Current Cardiology Reports最新文献

Purpose of review: Explore the clinical progression, diagnostic challenges, and evolving treatments of systemic right ventricular (SRV) failure, highlighting key gaps and advances.

Recent findings: Recent evidence highlights the distinct pathophysiology of SRV failure and limited efficacy of conventional heart failure (HF) treatments. Emerging drugs like SGLT2 inhibitors are being studied for modulating ventricular remodeling and fibrosis. Echocardiography, enhanced by speckle-tracking and 3D imaging, is first-line, while cardiac MRI remains the gold standard for volumetric, functional, and tissue characterization. SRV-specific machine learning models improve prognostication and personalized care. Advances in transcatheter tricuspid valve interventions offer less invasive options for high-risk patients. In end-stage SRV failure, ventricular assist devices effectively unload the ventricle, enhance transplant candidacy, may be combined with tricuspid procedures, and are increasingly used as long-term destination therapy. SRV failure is a unique condition requiring personalized, multidisciplinary management, with advances in risk stratification and treatments shaping future care.

Purpose of review: To review the current state of the science relating adverse childhood experiences (ACEs) and cardiovascular health and disease.

Recent findings: Recent work has demonstrated associations between ACEs and development of cardiovascular disease (CVD) and has additionally shed a light on potential mechanistic pathways noting associations between ACEs and genomics, vascular health and cardiac structure. Existing work has advanced our understanding of the mechanisms by which ACEs are associated with CVD, yet much work remains particularly as we strive to understand how to ameliorate the impact of ACEs on CVD. Future research on interventions that promote cardiovascular health and integrate ACEs and emotional wellbeing are needed. A multilevel framework that understands how sociopolitical, neighborhood and family level factors contribute to childhood experiences is necessary to address the root causes of ACEs.

Purpose of review: Cardiomyocyte postnatal maturation is a critical step of the mammalian heart development continuum, involving a myriad of phenotypic changes at morphological, molecular, and functional levels. While the phenotypic hallmarks of cardiac maturation are well characterized, the molecular mechanisms that govern this maturation process are still poorly defined. This review aims to explore the recent findings on how post-transcriptional regulations orchestrate the fetal-to-adult cardiomyocyte transition and to highlight their clinical implications for cardiac diseases and regeneration medicine.

Recent findings: The molecular regulations of cardiac maturation are distinct from the gene regulatory network implicated in embryonic stages of cardiac development. RNA alternative splicing and the resulting isoform switching events are significant part of the post-transcriptional reprogramming during the transitional stage of maturation, driving functional refinement through a network of RNA-binding proteins. Cardiomyocytes undergo significant changes in structure, physiology, metabolic activity, and proliferative capacities during fetal to adult maturation. Recent findings highlight the importance of post-transcriptional regulation in this process, in particular RNA alternative splicing and isoform switch. Understanding the post-transcriptional regulatory mechanisms, including key molecular players that contribute to the fetal-to-adult transition, can provide a new conceptual framework for cardiac development, diseases, and regenerative medicine.

Purpose of review: This review explores the historical, structural, and biological foundations of cardiovascular (CV) health inequities in the U.S. It examines how disparities by ancestry, sex, geography, income, immigration status, and race have emerged, persisted, and, in some cases, worsened while evaluating strategies for advancing equity.

Recent findings: Despite progress in prevention and treatment, key disparities remain entrenched. Structural inequities, socioeconomic exclusion, and underrepresentation in research continue to shape outcomes. Social adversity is increasingly understood to exert biological effects through mechanisms such as chronic stress, cardio-kidney-metabolic dysfunction, and epigenetic aging. Novel tools, including place-based deprivation indices, precision risk prediction models, and community-driven interventions offer actionable pathways forward but remain underutilized or unevenly implemented. Cardiac health equity requires more than clinical innovation; it demands structural reform, inclusive science, and equity-centered implementation. Future solutions must embed social context into care, research, and policy to drive durable, population-level impact.

Purpose of review: Lead failure in cardiac implantable electronic devices (CIEDs) presents a critical challenge in clinical electrophysiology. These failures can result in inappropriate therapies, ineffective pacing, and even life-threatening outcomes. Despite technological advances in device design, transvenous leads remain an important source of complications.

Recent findings: Novel developments in lead extraction strategies including pre-procedure risk prediction instruments, estimation of short-term mortality after lead extraction procedure, use of new technologies including shock-wave lithotripsy to facilitate disruption of intravascular calcium, cardioneural ablation to avoid need for reimplantation of cardiac devices, and the use of leadless pacemaker/defibrillator systems followed transvenous extraction are discussed. This review explores the underlying mechanisms of lead failure, highlighting notable cases such as the Riata and Fidelis recalls, and discusses the complex decision-making process surrounding lead abandonment, extraction, or replacement.

