Cardiac rehabilitation (CR) has been categorized as a class Ia recommendation for secondary prevention after major cardiac interventions or in patients with certain cardiac comorbidities. The benefits of CR have been established and range from reducing readmissions to improving quality of life. Given the increasing amount of literature on CR over the past few years and the evolution of this field, there is a need to synthesize these data. Thus, this review aims to combine the latest research findings to provide a comprehensive review of CR literature. We discuss the components needed to create a successful CR program, including individualized training plans, routine clinical assessments, exercise supervision, and nutritional assessments. Overall rates of CR utilization remain low. Therefore, we explore potential reasons for this underutilization observed in the literature, including CR deserts, under-referral, and the lack of education on benefits, time, and transportation. Moreover, we discuss solutions for underutilization that have been analyzed in the literature, including motivational interviewing, gender-specific regimens, transportation assistance, and automatic referrals. Realizing the underutilization of CR, we also assess virtual CR (VCR) and variations in various regimens within the programs. We compare exercise and body metrics, patient outcomes, feasibility, and patient preferences between VCR and traditional CR published in the literature. VCR does not appear to be inferior to conventional CR in many metrics, although more research is needed to compare the two modalities. We recommend that providers explain the outcomes of the two modalities and allow patients to choose the regimen that works best for them. We discuss how VCR may be better suited to patient populations with specific barriers to care. We also discuss the ongoing current CR trials, many of which are focused on solutions to underutilization. Lastly, we further discuss the remaining gaps in the CR literature and areas where future research could be beneficial, such as establishing large-scale VCR studies and studies focused on expanding CR indications.

Heart failure with preserved ejection fraction (HFpEF) represents a major phenotype of heart failure and accounts for over 50% of clinical cases. The complex pathophysiological mechanism involved in HFpEF promotes diagnostic difficulties and limited treatment options, posing a significant challenge in modern cardiology. Conventional imaging methods have significant limitations in comprehensively evaluating the heterogeneous etiologies and key pathological mechanisms of HFpEF. Radionuclide myocardial imaging, through the application of targeted radioactive tracers, enables , non-invasive quantitative assessment of multiple pathological and physiological processes such as myocardial perfusion, energy metabolism, sympathetic nervous activity, inflammatory responses, and fibrotic progression. Moreover, this technology offers a transformative approach to the precise diagnosis, molecular phenotyping, risk stratification, therapeutic monitoring, and prognostic assessment of HFpEF. Therefore, this review systematically summarizes the latest progress in radionuclide myocardial imaging techniques in diagnosing and treating HFpEF, with a particular focus on analyzing the unique clinical value of this technology in identifying specific etiologies (such as cardiac amyloidosis, cardiac sarcoidosis, and coronary microvascular dysfunction) and elucidating pathological mechanisms (including metabolic remodeling, inflammatory, fibrosis, and alterations in sympathetic innervation). Furthermore, we discuss the future directions of this imaging modality, including the development of novel molecular probes, integration with multimodal imaging techniques, and the application of artificial intelligence-assisted analysis. These innovations are expected to facilitate a paradigm shift from symptom-oriented management to mechanism-targeted therapy, offering new perspectives for the precise classification and clinical management of HFpEF.

Takayasu's arteritis (TAK) is a rare chronic arteritis that can lead to serious consequences. Understanding of the pathogenesis of TAK remains limited, and effective therapeutic strategies for this condition are lacking. Previous studies have suggested that there may be an association between TAK and the interaction between Mycobacterium tuberculosis infection and genetic susceptibility. Emerging data indicate that the nucleotide-binding and oligomerization domain (NOD)-like receptor pyrin domain-containing protein 3 receptor (NLRP3) inflammasome may be involved in the pathogenesis of TAK, potentially contributing to the initiation of the disease. This review summarizes the current epidemiological data, possible mechanisms, and targeting strategies of TAK, focusing on the involvement of the NLRP3 inflammasome in the pathogenesis of TAK, and provides new insights into the prevention and treatment of this condition.

This study aimed to examine the prognostic value of pericoronary adipose tissue (PCAT) attenuation at three months after transcatheter aortic valve replacement (TAVR) in patients with aortic stenosis (AS) and obstructive coronary artery disease (CAD).

Atrial fibrillation catheter ablation (AFCA) success rates vary across different phenotypes of hypertrophic cardiomyopathy (HCM). Therefore, we compared long-term outcomes between apical (aHCM) and septal (sHCM) subtypes of HCM.

