Combined post- and pre-capillary pulmonary hypertension in heart failure with preserved ejection fraction (CpcPH-HFpEF) involves remodeling in both the heart and pulmonary vasculature. Despite significant mortality, there are no proven therapies.

Coronary vasomotor dysfunction is diagnosed by a coronary function testing (CFT). However, protocols vary, and the influence of access site and concomitant vasodilator medication on the diagnostic yield and safety of CFT is unclear. This study assessed the diagnostic yield and safety of CFT by radial access with intraarterial calcium channel blockers compared with CFT by femoral access.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) has several underlying causes, including mimicking conditions in some cases. Imaging is recommended to identify MINOCA etiologies, but it remains unclear which patients are most likely to have abnormal findings. We characterized MINOCA mechanisms, analyzed predictors of imaging abnormalities and explored sex differences.

Delayed or missed diagnosis of congenital heart disease (CHD) contributes to excess pediatric mortality worldwide. Echocardiography (echo) is central to diagnosing and triaging CHD, yet expert interpretation remains a scarce and maldistributed global resource. Artificial intelligence (AI) offers the potential to democratize diagnostics and extend expert-level interpretation beyond large academic centers, but its application in CHD remains underexplored.

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.

Heart failure (HF) is a significant global health problem. Left ventricular assist device (LVAD) implantation serves as a bridge for patients awaiting heart transplantation. Intriguingly, LVAD support often improves cardiac histology and function, sometimes enough to avoid transplantation after LVAD removal. However, the cellular programs underlying this recovery remain unclear.

Survival after Fontan palliation for single ventricle heart disease has improved substantially, yet the long-term trajectory remains poorly defined. The Fontan Outcomes Network, a learning health network of 38 congenital heart centers in the United States and Canada, was established to address this gap. We report baseline characteristics and early findings from the first 1121 participants enrolled in this prospective clinical registry.

Rare variant genetics have been associated with peripartum cardiomyopathy (PPCM), but the role of genetics remains unsettled. The study sought to compare dilated cardiomyopathy (DCM) genetic risk in first-degree relatives (FDRs) of female patients (probands) with DCM or PPCM to gain causal inference, and to assess DCM-relevant rare variant prevalence in DCM/PPCM probands and population controls.

The Get With the Guidelines-Heart Failure program is a national quality improvement initiative that was established in 2005 with the goal of improving the quality of care for patients hospitalized with heart failure.

Peptides such as angiotensin II and brain natriuretic peptide are pivotal in diagnosing and treating heart failure (HF). However, unbiased systematic studies of the peptidome in patients with HF are lacking. Deciphering the plasma peptidome might significantly improve the diagnosis, prognostication, and treatment of patients with HF.

Mild congenital heart diseases such as atrial septal defect, ventricular septal defect, patent ductus arteriosus, and pulmonary valve stenosis constitute a significant public health problem. Understanding long-term outcomes after interventions for mild congenital heart disease is essential to inform lifelong care.

In patients with obstructive coronary artery disease, early revascularization does not improve outcomes but may reduce angina symptoms. The objective of this study was to examine whether changes in health status outcomes following revascularization are explained by the extent of myocardial perfusion defects and improvement in myocardial perfusion.

Premature atrial contractions (PACs) are independently associated with atrial fibrillation, stroke, and heart failure, yet no pharmacological therapy is approved for PAC suppression. Experimental studies have identified a functional cardiac glutamatergic system in which N-methyl-D-aspartate receptors regulate atrial electrophysiology. Preclinical studies show that pharmacological antagonism of N-methyl-D-aspartate receptors with memantine suppresses atrial arrhythmias.