Fibrosis, with accumulation of type I collagen, is a hallmark of postthrombotic change after deep vein thrombosis (DVT), but tools for its direct detection are lacking. Here, we investigate whether molecular magnetic resonance imaging (MRI) using a collagen-specific gadolinium-based probe can detect and measure changes in collagen during thrombus resolution and in response to treatment in a mouse model of DVT.

Cardiac fibrosis is a major determinant of adverse clinical outcomes of many heart diseases; currently, therapeutic strategy directly targeting fibroblasts is lacking. Nitric oxide-mediated nitrosative stress is associated with cardiac injury, and excessive nitric oxide can trigger S-nitrosylation (SNO) to specific cysteine thiol. This study aims to investigate the role of SNO in cardiac fibrosis and to identify potential therapeutic target.

Although disease-specific patient-reported outcomes (PROs) are well accepted as direct and indirect clinical outcomes in various diseases, data on PRO performance in adult congenital heart disease (ACHD) are limited to nondisease-specific metrics. We, therefore, investigated the association between responses to a novel ACHD-specific PRO metric and both clinical variables and gold standard PROs.

Guidelines recommend 3-hour cardiac amyloid radionuclide imaging (CARI) for transthyretin amyloid cardiomyopathy. Citing rapid blood clearance of 99mTc-hydroxymethylene-diphosphonate (HMDP) and efficient laboratory throughput, 1-hour imaging is increasingly practiced despite limited supporting evidence. We sought to compare diagnostic performance and interpreter experience of 1-hour versus 3-hour HMDP-CARI.

Inhibiting SGLT2 (sodium-glucose cotransporter 2) has recently transformed the medical care of patients with left heart disease. Right ventricular failure is a major predictor for patients suffering from pulmonary hypertension of various causes, including those with postcapillary pulmonary hypertension due to left heart disease. Similar to how SGLT2 inhibition benefits patients with left heart failure, recent studies have suggested utilizing these molecules to enhance right ventricular function in pulmonary hypertension. In this review, we summarize the current knowledge on the use of SGLT2is (SGLT2 inhibitors) in pulmonary hypertension. Further dedicated trials are necessary to establish their role in right ventricular pulmonary vascular disease.

Chronic aortic regurgitation (AR) is associated with significant cardiac remodeling, but the prevalence and prognostic impact of extravalvular cardiac damage remain unexplored.

Studies have demonstrated that patients with myocarditis may have a higher burden of cardiomyopathy-associated genetic variants than the general population. However, data on children are limited. We compared the prevalence of rare predicted-damaging variants and clinically pathogenic variants in children with dilated cardiomyopathy (DCM) secondary to myocarditis with that in children with DCM alone and in heart-healthy controls.

Hypertrophic cardiomyopathy (HCM) is an important cause of morbidity and mortality in children, but treatment options are limited. Aficamten, a next-in-class cardiac myosin inhibitor, directly targets the hypercontractility underlying HCM. Aficamten improved exercise capacity, health status, and symptoms in adults with obstructive HCM in the pivotal, phase 3 SEQUOIA-HCM trial (Safety, Efficacy, and Quantitative Understanding of Obstruction Impact of Aficamten in HCM; NCT05186818).

Air pollution is a major global environmental health threat and the leading environmental risk factor contributing to cardiovascular morbidity and mortality. Emerging evidence increasingly implicates air pollution as a critical, modifiable driver in the pathogenesis, progression, and prognosis of heart failure. Air pollution is increasingly recognized as part of the exposome-a complex interplay of environmental, social, and behavioral exposures accumulated across the life course. In this review, we synthesize experimental data demonstrating mechanistic links between air pollution and heart failure, along with growing experimental, clinical, and epidemiological evidence connecting both short- and long-term air pollution exposure with increased risk of heart failure progression across heart failure stages. We further examine how air pollution interacts with other exposomic risk domains-such as the social exposome, built environment, and access to greenery-compounding vulnerability in marginalized and underserved populations. The review will also summarize current approaches to communicate air pollution risk and propose practical strategies for both individuals and healthcare systems to mitigate its cardiovascular impact. Finally, we present a clinical framework for assessing and managing air pollution exposure in patients with heart failure, emphasizing the need for targeted risk stratification and the development of context-specific mitigation interventions.

Current national performance metrics rank transcatheter aortic valve replacement (TAVR) centers based on risk-adjusted outcomes. This could make operators/centers less inclined to offer TAVR in high-risk cases.

A formal prognostic staging system in wild-type transthyretin amyloid cardiomyopathy (ATTRwt-CM), based on echocardiographic imaging, is lacking. We evaluated the prognostic performance of global longitudinal strain (GLS) staging in a large cohort of patients with ATTRwt-CM, including under tafamidis treatment and relative to National Amyloidosis Center (NAC) biomarker staging.

The safety, yield, and prognosis of a type 1 procainamide-induced Brugada pattern are incompletely understood and may differ from those of other sodium channel blockers with greater potencies.