Atherosclerosis (AS) is a significant contributor to cardiovascular disease, characterized by abnormal lipid metabolism, cellular apoptosis, oxidative stress, and chronic inflammation. Ferroptosis represents a form of non-apoptotic programmed cell death characterized by the iron-dependent accumulation of lethal lipid reactive oxygen species (ROS) and the peroxidation of membrane polyunsaturated fatty acid phospholipids (PUFA-PLs). The ferroptosis of endothelial cells (ECs) and macrophages plays a crucial role in the development of atherosclerotic plaques. This review summarizes the mechanisms and associated therapeutic targets related to ferroptosis in macrophages and ECs within the context of AS. Recent research has made substantial progress in elucidating the mechanisms through which ferroptosis influences AS progression; however, a comprehensive understanding of the precise molecular basis for AS remains essential. Moreover, further clinical trials of drugs targeting ferroptosis are necessary. This review updates the knowledge of ferroptosis in ECs and macrophages related to AS, identifies potential links and the subsequent implications for plaque stability, and serves as a reference for developing new pharmacological strategies to address AS and stabilize vulnerable plaques.

Acute type A aortic dissection (ATAAD) is a life-threatening cardiovascular surgical emergency with a mortality of 20-25%. This review offers an overview of current research on the morphology, taxonomy, epidemiology, and anesthetic, perfusion, and surgical strategies involved in ATAAD. Moreover, this review examines methods for predicting mortality risk and explores clinician-patient interactions, particularly those involving patients who refuse blood transfusions. The literature search included PubMed, Google Scholar, Web of Science, and ScienceDirect databases, as well as any relevant books. This review references 144 sources: 129 peer-reviewed articles and 15 book chapters or books. Modern classification systems utilize aortic zones based on the location of intimal tears and the extent of dissection; recent updates have included coronary artery dissection as an additional mapping criterion. Socioeconomic factors are linked to higher ATAAD incidence and poorer long-term survival post-surgery. The duration of global myocardial ischemia correlates with mortality and is a key element in the surgical strategy. Compared to deep hypothermic circulatory arrest (HCA), moderate HCA with cerebral perfusion provides benefits such as reduced bleeding and improved survival. Standard prediction models may not accurately assess risks in patients with life-threatening anemia who refuse blood transfusion. Therefore, incorporating Auckland and Hamilton anemia mortality risk scores alongside conventional tools can improve prognostic accuracy and support personalized management. An interpretive-deliberative model balances patient preferences with surgical outcomes, especially in bloodless surgery. Advances in surgical and endovascular management, as well as postoperative strategies for residual aortic disease, have also been explored. Significant progress has been made in assessing in-hospital mortality, improving doctor-patient communication, refining anesthetic and perfusion techniques, and enhancing surgical management of ATAAD. However, further research is needed to validate these approaches.

Serum chloride levels and the advanced lung cancer inflammation index (ALI) score are independent prognostic factors in patients with heart failure (HF). Nevertheless, the interactive relationship between serum chloride levels and the ALI score in predicting all-cause mortality among individuals with acute decompensated heart failure (ADHF) remains undefined.

Atrial fibrillation (AF) can increase the risk of stroke by five-fold; strokes associated with AF are more likely to lead to death or severe disability in patients. Thus, preventing the formation of thrombosis is of vital importance in the treatment of patients with AF. Epicardial adipose tissue (EAT) is a risk factor for AF and is closely associated with many AF-related complications. However, to our knowledge, no in-depth studies on the relationship between the incidence of thrombosis in AF patients and EAT have been conducted. Therefore, it is of great clinical significance to explore the potential of EAT quantification in predicting intra-atrial thrombosis in patients with AF.

Pulsed field ablation (PFA) represents a paradigm shift in cardiac ablation technology. Indeed, PFA, a non-thermal technique, achieves homogeneous tissue effects by delivering ultrashort, high-frequency electric pulses. Moreover, PFA has emerged as a prominent ablation strategy in electrophysiology laboratories worldwide. While current clinical evidence demonstrated promising outcomes and expanded applications for existing PFA platforms, energy-specific difficulties complicated the definition of safety boundaries, particularly in patients with clinical complications. Furthermore, substantial heterogeneity among commercial PFA systems impeded procedural standardization. Therefore, this review aimed to synthesize contemporary perspectives on mitigating these energy-specific adverse events, with emphasis on modifiable perioperative factors. The evidence of safety across commercially available PFA systems with divergent catheter design philosophies was concurrently evaluated to examine how design strategies influence procedural safety profiles.

