Nationally, there has been a rise in the number of children and adolescents with congenital and acquired heart disease presenting with acute decompensated heart failure. Compared with adults, these children have increased morbidity and mortality and use significantly more health care resources once admitted. Currently, there is little guidance on how to assess, manage, and create successful discharge plans for children presenting with acute decompensated heart failure. Given that this population represents an intersection among emergency medicine, cardiology, surgery, critical care, and psychology, a guidance document for the comprehensive management of this high-risk population is needed. This scientific statement reflects the state of current evidence and highlights important knowledge gaps in this domain.

Right ventricular (RV) dysfunction is a key predictor of outcomes in pulmonary hypertension (PH), substantially contributing to illness and death. As PH progresses, increased pulmonary vascular resistance places chronic pressure overload on the right ventricle. Initially, the right ventricle adapts through hypertrophic remodeling, thickening the heart wall to maintain cardiac output. Over time, this adaptive phase shifts to maladaptive remodeling, marked by RV dilation, fibrosis, stiffness, and decoupling from the pulmonary artery, known as RV-pulmonary arterial uncoupling. This uncoupling reflects the inability of the right ventricle to sustain contractility against elevated afterload, ultimately leading to right heart failure, the primary cause of death in late-stage PH. Awareness of RV dysfunction has grown, extending beyond PH and pulmonary arterial hypertension to systemic conditions, such as heart failure with preserved ejection fraction, congenital heart disease, COVID-19, and complications of left ventricular assist device implantation. Research is increasingly focused on understanding the molecular and hemodynamic drivers of RV failure, including inflammation and altered cellular signaling. Innovations in imaging and biomarker discovery are improving the detection of maladaptive RV remodeling. Promising treatments, such as the activin signaling inhibitor sotatercept, may reduce pulmonary vascular resistance and support RV recovery. Further work is needed to enhance RV function and prevent failure. This review summarizes current knowledge on RV dysfunction in PH, emphasizing its mechanisms, clinical relevance, and therapeutic potential. Recognizing the right ventricle as a central therapeutic target may lead to more personalized, effective interventions and improved patient outcomes in PH and related conditions.

Poor diet quality is strongly associated with elevated cardiovascular disease morbidity and mortality risk. This American Heart Association scientific statement for food-based cardiovascular health optimization and cardiovascular disease risk reduction guidance summarizes available evidence and provides contextual guidance for the key features of heart-healthy dietary patterns. It enumerates collateral benefits of adopting a heart-healthy dietary pattern in terms of nutrient intake adequacy and compatibility with other chronic disease risk reduction guidance. The features of a heart-healthy dietary pattern include (1) adjusting energy intake and expenditure to achieve and maintain a healthy body weight; (2) eating plenty of vegetables and fruits and choosing a wide variety; (3) choosing foods made mostly with whole grains rather than refined grains; (4) choosing healthy sources of protein; (5) choosing sources of unsaturated fats in place of sources of saturated fat; (6) choosing minimally processed foods instead of ultraprocessed foods; (7) minimizing intake of added sugars in beverages and foods; (8) reducing sodium intake by choosing foods low in sodium and preparing foods with minimal or no salt; and (9) if alcohol is not consumed, do not start; if alcohol is consumed, limit intake.

Ambient temperature is a key environmental driver of cardiovascular health. With rising global temperatures and increasing frequency, intensity, and duration of extreme temperature events, understanding the cardiovascular impacts of nonoptimal temperature is more urgent than ever. Short-term exposures to both heat and cold increase the risk of cardiovascular events, including myocardial infarction, stroke, heart failure decompensation, arrhythmias, and sudden cardiac death. Climate, built environment, socioeconomic variables, physiological vulnerability, and systemic inequities exacerbate these risks. There is also a growing appreciation of the importance of contextual factors such as geographic location, housing, occupation, and individual-level exposure. A range of biological mechanisms, including autonomic and neurohormonal activation, endothelial dysfunction, inflammation, hemoconcentration, and impaired thermoregulation, mediate temperature-related cardiovascular risk. Nonoptimal temperatures affect not only the incidence of cardiovascular disease but also health care access and delivery. They can increase demand for emergency care, disrupt operations, and pose challenges to the resilience and sustainability of health systems. Meanwhile, cardiovascular care contributes significantly to health care-related greenhouse gas emissions, highlighting a paradox in which efforts to protect cardiovascular health can indirectly contribute to climate-driven risks. This scientific statement synthesizes current knowledge of the relationship between nonoptimal temperature and cardiovascular health, highlights inequalities in exposure and outcomes, and identifies actionable strategies at the individual, community, health system, and public policy levels. Last, this scientific statement outlines significant research gaps and future priorities, including the need for improved exposure assessment, better understanding and measurement of the impact of long-term exposures, interactions with medications and coexposures, and identification of risk modifiers. Coordinated action is needed in research, clinical practice, and policy to mitigate the rising risks of nonoptimal temperatures on cardiovascular health in a changing climate.

