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."

Peripheral artery disease (PAD) and its severe form, chronic limb-threatening ischemia (CLTI), significantly impair blood flow to the lower extremities, affecting millions of adults globally. Intramuscular adipose tissue (IMAT) and fibrosis accumulation distinguish patients with CLTI from those with mild PAD, suggesting a role in CLTI pathobiology. However, the functional consequences of IMAT in CLTI remain unclear.

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.

Sarcomere gene variants are a key cause of hypertrophic cardiomyopathy (HCM), and have been associated with worse prognosis. However, it is unclear how comorbidities influence clinical trajectories, the timing of events, and causes of death in sarcomeric and nonsarcomeric HCM.

Aortic valve calcification increases leaflet stiffness and contributes to the development of calcific aortic valve disease. The molecular and cellular mechanisms underlying calcification remain unclear. Here, we aimed to investigate the role of PRMT3 (protein arginine methyltransferase 3) in valvular calcification and calcific aortic valve disease progression.

Right ventricular failure drives both morbidity and mortality in pulmonary arterial hypertension (PAH), but the mechanism of transition from compensated right ventricle (cRV) to decompensated RV (dRV) is unknown, and some PAH patients develop dRV faster than others.

Myocardial ischemia/reperfusion (I/R) injury is a common and severe clinical complication in patients with ischemic heart disease after reperfusion therapy. Effective therapeutic strategies for myocardial I/R injury remain limited. Ferroptosis is a form of regulated cell death characterized by iron-dependent lipid peroxidation. However, the mechanisms underlying ferroptosis in myocardial I/R injury are not fully understood.

Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) is useful for identifying ventricular tachycardia (VT) substrate in patients with structural heart disease. While preprocedural LGE-CMR is widely used for planning, the role of postprocedural LGE-CMR in evaluating VT ablation success and long-term scar evolution has been less explored. This study aimed to prospectively and systematically assess the long-term evolution of scar and ablation lesions using serial postablation LGE-CMR with long-term follow-up.

Nutrition insecurity is a major driver of poor cardiovascular health in Indigenous communities. Medically tailored meals may improve heart failure outcomes and quality of life. There is growing momentum among Indigenous communities to reclaim traditional precontact foods to improve cardiovascular health. In this context, utilizing community-based-participatory methods, we designed MUTTON-HF (Medically Utilized Tailored Traditional Foods to Optimize Nutrition in Heart Failure)-an Indigenous culturally and medically tailored meals program that locally sources Native produce and meat and incorporates traditional Diné (Navajo) foods and recipes.

Mortality from acute myocardial infarction (MI) has declined significantly in the past decade for nondiabetic patients. However, both morbidity and mobility of ischemic heart failure (IHF) persistently escalate in the diabetic population via incompletely understood mechanisms. Recent studies demonstrated that small extracellular vesicles (sEVs) released from nondiabetic and diabetic adipocytes (ADps) exert opposite effects on acute myocardial ischemia and reperfusion (MI/R) injury. However, whether and how ADp sEVs may protect against post-MI remodeling and IHF, and more important, whether and how diabetes may impair this protective effect, remain unknown.