The 2021 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, which incorporates both creatinine and cystatin C, provides enhanced estimation of glomerular filtration rate (eGFR) compared to creatinine-only equations. This study aimed to explore the incremental prognostic value of eGFR estimates in patients with acute coronary syndrome (ACS).

Increasing evidence suggests a positive correlation between serum uric acid (SUA) levels and incident hypertension (IHT). However, few studies have focused on the sex-differential impact of SUA levels on IHT in populations with a normal body mass index (BMI).

Coronary artery disease (CAD) remains a leading cause of morbidity and mortality worldwide. Percutaneous coronary intervention (PCI) represents the standard treatment for CAD; however, significant challenges, such as in-stent restenosis, late thrombosis, and delayed endothelial healing, remain issues for long-term outcomes. The evolution of stents from bare metal and drug-eluting platforms to bioabsorbable and nanoengineered designs has reduced, but not eliminated, these complications. Meanwhile, exosome-mimetic nanovesicle (EMNV)-coated stents have emerged as a potential approach to address these limitations since EMNVs mimic the structure and biological function of natural exosomes. This mimetic ability enables targeted delivery of therapeutic agents such as microRNAs, growth factors, and anti-inflammatory molecules. Indeed, preclinical studies have previously demonstrated the ability of these stents to reduce neointimal hyperplasia, enhance endothelialization, and modulate inflammatory responses. Engineering strategies, including stimuli-responsive release triggered by pH or enzymatic activity, further improve the precision of therapeutic delivery. However, the transition to clinical application remains in its early stages, with key obstacles including the scalability and reproducibility of EMNV production, the stability of biologic coatings during application, and regulatory classification as combination products. Therefore, clinical translation will require standardized manufacturing standards, reliable potency testing, and long-term safety studies to overcome these challenges. Personalized medicine approaches using patient-derived exosomes and artificial intelligence (AI)-assisted stent design may provide additional opportunities to accelerate the transition. This review summarizes the evolution of coronary stent technology and discusses the potential and limitations of EMNV-based platforms. This article also outlines future directions that will guide the development of EMNV-based platforms as next-generation devices in interventional cardiology.

Total anomalous pulmonary venous connection (TAPVC) is a congenital heart defect requiring surgical correction and is associated with significant postoperative risks, such as prolonged ventilatory support and mortality. This study aimed to identify perioperative factors that contribute to protracted ventilatory support in infants undergoing TAPVC repair.

Sepsis-induced cardiomyopathy (SICM) constitutes a critical myocardial impairment that substantially elevates mortality risk in septic patients. The structural and functional changes of SICM are accompanied by metabolic disturbances, including mitochondrial dysfunction and altered myocardial metabolism. Diagnostic advancements feature biomarkers, circulating microRNAs, and imaging tools, such as speckle-tracking echocardiography. Therapies extend from vasopressors to immunomodulators, mitochondrial-targeted antioxidants, and mesenchymal stem cell-based approaches. Despite progress, challenges related to heterogeneity and the need for long-term data persist. Thus, integrated approaches leveraging machine learning and omics are essential for optimizing personalized care and reducing the global burden of SICM.

Diabetes is widely recognized as a major contributor to stroke risk. Certain antidiabetic medications have demonstrated promising effects on reducing stroke incidence and improving outcomes.

Hypertrophic cardiomyopathy (HCM) is a prevalent cardiac disease characterized by marked phenotypic variability. Recent advances in diagnosis and treatment have allowed a personalized approach to the treatment of this disease. Depending on the predominant phenotype, management can be tailored to address left ventricular outflow tract obstruction, heart failure, arrhythmia control, and/or sudden cardiac death prevention. This review highlights recent advances that have transformed the therapeutic landscape of HCM. Modern imaging techniques have improved sudden cardiac death risk stratification. The development of myosin inhibitors represents a paradigm shift in the treatment of symptomatic obstructive HCM. Invasive septal reduction techniques have also evolved, with novel approaches such as percutaneous intramyocardial septal radiofrequency ablation and transapical beating-heart septal myectomy. Finally, gene-targeted therapies including replacement, editing and silencing approaches, are emerging as promising strategies for HCM management.