Heart failure with preserved ejection fraction is a complex and increasingly prevalent condition often associated with metabolic comorbidities such as obesity, diabetes, and hypertension. Although its burden is substantial, therapeutic progress has lagged compared with heart failure with reduced ejection fraction. GLP-1RAs (glucagon-like peptide-1 receptor agonists), initially developed for glycemic control in type 2 diabetes, have emerged as promising therapeutic agents for the obese/cardiometabolic heart failure with preserved ejection fraction phenotype. Recent trials, including STEP-HFpEF and SUMMIT, have demonstrated improvements in symptoms, quality of life, and reductions in heart failure events. Beyond inducing substantial weight loss, GLP-1RAs exert a range of metabolic, cardiovascular, and anti-inflammatory effects. In this review, we summarize weight-dependent and weight-independent actions of GLP-1RAs and outline how these mechanisms may influence cardiovascular physiology, myocardial remodeling, cardiac metabolism, renal sodium handling, and systemic inflammation in heart failure with preserved ejection fraction.

The "2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia" retires and replaces the "2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol."

The arterial vasculature is the second most frequently calcified structure in the human body after the skeleton. Calcification of the aorta and aortic valves occurs in most individuals in westernized societies with advancing age, with abdominal aortic calcification generally preceding ascending thoracic aortic disease. In cardiac valves and the thoracic aorta, however, calcification often arises earlier in common disease contexts characterized by metabolic, mechanical, or inflammatory injury (eg, metabolic syndrome, chronic kidney disease, irradiation). In these settings, calcification frequently involves the arterial media as a histoanatomic feature, and is associated with accelerated neurocognitive decline and increased cardiovascular mortality, reflecting a form of precocious aging. The term arteriosclerosis was coined nearly 2 centuries ago to describe the calcium-mediated hardening of the aorta and conduit arteries observed at autopsy with aging. However, much of our understanding of the causes, characterization, and consequences of aortic calcium deposition has emerged only within the past decade. Features of disease biology, including engagement of innate immunity, senescence (inflammaging), and ectopic activation of osteogenic mechanisms, are consistently revealed. In this article, we briefly review the burgeoning literature, highlighting recent advances in clinical and discovery science with translational implications. Given the current trajectory, after 2 centuries of disease recognition, the next decade of innovation promises meaningful progress toward effective medical treatments to prevent and treat the clinical consequences of calcific aortopathy.

Forecasts for the future prevalence of cardiovascular disease and stroke are crucial to guide efforts to improve health outcomes across the life course for women.

Malnutrition can affect patients with various acute cardiovascular disease conditions, including acute coronary syndromes, arrhythmias, or valvular disease; however, most of the literature has focused on patients with heart failure. Malnutrition prevalence estimates range from 20% to 60% for hospitalized patients. Use of Global Leadership Initiative on Malnutrition criteria for malnutrition diagnosis for patients with cardiovascular disease has confirmed prognostic value, correlating with poorer physical function and higher mortality. Nutritional support plays a key role for inpatients, particularly in the cardiac intensive care unit, and includes initiation of feeding within 48 hours of hospitalization, preferably through enteral nutrition. Enteral nutrition is more cost-effective compared with parenteral nutrition and can decrease mortality and shorten lengths of stay. Parenteral nutrition is reserved for patients with severe gastrointestinal dysfunction or to supplement nutrition when enteral nutrition is contraindicated, for example, during high pressor doses that preclude adequate intestinal perfusion or when achieving <70% of nutritional targets after the first week. The optimal protein intake for patients with cardiogenic shock is an area of ongoing research, with higher protein approaches not appearing beneficial in recent critical care trials.

