Hypertension is the leading modifiable risk factor for atrial fibrillation (AF) and is estimated to be present in >70% of AF patients. This Frontiers Review was prepared by 29 expert members of the AF-SCREEN International Collaboration to summarize existing evidence and knowledge gaps on links between hypertension, AF, and their cardiovascular sequelae; simultaneous screening for hypertension and AF; and the prevention of AF through antihypertensive therapy. Hypertension and AF are inextricably connected. Both are easily diagnosed, often silent, and frequently treated inadequately. Together, they additively increase the risk of ischemic stroke, heart failure, and many types of dementia, resulting in greater all-cause mortality, considerable disease burden, and increased health care expenditures. Automated upper arm cuff blood pressure devices with implemented technology can be used to simultaneously detect both hypertension and AF. However, positive screening for AF with an oscillometric blood pressure monitor still requires ECG confirmation. The current evidence suggests that high-risk individuals aged ≥65 years or with treatment-resistant hypertension could benefit from AF screening. Since antihypertensive therapy effectively lowers AF risk, particularly in individuals with left ventricular dysfunction, hypertension should be the key target for AF prediction and prevention rather than merely a comorbidity of AF. Nevertheless, several important gaps in knowledge need to be filled over the next years, including the ideal method and selection of patients for simultaneous screening of hypertension and AF and the optimal antihypertensive drug class and blood pressure targets for AF prevention.

Cardiovascular health (CVH) is affected by genetic, social, and genomic factors across the life course, yet little research has focused on the interrelationships among them. An extensive body of work has documented the impact of social determinants of health at both the structural and individual levels on CVH, highlighting pathways in which racism, housing, violence, and neighborhood environments adversely affect CVH and contribute to disparities in cardiovascular disease. Genetic factors have also been identified as contributors to risk for cardiovascular disease. Emerging evidence suggests that social factors can interact with genetic susceptibility to affect disease risk. Increasingly, social factors have been shown to affect epigenetic markers such as DNA methylation, which can regulate gene and protein expression. This is a potential biological mechanism through which exposure to poor social determinants of health becomes physically embodied at the molecular level, potentially contributing to the development of suboptimal CVH and chronic disease, thus reinforcing and propagating health disparities. The objective of this statement is to highlight and summarize key literature that has examined the joint associations between social, genetic, and genomic factors and CVH and cardiovascular disease.

T2-weighted imaging is commonly used to measure myocardial salvage in reperfused myocardial infarction but is hindered by poor reproducibility and indistinct boundaries. Early gadolinium enhancement (EGE) emerges as an alternative for measuring the area at risk. This study aims to evaluate the determinants of the myocardial salvage index (MSI) derived from EGE and its prognostic implications.

The optimal antispastic treatment after coronary artery bypass grafting using radial artery (RA) grafts is controversial. This clinical trial aimed to generate pilot comparative data on the effects of nicorandil, isosorbide mononitrate, or diltiazem on RA grafts.

The use of ionizing radiation during cardiac catheterization procedures poses risks to patients and medical staff, both directly and indirectly through orthopedic injuries caused by lead aprons. In this review, we summarize recent advances in radiation protection in the cardiac catheterization laboratory and discuss the effectiveness of traditional and novel radiation protection strategies and equipment.

Many patients are unaware of their stroke risk. The purpose of this research was to compare the effect of behaviorally tailored mailed messages on patient activation to reduce stroke risk.

Genetic variants in desmosomal cadherins, desmoglein 2 (DSG2) and desmocollin 2 (DSC2), cause a distinct form of arrhythmogenic right ventricular cardiomyopathy (ARVC), which remains poorly reported. In this study, we aimed to provide a comprehensive description of the phenotypic expression, natural history, and clinical outcomes of patients with this ARVC subset.

Tricuspid regurgitation (TR) is associated with increased mortality and is often underdiagnosed due to limitations in imaging modalities. While routine 2-dimensional echocardiography (2DE) demonstrates frequent disagreement with cardiac magnetic resonance imaging (CMR) in classifying TR severity, the incremental value of 3-dimensional echocardiography (3DE) remains unknown also due to the lack of a generalizable grading scheme across imaging modalities. Therefore, this study provides an intermodality comparison of all 3 imaging modalities (2DE, 3DE, and CMR) in evaluating TR severity and proposes an adapted 5-class grading scheme for TR severity using CMR.

Patients with paradoxical low-flow, low-gradient severe aortic stenosis exhibit low transvalvular flow rate (Q), while maintaining preserved left ventricular ejection fraction. Severe mitral regurgitation (MR) also causes a low-flow state, adding complexity to diagnosis and management. This study aimed to examine the impact of severe MR on outcomes in paradoxical low-flow, low-gradient severe aortic stenosis.

Recent studies have shown that vasospastic angina (VSA) is associated with myocardial bridge (MB) and pericoronary adipose tissue inflammation. We aimed to investigate the clinical and coronary computed tomography angiographic (CCTA) features that could predict VSA in patients with angina and nonobstructive coronary arteries.

Magnetic resonance imaging (MRI)-derived myocardial extracellular volume fraction (ECV) is elevated in the presence of fibrosis, amyloid deposition, inflammation, and edema. In patients with cardiac amyloidosis and prolonged T2 due to concomitant inflammation or edema, MRI-ECV may not correctly reflect histological amyloid load. The authors sought to determine whether MRI-ECV can accurately reflect histological amyloid load in 2 groups of patients with wild-type transthyretin amyloid cardiomyopathy (ATTRwt-CM), with and without T2 prolongation.