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.

Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of morbidity and mortality worldwide. Preventing ASCVD is of utmost importance; however, a large proportion of preventable cases is not discovered early enough to initiate relevant treatment. Risk stratification for ASCVD includes classical risk factors, such as sex, age, smoking habits, blood pressure, cholesterol levels, and diabetes. Current risk prediction models, including the Systematic Coronary Risk Evaluation 2 algorithms, are designed for individuals aged 40 to 69 years and relate to 10-year risk and not to lifetime risk, thereby being inaccurate for the young. Another problem is the underdiagnosis of events in women, thereby underestimating risk. Multiomics, encompassing genomics, epigenomics, transcriptomics, epitranscriptomics, proteomics, and metabolomics, offers new opportunities. Polygenic risk scores derived from genomic data may improve ASCVD risk classification. While genomic risk is established at inception, epigenomics captures the influence of environmental exposures over the lifespan through dynamic DNA modifications that regulate gene expression. Proteomics-based prediction reflects interactions between genetic inheritance, and modifiable and nonmodifiable influences. Transcriptomic analyses of carotid plaques have clustered human atherosclerotic lesions into distinct molecular subgroups, and changes in RNA methylation of circulating blood cells have been linked to clinical outcomes after ASCVD. Metabolomics identifies metabolic signatures, including lipid subclass alterations, amino acid imbalances, and inflammatory markers, all associated with cardiovascular disease incidence. In this review, we highlight current challenges, explore potential solutions, and discuss how integrating multiple omic layers through computational modeling (multiomics) could enhance patient stratification, optimize clinical management, and reduce the global burden of ASCVD.

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.

Surgical aortic valve (AV) replacement has been the standard treatment for patients with severe symptomatic degenerative AV stenosis (AS). In recent years, transcatheter AV replacement has emerged as an established alternative in selected patient populations, supported by robust evidence in tricuspid AS. However, there has been limited evaluation of transcatheter AV replacement in bicuspid AV AS. Recently, several observational studies have demonstrated the feasibility and safety of transcatheter AV replacement in bicuspid AV AS, and the use of newer-generation devices has shown encouraging outcomes. However, the incidence of procedural complications such as paravalvular regurgitation, permanent pacemaker implantation, and aortic root injury was more frequent in patients with bicuspid AV AS compared with tricuspid AS. We review the clinical evidence of transcatheter AV replacement for bicuspid AV AS and suggest the appropriate criteria for patient and device selection, implantation techniques, and further management.

Pericarditis spans acute, recurrent/incessant, effusive, and constrictive phenotypes, and accurate assessment of inflammatory activity and chronicity is essential to guide therapy and anticipate outcomes. Although transthoracic echocardiography remains the first-line modality to evaluate pericardial effusion, tamponade physiology, and constrictive hemodynamics, it is limited for tissue characterization. Multimodality imaging integrates complementary strengths: cardiac magnetic resonance provides the most sensitive noninvasive assessment of pericardial edema and late gadolinium enhancement to phenotype active inflammation versus chronic fibrotic disease and to support prognostication (including identification of potentially reversible constriction); cardiac computed tomography offers superior anatomic detail for pericardial thickness, calcification, complex effusions, and preoperative planning for pericardiectomy, and can serve as an alternative when cardiac magnetic resonance is contraindicated; and 18F-fluorodeoxyglucose positron emission tomography/computed tomography adds targeted value by detecting metabolically active pericardial inflammation in diagnostically ambiguous or refractory cases and may inform escalation to advanced therapies. We synthesize practical, guideline-aligned applications of these modalities, highlight common pitfalls and system-level constraints, and propose a simplified framework using key imaging biomarkers edema/inflammation, neovascularization (late gadolinium enhancement), thickening, effusion/tamponade, constriction, and fibrosis/calcification to enable imaging-guided therapy, including treatment escalation and tapering strategies in recurrent disease and selection of patients for pericardiectomy.

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.

