockers, calcium channel blockers, disopyramide, or invasive septal reduction in advanced cases. The identification of pathogenic sarcomere variants and the recognition of hypercontractility as a central disease mechanism have paved the way for cardiac myosin inhibitors (CMIs), the first truly disease-specific pharmacological therapy for HCM. Indeed, CMIs represent a revolutionary therapeutic paradigm that redefines the standard of care by translating molecular discovery into clinical application. This review provides a guide to the mechanistic basis of sarcomere modulation, summarizes the clinical evidence for mavacamten and aficamten, and critically evaluates the evolving roles of both medications in obstructive and non-obstructive HCM.

Background: Various anatomical factors have been related to mortality after endovascular aortic aneurysm repair (EVAR). This systematic review investigated the impact of the pre-operative maximum aortic aneurysm diameter on mortality after standard and complex EVAR.

Methods: The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines were followed to search the MEDLINE, EMBASE, via Ovid and CENTRAL databases, until 31st July 2025. Randomized controlled trials and observational studies were eligible if they were published between 2015 and 2025 and reported on the association of the pre-operative maximum aortic aneurysm diameter with a 30-day and midterm mortality follow-up in standard and complex EVAR patients. The Newcastle-Ottawa Scale assessed the risk of bias. The primary outcome was the impact of the pre-operative maximum aortic aneurysm diameter on 30-day mortality after standard and complex EVAR.

Results: From 1182 studies, 25 were included; 19 reporting on standard (130,476) patients and six on complex EVAR (14,097) patients. A significant heterogeneity in terms of maximum pre-operative aortic aneurysm diameter threshold to identify larger aneurysms was detected. Regarding standard EVAR, eight studies evaluated the impact of the pre-operative maximum abdominal aortic aneurysm (AAA) diameter on 30-day mortality (smaller: 0.3-13.2% vs. larger: 0.7-20.8%) with conflicting outcomes. Four studies (4/8 studies; 50%) concluded that a larger diameter was related to higher 30-day mortality in patients with standard EVAR, while four showed no statistical significance. Two out of five standard EVAR studies that investigated the pre-operative AAA diameter as an independent predictor for 30-day mortality confirmed this finding. During the mid-term follow-up, ten studies showed that the pre-operative maximum AAA diameter was independently related to mortality after standard EVAR. In complex EVAR, four out of six studies showed that the 30-day mortality was higher (smaller: 0.5-7.0% vs. larger: 4.0-15.0%) in larger aortic aneurysms, including juxta-, para-, supra-renal, and thoracoabdominal aortic aneurysms. Four out of five (80.0%) studies showed that a larger diameter was an independent predictor for follow-up mortality after complex EVAR.

Conclusions: The pre-operative aortic aneurysm diameter seems to be related to mortality after standard or complex EVAR. However, the impact of the pre-operative aortic aneurysm diameter on mortality seems to be more prominent in complex EVAR cases, with 80% of studies confirming this finding.

Heart failure (HF) remains a global health challenge characterised by significant clinical heterogeneity, necessitating more precise tools for diagnosis and risk stratification. Olink proteomics, a high-throughput platform based on proximity extension assays (PEAs), has emerged as a powerful technology for exploring the molecular landscape of HF. Despite a growing number of studies utilising this platform, a comprehensive synthesis of its clinical and mechanistic contributions is still lacking. This review systematically examines the application of Olink proteomics across the HF continuum. We synthesised evidence regarding its role in biomarker discovery for early detection and prognosis, its ability to dissect key pathophysiological pathways such as inflammation and fibrosis, and its emerging potential to guide precision medicine. By critically evaluating technological advances, current challenges, and future directions, this review concludes that Olink proteomics is pivotal for transitioning HF management from a phenotype-driven to a mechanism-based paradigm, paving the way for targeted therapies and improved patient outcomes.

With ongoing technological advancements and device innovations, transcatheter aortic valve replacement (TAVR) has become a well-established therapeutic approach for managing aortic stenosis and regurgitation. As indications for TAVR expand, particularly into younger patient populations, the incidence of TAVR-associated infective endocarditis (TAVR-IE) has concurrently increased. Although the reported incidence of TAVR-IE remains relatively low (0.3%-2.0% per 100 patient-years), its clinical outcomes are notably poor, with mortality rates considerably higher than those observed in general infective endocarditis (IE). Moreover, the microbiological profile of TAVR-IE differs distinctly from surgical aortic valve replacement-associated IE (SAVR-IE), predominantly involving Enterococcus spp., Staphylococcus aureus, and coagulase-negative staphylococci. This review systematically summarizes the epidemiology, diagnosis, microbial etiology, prevention strategies, clinical prognosis, and management approaches for TAVR-IE, providing clinical insights and identifying key areas for future research.

Resistant hypertension (RH) is a high-risk phenotype characterized by blood pressure readings ≥130/80 mmHg despite maximally tolerated therapy with three antihypertensive agents, including a diuretic, or controlled blood pressure requiring four or more medications. The diagnosis of RH requires a structured evaluation that confirms accurate blood pressure measurement, excludes pseudoresistance-particularly nonadherence and white coat hypertension-and identifies secondary causes such as obstructive sleep apnea, primary aldosteronism, renovascular disease, pheochromocytoma, and Cushing syndrome. RH arises from overlapping mechanisms, including activation of the renin-angiotensin-aldosterone system (RAAS), sympathetic overactivity, arterial stiffness, volume expansion, and immune-mediated pathways. Management begins with lifestyle modification and optimized triple therapy, followed by mineralocorticoid receptor antagonists as the preferred fourth-line treatment. Emerging pharmacological options, such as sodium-glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, endothelin receptor antagonists, aldosterone synthase inhibitors, and angiotensin receptor and neprilysin inhibitors (ARNIs), offer additional therapeutic potential; meanwhile, device-based interventions, including renal denervation and baroreflex activation therapy, have shown sustained blood pressure reductions in selected patients. Future directions highlight precision medicine, digital health technologies, and artificial intelligence as methods to improve diagnosis, guide individualized therapy, and enhance long-term blood pressure control.