Purpose of review: This review summarizes recent advances in the evaluation of diastolic dysfunction and management considerations in the unique congenital heart disease population.

Recent findings: Diastolic dysfunction is prevalent in a number of congenital lesions. Non-invasive assessment methods have varying applicability depending on the specific lesion. Lesions with a systemic left ventricle can likely be accurately assessed with traditional echocardiographic techniques while higher complexity lesions may be better suited to emerging techniques including 4D-flow cardiac MRI and analysis of late gadolinium enhancement. Diagnosis and management are tailored to the individual patient and include surveillance, medication, lifestyle modification and occasionally device therapy. Diastolic dysfunction is increasingly recognized across the spectrum of the expanding, aging congenital heart population. Ongoing study of the unique mechanisms in individual lesions is needed to determine how best to assess for and intervene upon this pathology.

Purpose of review: Patients living with cancer are at risk for significant potential cardiovascular complications as a direct result of cancer treatment or due to underlying comorbid cardiovascular disease. This article reviews the methods of risk stratification as well as pharmacologic and nonpharmacologic approaches to cardioprotection in cardio-oncology.

Recent findings: Several cancer-specific risk stratification tools have incorporated variables such as age, sex, cancer subtype, traditional cardiovascular risk factors and cancer treatment-related parameters to assess cardiovascular specific risk prior to cancer therapy. Cardioprotective strategies, namely neurohormonal blockade and statins, have yielded mixed results in patients with cancer. Non-pharmacologic strategies, including exercise and dietary interventions, have shown potentially promising results in observational and randomized studies. Ultimately, the optimal cardioprotective strategy should be personalized based on each patient's unique risk profile and clinical context. Further research is needed to better define the role of cardioprotection across different cancer subtypes and cardiovascular risk groups, with an emphasis on refining individualized prevention and treatment strategies.

Purpose of review: VO₂ max is a fundamental marker of cardiorespiratory fitness with substantial prognostic and diagnostic value within the field of cardiology. This review analyzes current and emerging evidence regarding its clinical uses, highlights key evidence gaps, and explores emerging developments poised to broaden its clinical application.

Recent findings: Evidence supports VO2 max as a powerful independent predictor for heart failure, coronary artery disease, hypertrophic cardiomyopathy, and cardiac amyloidosis, supporting it use in identifying high-risk patients for advanced interventions. Recent developments including the integration of machine learning and wearable devices can facilitate accurate VO2 estimation in routine clinical practice without the necessity of specialized diagnostic tools. Despite its robust diagnostic and prognostic value, VO₂ max assessment remains underutilized in routine cardiovascular care, primarily due to the need for specialized equipment and personnel. Future research should explore emerging technological innovations for VO2 max estimation and the development of evidence-based protocols to support its broader clinical implementation for improved cardiovascular outcomes.

Purpose of review: Metabolic changes can play a critical role in the structural and functional decline of the aging cardiovascular system. In this review, we examine how key metabolic pathways and regulatory mechanisms influence cardiovascular aging, highlighting recent studies into metabolic flexibility, mitochondrial function, nutrient sensing, and energy utilization in the aging heart. Potential metabolic-based interventions to mitigate cardiac aging are also discussed.

Recent findings: Various metabolic changes have been observed in the aging heart. Impaired metabolic flexibility, as seen by reduced fatty acid oxidation with an increased reliance on glucose, is observed. Mitochondrial dysfunction and increased oxidative stress in aged cardiomyocytes may lead to energy deficits, contributing to myocardial fibrosis and diastolic dysfunction. Accelerated cardiovascular aging is also connected to the dysregulation of nutrient-sensing pathways- such as AMP-activated protein kinase (AMPK), sirtuins, and the mechanistic target of rapamycin (mTOR). Enhancing the age-dependent decline in autophagy and mitophagy, which clears damaged organelles, appears to preserve cardiac function in aging. Recent studies have shown that interventions such as caloric restriction, exercise, and metformin can favorably remodel cardiac metabolism and delay age-related cardiac deterioration. Metabolic changes, including energy substrate shifts, mitochondrial oxidative stress, and impaired nutrient signaling, play a direct role in cardiovascular aging. Targeting these metabolic factors and pathways holds promise for alleviating age-associated cardiac dysfunction. Recent studies focusing on lifestyle or pharmacologic means of metabolic modulation provide and outline for the promotion of healthy cardiovascular aging, thereby reducing the burden of cardiovascular disease in the growing aging population.