The optimal strategy for lower extremity revascularization (surgical bypass versus endovascular intervention) in patients with chronic limb-threatening ischemia (CLTI) is unclear. We examined the effectiveness of open surgical bypass using single-segment great saphenous vein conduit (SSGSV), alternative conduits (AC), or endovascular interventions (ENDO) among patients with CLTI deemed acceptable for either open surgical bypass or ENDO treatment.

Current guidelines recommend implantable cardioverter defibrillators for the primary prevention of sudden cardiac death (SCD) in patients with dilated cardiomyopathy with left ventricular ejection fraction (LVEF)≤35%. However, its effectiveness is hindered by the inability to reliably discriminate between the risk of SCD and competing death of heart failure deterioration, thereby limiting its clinical utility. We aimed to refine the SCD risk stratification model based on cardiac magnetic resonance imaging for patients with dilated cardiomyopathy with LVEF≤35%.

Myocardial infarction (MI) elicits mitochondria reactive oxygen species (ROS) production and cardiomyocyte (CM) apoptosis. Nrf3 (nuclear factor erythroid 2-related factor 3) has an established role in regulating redox signaling and tissue homeostasis. Here, we aimed to evaluate the role and mechanism of Nrf3 in injury-induced pathological cardiac remodeling.

Limited evidence exists on the prognostic role of continuing medical therapy in patients with heart failure (HF) and an ejection fraction (EF) that has improved over time. This study assessed rates of, patient profiles, and associations with morbidity/mortality of renin-angiotensin inhibitors (RASi), angiotensin receptor-neprilysin inhibitors (ARNi), beta-blockers (BBL), and mineralocorticoid receptor antagonists (MRA) withdrawal in patients with HF with improved EF.

Very preterm-born infants are at risk for developing bronchopulmonary dysplasia (BPD), a chronic lung disease. Nowadays, the majority of these infants reach adulthood. Very preterm-born young adults are at risk for developing pulmonary arterial (PA) hypertension later in life. An early sign of PA hypertension is increased PA stiffness. This study aims to use cardiovascular magnetic resonance to compare PA stiffness using PA relative area change (RAC) and pulse wave velocity (PWV) to identify early signs for PA hypertension in young adults born very premature, with and without BPD.

Despite insufficient evidence to support direct-to-consumer genetic testing in routine clinical care, cardiovascular clinicians increasingly face questions about its utility and interpretation because individuals can purchase these tests directly from laboratories. A burgeoning marketplace offers an expanding array of testing options. In many cases, direct-to-consumer genetic testing advertises information that could inform one's risk of heritable disease, including insight into having a genetic predisposition to cardiovascular disease or data about gene-drug interactions that could affect response to cardiovascular medications. Navigating clinical questions about direct-to-consumer genetic testing involves understanding the evolution and oversight of the marketplace; the scope of direct-to-consumer genetic testing offerings; and the risks, benefits, and limitations of said testing. In this American Heart Association scientific statement, we summarize the state of the direct-to-consumer genetic testing industry, review types of cardiovascular genetic information that may be included in direct-to-consumer genetic testing, describe approaches to evaluate test quality, and provide resources for clinicians navigating questions about direct-to-consumer genetic testing. If direct-to-consumer genetic test information is used in clinical care, care should be taken to assess the limitations of the test, to contextualize the information specifically to the patient, and to corroborate potentially actionable monogenic findings.

Cardiac β3-adrenergic receptors (ARs) are upregulated in diseased hearts and mediate antithetic effects to those of β1AR and β2AR. β3AR agonists were recently shown to protect against myocardial remodeling in preclinical studies and to improve systolic function in patients with severe heart failure. However, the underlying mechanisms remain elusive.

Sex differences in the risk factors, diagnosis, treatment, and outcomes of patients with cardiovascular disease have been well described; however, the bulk of the literature has focused on heart disease in women. Data on sex differences in peripheral vascular disease are ill defined, and there is a need to report and understand those sex-related differences to mitigate adverse outcomes related to those disparities. Although peripheral vascular disease is a highly diverse group of disorders affecting the arteries, veins, and lymphatics, this scientific statement focuses on disorders affecting the peripheral arteries to include the aorta and its branch vessels. The purpose of this scientific statement is to report the current status of sex-based differences and disparities in peripheral vascular disease and to provide research priorities to achieve health equity for women with peripheral vascular disease.

Despite favorable hemodynamic and neurohormonal effects, endothelin receptor antagonists have not improved outcomes in patients with heart failure (HF), possibly because they cause fluid retention.

Muscle proteins of the obscurin protein family play important roles in sarcomere organization and sarcoplasmic reticulum and T-tubule architecture and function. However, their precise molecular functions and redundancies between protein family members as well as their involvement in cardiac diseases remain to be fully understood.

Nickel-containing devices, such as the Amplatzer PFO Occluder and Gore Cardioform Septal Occluder, are used for transcatheter patent foramen ovale closure. However, the impact of nickel hypersensitivity on postprocedural outcomes remains poorly understood. This study aimed to evaluate the risk of adverse events in patients with nickel hypersensitivity undergoing patent foramen ovale closure.

Therapies targeting the LPL (lipoprotein lipase) pathway are under development for cardiometabolic disease. Insights into their efficacy-both alone and in combination with existing lipid-lowering therapies-modes of action, and safety of these agents are essential to inform clinical development. Using Mendelian randomization, we aimed to (1) evaluate efficacy, (2) explore shared mechanisms, (3) assess additive effects with approved lipid-lowering drugs, and (4) identify secondary indications and potential adverse effects.

We derived and validated proteomic risk scores (PRSs) for heart failure (HF) prognosis that provide absolute risk estimates for all-cause mortality within 1 year.

Heart rate (HR) affects heart failure outcomes, via uncertain mechanisms that may include left ventricular remodeling. However, in human ventricular myocardium, HR change has not been associated with a particular remodeling molecular phenotype.

Lymphedema is an incurable disease associated with lymphatic dysfunction that causes tissue swelling and fibrosis. We investigated whether lymphedema could be attenuated by interfering with uPARAP (urokinase plasminogen activator receptor-associated protein; Mrc2 gene), an endocytic receptor involved in fibrosis and lymphangiogenesis.