The "2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults" is a de novo guideline that provides comprehensive recommendations for the evaluation, management, and follow-up of adult patients (≥18 years of age) with acute pulmonary embolism (PE). A key feature of this guideline is the introduction of the AHA/ACC Acute Pulmonary Embolism Clinical Categories, which enhance the precision of severity classification, prognosis assessment, and evidence-based therapeutic decision-making.

Right ventricular (RV) failure is a principal determinant of morbidity and mortality in children with pulmonary hypertension, making accurate RV assessment a cornerstone of risk stratification and long-term management. Noninvasive imaging plays a central role in this evaluation; however, commonly used modalities, including 2- and 3-dimensional echocardiography and cardiac magnetic resonance imaging, each have distinct advantages and limitations in the pediatric population. Consequently, an integrated, multimodal imaging strategy is required. This review provides a contemporary, critical appraisal of the existing evidence and key knowledge gaps related to noninvasive multimodality imaging of the RV in pediatric pulmonary hypertension. The discussion is structured around fundamental aspects of RV physiology, including chamber size and mass, systolic function, diastolic function and stiffness, RV-left ventricle interactions, ventriculoarterial coupling, and exercise assessment. Echocardiography and cardiac magnetic resonance imaging are presented in parallel to highlight their complementary roles within a multimodality framework. Current prognostic thresholds in pediatric pulmonary hypertension imaging are largely supported by level of evidence C, underscoring persistent gaps that limit the development of definitive clinical recommendations and a unified approach. We propose a roadmap to guide future research efforts and collaborative initiatives among pediatric pulmonary hypertension and imaging specialists, emphasizing the role of professional networks in advancing the field.

Risk prediction has been used in the primary prevention of cardiovascular disease for >3 decades. Contemporary cardiovascular risk assessment relies on multivariable models, which integrate established cardiovascular risk factors and have evolved over time from the Framingham Risk Model to the pooled cohort equations to the PREVENT (Predicting Risk of CVD Events) equations. Recent scientific (ie, genomics, proteomics, metabolomics) and methodologic (ie, artificial intelligence) advances have led to a proliferation of novel models, biomarkers, and tools for potential use in risk prediction. In parallel, the growing armamentarium of preventive therapies, some with considerable cost, underscores the need for more accurate and precise risk assessment to prioritize those at highest risk who will derive the greatest absolute benefit. Accompanying the considerable enthusiasm for the potential of newer approaches to improve risk prediction is the need for rigorous evaluation and assessment of their performance (ie, accuracy, precision, incremental performance when added to contemporary multivariable risk models or established risk factors) and clinical utility (ie, actionability, scalability, generalizability) before adoption in clinical practice. Additional considerations in risk tool evaluation include reproducibility, cost-value considerations (including impact on downstream health care costs), and implications for health equity. This scientific statement defines a standardized framework for general considerations in risk prediction, statistical assessment of predictive utility, and critical appraisal of clinical utility and readiness. This scientific statement is intended to support clinicians, researchers, and policymakers in how best to evaluate current and emerging risk prediction tools and ultimately improve the prevention of cardiovascular disease in diverse populations.

Clonal hematopoiesis (CH), the benign clonal expansion of hematopoietic stem cells, is often caused by somatic sequence variations in genes associated with hematologic malignancies. Over the past decade, CH has emerged as a risk factor for a wide range of cardiovascular diseases (CVDs), including atherosclerosis, heart failure, atrial fibrillation, and thrombosis. The cardiovascular risk associated with CH is heterogeneous; it varies on the basis of specific genes and variants, clone size, and various extrinsic features. Mechanistic studies suggest that CH contributes to CVDs through both gene-specific pathways and broader inflammatory processes. These include aberrant cytokine production, inflammasome activation, and other proinflammatory mechanisms, which can accelerate atherosclerosis, promote thrombogenesis, and impair vascular or myocardial function. These findings underscore the importance of addressing CH as a potential contributor to CVDs. CH is predominantly considered an age-related phenomenon, but lifelong influences on the fitness of genetic variants, including germline predispositions, obesity, chronic inflammation, and exposure to environmental toxins (eg, tobacco, certain cancer treatments), influence CH. A greater understanding of CH risk factors is therefore important for both individual and population-level risk assessments. Incorporating CH-associated risk into existing CVD risk prediction models may inform new personalized preventive or therapeutic approaches. No CH-specific therapies have proven efficacy in CVD treatment or prevention, but multiple molecular-based therapeutic hypotheses are beginning to be tested.

