Catecholaminergic polymorphic ventricular tachycardia (CPVT) is strongly associated with rare missense variants in RYR2, the gene encoding the intracellular calcium release channel RyR2.

The impact of proportionality to heart valve regurgitation has been widely investigated in mitral regurgitation, helping to better characterize the best candidates for therapies. However, it has never been studied in tricuspid regurgitation (TR). The aim of the present study is to investigate the impact of the proportionality of TR on outcomes.

The prognostic value of rapid atrial pacing (RAP)-induced Wenckebach atrioventricular block (W-AVB) as a diagnostic test for predicting permanent pacemaker implantation (PPI) after transcatheter aortic valve replacement (TAVR) remains unclear and requires further validation. The objective of this study was to evaluate the predictive value of RAP-induced W-AVB for PPI and sudden cardiac death within 30 days post-TAVR.

The COMPASSION S3 trial (Congenital Multicenter Trial of Pulmonic Valve Dysfunction Studying the SAPIEN 3 Interventional Transcatheter Heart Valve) was designed to evaluate the safety and effectiveness of the SAPIEN 3 transcatheter heart valve (THV) for transcatheter pulmonic valve replacement in patients with a dysfunctional right ventricular outflow tract (RVOT) conduit or previously implanted valve in the pulmonic position. Here, 5-year clinical and hemodynamic outcomes for patients in the main cohort and the continued access protocol are reported.

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.

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.