The current guidelines contraindicate intravenous amiodarone in patients with Wolff-Parkinson-White syndrome presenting with preexcited atrial fibrillation (AF) due to the risk of degeneration into ventricular fibrillation (VF). However, these recommendations are based predominantly on isolated case reports, which is concerning given the drug's widespread global use as a first-line antiarrhythmic in resource-limited settings. To evaluate the safety of intravenous amiodarone in this context, we conducted a systematic review of (1) studies enrolling patients with electrocardiographically confirmed preexcited AF who received intravenous amiodarone and (2) studies quantifying antegrade accessory-pathway effective refractory period during intravenous amiodarone administration. All observational and interventional studies assessing patients with preexcited AF were pooled under a conjugate β-binomial model with prespecified weak priors to estimate the risk of VF during or following infusion. Concomitantly, to assess real-world access to alternative class IIa/IIb European Society of Cardiology-recommended antiarrhythmic agents for preexcited AF, we performed a multinational survey of Latin American emergency departments. Twelve studies comprising 177 patients were included in the review (7 case reports, 2 cohorts, 3 before-and-after interventional studies). Four case reports described transient ventricular rate acceleration or VF following intravenous amiodarone. However, across the observational and interventional cohorts assessing patients with preexcited AF (n=146), no acceleration or VF was observed. The posterior mean estimates of VF risk ranged 0.12% to 0.68% over priors. Across 3 interventional before-and-after studies, there was a significant increase in the anterograde effective refractory period of the atrioventricular node and AP following amiodarone administration. The survey responses from 10 emergency centers indicated that none had access to class IIa/IIb indicated agents, while all had intravenous amiodarone available. Taken together, population-level evidence suggests that the risk of VF in preexcited AF following intravenous amiodarone administration is rare. In settings where guideline-recommended drugs are inaccessible, intravenous amiodarone may represent a clinically reasonable alternative for rhythm or rate control.

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.

Kidney dysfunction after heart transplantation (HT) is associated with significant morbidity and mortality. Recipient and perioperative factors may all influence the risk of kidney injury. Furthermore, data suggest that the incidence of kidney dysfunction, both acute and chronic, is increasing after the implementation of the United States' 2018 allocation system due to increasing use of temporary mechanical circulatory support and changing recipient characteristics. While data are robust regarding nephroprotective therapies such as renin-angiotensin-aldosterone system inhibition and SGLT2 (sodium-glucose cotransporter 2) inhibitors to minimize the progression of chronic kidney disease in patients with heart failure, data in HT recipients are beginning to emerge. This state-of-the-art review will critically examine the existing literature regarding the epidemiology of kidney dysfunction after HT, mitigation strategies for acute kidney injury and chronic kidney disease, including pharmacotherapeutics, the need for kidney transplantation after HT, and practical next steps for the larger HT community.

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.

Paravalvular leak (PVL) is a well-known complication of valve replacement, occurring in up to 10% of aortic and 17% of mitral prosthetic valves. Although many leaks are small and clinically insignificant, ≈1% to 5% of cases are associated with clinically relevant complications, such as heart failure symptoms and hemolytic anemia. Surgical reoperation is currently considered the first-line option; however, it encompasses high mortality and morbidity risks. In the past years, transcatheter PVL closure has proven to be highly effective when performed in experienced centers. Transcatheter PVL closure requires advanced imaging modalities, specialized materials, and techniques, reflecting the high complexity of the procedure. We review the complex nature of PVL, including its diagnostic workup and the available transcatheter treatment strategies, with a special focus on the treatment of mitral and aortic PVL using plugging devices.

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.

Btk (Bruton's tyrosine kinase), a Tec-family kinase initially recognized for its role in B-cell signaling, has emerged as a critical player in thrombosis and cardiovascular disease. Beyond the established therapeutic effects of Btk inhibitors in B-cell malignancies, its expression in platelets, macrophages, and neutrophils implicates Btk in platelet activation, atherothrombosis, and innate immunity. This state-of-the-art review synthesizes the current understanding of Btk's mechanistic contributions to thrombosis and cardiovascular disease, evaluates the evolution of Btk inhibitors (BTKi), and explores their therapeutic potential. Patients with X-linked agammaglobulinemia who lack Btk do not have a bleeding diathesis, indicating that platelet-selective Btk inhibition would be a safe antithrombotic strategy. In platelets, Btk mediates immunoreceptor tyrosine-based activation motif-dependent and -independent signaling, driving atherothrombosis, venous thrombosis, and immunothrombosis without affecting hemostatic platelet functions. In myeloid cells, Btk amplifies inflammation via NLRP3 inflammasome activation and neutrophil extracellular trap formation, linking it to thromboinflammation and atherosclerosis. First-generation BTKi such as ibrutinib demonstrate antithrombotic efficacy but are limited by off-target effects, including bleeding and atrial fibrillation. Second- and third-generation inhibitors (eg, acalabrutinib, zanubrutinib, and pirtobrutinib) show enhanced selectivity, reducing cardiovascular toxicity in patients with B-cell malignancies. Highly selective BTKi (fenebrutinib and remibrutinib) do not show bleeding in clinical trials of various autoimmune disorders, and covalent selective BTKi applied at low dosage are expected to selectively inhibit Btk in platelets without bleeding side effects. Preclinical data and early observations from compassionate use in patients with atypical autoimmune thrombosis highlight the potential of BTKi as selective antithrombotic agents beyond traditional therapies. This review conceptualizes and underscores Btk's pivotal role at immune-thrombosis interfaces in atherothrombosis, advocating for precision medicine approaches and innovative platforms to unlock its full therapeutic potential in cardiovascular disease management.

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.