There is an emerging convergence between atherosclerotic cardiovascular disease and cancer, driven by shared risk factors and overlapping pathophysiologic mechanisms. Traditional factors, such as smoking, aging, obesity, hypertension, and diabetes, alongside novel markers, such as clonal hematopoiesis of indeterminate potential, not only predispose individuals to both malignancies and coronary atherosclerosis but also amplify the risk of cardiotoxicity from cancer therapies. Inflammatory processes play a central role in atherogenesis, a process further accelerated by oncologic treatments-including chemotherapy (eg, anthracyclines, 5-fluorouracil), targeted and hormone therapies (eg, tyrosine kinase inhibitors, androgen deprivation, aromatase inhibitors), immune checkpoint inhibitors, and radiation therapy (RT)-that contribute to endothelial dysfunction and plaque instability. This scientific statement synthesizes the evidence on the interplay between cancer and coronary atherosclerosis, highlighting advances in noninvasive imaging modalities (ie, cardiac CT, nuclear imaging, cardiac magnetic resonance, echocardiography) for early detection, risk stratification, and surveillance of coronary artery disease in oncologic populations, and examines the role of invasive imaging techniques in guiding revascularization decisions. Given the elevated bleeding and thrombotic risks in these patients, individualized management of post-percutaneous coronary intervention medications and abbreviated dual antiplatelet therapy regimens is emphasized. This scientific statement also addresses knowledge gaps and reinforces the need for more evidence to improve risk stratification for atherosclerotic cardiovascular disease in patients with cancer. The shared pathobiology between coronary atherosclerosis and cancer necessitates an integrated, multidisciplinary approach to screening, diagnosis, and management.

Bicuspid aortic valve (BAV) is a frequent congenital heart defect with a high heritability. Despite this, only a limited number of genes have been associated with the disease, and the molecular mechanisms remain unexplained in most cases. This study aimed to further understand the genetic architecture of BAV.

Premenopausal women presenting with acute coronary syndrome (ACS) are a unique and often underrecognized patient population. Although they are traditionally considered at lower cardiovascular risk than other groups, we have begun to appreciate the potential risk for ACS in this younger subset of women. Whereas atherosclerotic disease (obstructive or nonobstructive) accounts for most presentations, a substantial number are attributable to nonatherosclerotic causes, including spontaneous coronary artery dissection, epicardial coronary artery spasm, and coronary embolism. A major challenge at present is the lack of specific data and evidence for the diagnosis and management of these women. Unfortunately, as a result of several factors, diagnostic delays, misclassification, and mistreatment appear to be more frequent than for other patient groups. Of great concern, younger women less often receive guideline-directed therapies after ACS, and younger women with ACS have been shown to have worse outcomes than young men with ACS. Management should be tailored to the unique pathophysiology in premenopausal women, emphasizing early diagnosis, a low threshold for invasive angiography if appropriate, and special consideration in the pregnant patient. Secondary prevention must address traditional cardiovascular and disease-specific risk factors, with consideration of current or future pregnancies and lactation. Participation in cardiac rehabilitation is associated with improved outcomes and must be strongly encouraged, whereas attention to potential post-ACS depression and anxiety is an important aspect of holistic care. Increased patient and health care professional awareness and improved representation in research are critical to closing the knowledge and outcome gaps in premenopausal women with ACS.