Heart failure (HF) is a major contributor to morbidity and mortality in the US and worldwide. HF is a complex condition characterized by the disruption of normal physiology and the activation of neurohumoral pathways, including the renin-angiotensin-aldosterone system, the sympathetic system, and inflammatory pathways. These have adverse effects on renal handling of salt and water balance, leading to salt and water retention and a vicious cycle of worsening congestive changes with progressive volume overload. Meanwhile, diuretics are pharmacologic agents that are essential in the management of HF. Indeed, diuretics induce natriuresis to disrupt this vicious cycle of progressive volume overload, thereby reducing congestive changes and alleviating the symptoms of HF. In this review, we discuss the different classes of diuretics and their sites and mechanisms of action across the nephron. We highlight differences in the potency and usefulness of these diuretics. Moreover, we examine their application in the management of various stages of HF, focusing on their optimal and effective use in clinical practice. In this review, we also cover several aspects of the pathophysiology of HF. We address the milder forms of HF that are treated in outpatient clinics, as well as the more advanced states of HF, including acute decompensated HF (ADHF), which are usually managed in a hospital setting. We discuss management strategies in the outpatient setting, with a specific focus on maintaining sufficient decongestion of patients to prevent hospitalization. We stress the importance of closely monitoring congestive symptoms and weight trends, as well as electrolyte and renal parameters. We recommend setting a "target weight goal" for the patient between clinic visits, which helps with outpatient diuretic therapy adjustments and avoids drifts in volume status. We also examine the usefulness of diuretics in hospitalized patients with ADHF. For these more challenging conditions, we discuss the use of combination diuretics to overcome diuretic resistance and highlight current recommendations for achieving the desired goals and speed of diuresis. Patients with HF commonly have chronic kidney disease (CKD), which frequently complicates overall management strategies. CKD also leads to diuretic resistance, necessitating escalation of diuretic dosing and more frequent changes in diuretic prescription. Hence, this review also discusses management strategies for CKD patients and highlights the importance of close monitoring of kidney function in both inpatient and outpatient settings when using diuretics in patients with HF. We briefly discuss the benefits of monitoring central venous filling pressures in patients with ADHF as a tool to guide the optimization of diuresis. Finally, we allude to new advanced technologies such as remote monitoring of outpatients with HF. These can be used to detect early signs of impending HF decompensation that earlier adjustments to the diuretic dose could then address.

Limited evidence exists for an association between dilated cardiomyopathy (DCM) and the angiotensin-converting enzyme () gene with an insertion/deletion () angiotensinogen () gene polymorphism. A systematic review and meta-analysis were conducted to elucidate the role of and in the morbidity of DCM. This meta-analysis was performed following the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) 2020 guidelines for Abstracts.

Myocardial fibrosis represents a common pathological hallmark of various cardiovascular diseases progressing to heart failure, with the immunoinflammatory response playing a pivotal role in the pathogenesis of myocardial fibrosis. Accumulating evidence suggests that the immune microenvironment modulates myocardial fibrosis by regulating RNA epigenetic modifications, with 5-methylcytosine (m5C) methylation emerging as a key player in this process. This review systematically summarizes the characteristics of m5C methylation modification, the regulatory enzymes involved, and their biological functions in immunoinflammatory responses and myocardial fibrosis. Furthermore, this review examines the molecular mechanisms underlying m5C methylation-mediated regulation of myocardial fibrosis, encompassing the activation of immune cells, the transdifferentiation of cardiac fibroblasts, and the regulation of collagen metabolism. Moreover, the potential clinical implications of targeting m5C methylation for treating myocardial fibrosis are discussed, with an emphasis on future therapeutic prospects.

Minimally invasive mitral valve repair (MI-MVr) is the preferred treatment approach in experienced centers for mitral valve disease (MVD), offering reduced surgical trauma and fast recovery. However, limited operative exposure and increased procedural complexity can represent a challenge in complex MVD. This narrative review provides an overview of current literature on clinical outcomes of MI-MVr in challenging MVD scenarios, such as mitral valve (MV) endocarditis, annulus calcification, and mitral annular disjunction, in the context of myxomatous MVD. Despite the complex anatomy and MVD, MI-MVr is non-inferior in long-term outcomes in treating MV endocarditis, MV calcification, and myxomatous MVD with mitral annular disjunction. Nonetheless, careful patient selection and referral to high-volume centers, where surgeons with expertise in MI-MVr operate, are key elements for achieving a durable, patient-tailored repair with an optimal long-term outcome in treating complex MVD.