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical syndrome affecting ≈32 million individuals worldwide. It accounts for at least half of all heart failure cases and is associated with substantial morbidity and mortality. Although the prevalence of HFpEF increases with age, a substantial proportion of the HFpEF subjects present with cardiometabolic alterations, marking a specific phenogroup of HFpEF. Obesity, diabetes, and hypertension are considered central features in the pathophysiology of HFpEF, driving its development and disease progression by a complex interplay of metabolic-, hemodynamic-, and neurohormonal impairments, resulting in systemic inflammation and immune system dysregulation. Cellular and systemic immunometabolic stress induces vascular endothelial microvascular dysfunction, infiltration of immune cells in the myocardium, and activation of innate and adaptive immune cells in cardiac tissue. The resulting bidirectional crosstalk between systemic and cardiac metabolism influences immune cell reprogramming, sustaining a vicious cycle of cardiac chronic inflammatory response, ultimately leading to adverse structural and functional cardiac remodeling. In this review, we discuss the role of cellular interactions and immunometabolic mechanisms of immune system dysregulation resulting in cardiometabolic HFpEF and elaborate on therapeutic strategies targeting cardiometabolic risk.

In vitro functional modeling of genetic variants has revolutionized our understanding of which variants can cause cardiac disorders, providing insights into their molecular underpinnings. This review provides an overview of high-throughput methods used for the functional assessment of variants implicated in inherited cardiac diseases. Advances in gene-editing technology now enable the efficient generation of cells expressing individual genetic variants or libraries of variants for robust functional studies. We discuss innovative assays that can evaluate dozens or hundreds of variants sequentially. For example, the electrophysiological properties of numerous cardiac ion channel variants in genes linked to inherited arrhythmias can be characterized using automated patch clamping. The mechanical properties of cardiomyocytes expressing candidate cardiomyopathy variants can be assessed using techniques such as atomic force microscopy, traction force microscopy, and impedance-based methods. Multiplexed assays of variant effect are an emerging family of techniques that use gene-specific or general assays, combined with next-generation sequencing, to characterize hundreds or thousands of pooled genetic variants. We examine the key advantages and limitations of each method and outline future goals for the field. Innovative in vitro studies of cardiac genetic variants will enhance our understanding of variant-disease relationships and improve diagnosis, screening, and treatment options for these disorders.

Takayasu arteritis (TAK) is a rare, immune-mediated large-vessel vasculitis that affects predominantly young women and carries a substantial risk of both vascular complications and long-term cardiovascular disease. Although glucocorticoids and conventional immunosuppressive therapies remain the cornerstone of treatment, relapse rates are high, and current strategies fail to adequately mitigate future cardiovascular risk. This review synthesizes evidence on current treatment strategies, unmet clinical needs, and novel approaches, including immunological and vascular-targeted therapies, and argues for a shift in management paradigm toward integrated cardiovascular risk reduction. We discuss advances in understanding the pathogenesis of TAK, highlighting the roles of innate and adaptive immunity in disease progression, and the challenges of early diagnosis and disease monitoring. We critically appraise current treatment paradigms, including glucocorticoids, conventional disease-modifying antirheumatic drugs, and biologics such as tocilizumab and tumor necrosis factor-α inhibitors, and outline emerging therapies targeting novel pathways, including interleukin-17, interleukin-12/23, Janus kinase/signal transducer and activator of transcription, and Notch-1/mammalian target of rapamycin complex signaling. We highlight the increasing recognition of cardiovascular morbidity as a major contributor to mortality in TAK and the need for integrated approaches to risk factor modification. We explore a road map for advancing management of cardiovascular disease in TAK, including comprehensive screening tools that integrate serological and imaging biomarkers to interrogate cardiovascular risk and potential therapeutic cardioprotective strategies such as sodium-glucose cotransporter 2 inhibitors and endothelin receptor antagonists. Despite recent progress, clinical management remains limited by diagnostic uncertainty, heterogeneous treatment approaches, and a paucity of high-quality randomized controlled trials. Future work should focus on interventions that target both immune-mediated vascular injury and cardiovascular disease progression. Achieving long-term disease remission while reducing cardiovascular mortality must become the primary therapeutic goal in TAK.

The American Heart Association annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, nutrition, sleep, and obesity) and health factors (cholesterol, blood pressure, glucose control, and cardiovascular-kidney-metabolic syndrome) that contribute to cardiovascular health. The 2026 Heart Disease and Stroke Statistics Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, brain health, complications of pregnancy, kidney disease, congenital heart disease, rhythm disorders, sudden cardiac arrest, subclinical atherosclerosis, coronary heart disease, cardiomyopathy, heart failure, valvular disease, venous thromboembolism, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs).