Carotid artery intima-media thickness (cIMT) is a highly heritable measure of subclinical atherosclerosis and a predictor of cardiovascular diseases. However, knowledge about its shared genetic basis remains limited. The majority of genome-wide association studies have been conducted in individuals of European ancestry, leaving the genetic determinants of cIMT in non-European ancestry populations largely understudied.

Aging is associated with increases in pulmonary pressure related to concomitant age-associated left ventricular remodeling, diastolic dysfunction, and declines in pulmonary function. Little is known regarding morphological changes in the pulmonary arterial vasculature underlying these associations. Our aim was to determine the associations between pulmonary vascular arterial remodeling, reflected in distal pruning and proximal dilation, and cardiac structure and function, pulmonary pressure, and functional outcomes.

Right atrioventricular coupling index (RACI), defined as the ratio of right atrial (RA) to right ventricular end-diastolic volume on cardiac magnetic resonance, is a novel parameter that reflects RA-right ventricular (RV) hemodynamic interplay. Its prognostic value in functional tricuspid regurgitation (TR) is unknown.

Although medically tailored groceries (MTG) hold promise to improve food and nutrition security and health among patients with diet-related illnesses and social needs, few randomized trials have been performed.

Cardiac sarcoidosis is a granulomatous myocarditis, classified by some authorities as an infiltrative cardiomyopathy and by others as an inflammatory cardiomyopathy, that carries an elevated risk of life-threatening arrhythmias, heart failure, and sudden cardiac death. Despite its clinical importance, diagnosis remains challenging. No single modality achieves both high sensitivity and specificity, and the 4 major consensus documents-comprising expert consensus statements, clinical practice guidelines, and a scientific statement-differ in diagnostic thresholds and can yield discordant diagnoses when applied to the same patient. Genetic cardiomyopathies account for a meaningful fraction of patients diagnosed with presumed isolated cardiac sarcoidosis. This primer organizes the diagnostic approach around 2 clinical contexts: de novo cardiac presentation with unexplained atrioventricular block, ventricular arrhythmia, or heart failure without previous sarcoidosis; and cardiac screening in patients with established extracardiac sarcoidosis. In nonurgent presentations, concordant cardiac magnetic resonance imaging and 18F-fluorodeoxyglucose positron emission tomography abnormalities are accepted as sufficient for diagnosis; endomyocardial biopsy is indicated when imaging is inconclusive or giant cell myocarditis must be excluded. Advanced imaging should precede permanent device implantation in all de novo presentations. Isolated cardiac sarcoidosis represents the most diagnostically challenging phenotype. A 5-step pathway is presented that integrates advanced imaging, tissue acquisition when it would change management, and genetic evaluation. Expert opinion on histologic confirmation in nonurgent presentations is divided, and no diagnostic approach has been prospectively validated.

At a time when there was no unifying hypothesis and no broadly effective treatments for heart failure with a preserved ejection fraction (HFpEF), it was proposed that HFpEF represented a multitude of different disorders. Accordingly, characterization of phenotypic heterogeneity was envisioned as a means of identifying novel causal pathways that could lead to new treatments while simultaneously discerning patients who would selectively benefit from a specific therapy. However, efforts over the past decade to characterize phenotypic diversity in diverse and complex ways have not achieved these goals. Subgroup analyses of neutral HFpEF trials have failed to reliably identify responders to treatments. Neither proteomics nor unsupervised cluster analysis across multiple phenotypic domains has yielded reproducible results (even in the same dataset), elucidated novel mechanistic pathways for new drug development, or identified patients most likely to benefit from treatment. In marked contrast to these efforts to characterize phenotypic heterogeneity, large-scale trials in HFpEF enrolled patients using broad eligibility criteria, and they established the benefits of sodium-glucose cotransporter 2 inhibitors and mineralocorticoid receptor antagonists without evidence for subgroup effects. However, it is noteworthy that patients enrolled in recent large-scale HFpEF trials were characterized by general uniformity with respect to the presence of excess adiposity, with central obesity being a feature of the vast majority of enrolled participants. Of note, patients with obesity showed particularly large benefits when treated with effective drugs for HFpEF. These observations raise the possibility that, if these trials had permitted the participation of patients with class III obesity or with lower natriuretic peptide levels, the magnitude of the observed treatment effects might have been greater than originally reported. These findings are consistent with a central role for visceral adiposity (and the secretion of an altered suite of adipokines) in the pathogenesis of HFpEF. Therefore, because the field of HFpEF has a unifying hypothesis (applicable to the large majority of patients), enrolled a broad population of patients in large-scale trials without subgroup interactions, and has several broadly applicable effective treatments (as is true for heart failure with a reduced ejection fraction), the motivation to characterize phenotypic heterogeneity in HFpEF in complex ways may no longer be supported or needed.

Metabolic adaptation and maladaptation are hallmarks of the failing heart and may be a target for therapeutic interventions. For example, sustained glucose oxidation during cardiac stress is associated with increased activity and abundance of ACL (ATP-dependent citrate lyase, Acly), which produces acetyl-coenzyme A (CoA) from citrate and CoA and supports de novo lipid synthesis. However, our understanding of how ACL supports cardiac metabolic adaptation and its potential to modulate disease pathophysiology has not yet been investigated.

Caffeine is one of the most commonly consumed drugs in the world. It is found in various naturally occurring substances and can be ingested in a synthetically derived pure form. The majority of human subject-based research is observational and has focused on beverages and foods that contain caffeine. The relationships between caffeine and cardiovascular risk factors and diseases are complex, exhibiting heterogeneity depending on the nature of the caffeine consumed and individual-level propensities. Acute versus chronic caffeine-associated cardiovascular effects are often different. Most studies suggest an inverse J-shaped relationship between consumption of naturally occurring caffeinated products and blood pressure. Data on relationships between caffeine and diabetes are not consistent, but habitual coffee consumption has been associated with a lower risk of incident type 2 diabetes. Whereas no clear relationship between caffeine and blood lipids is evident, unfiltered coffee raises low-density lipoprotein cholesterol. Caffeine, studied primarily in the context of coffee, has been shown either to have no relationship or to be associated with a lower risk of coronary artery disease and heart failure. Randomized controlled trial data among regular caffeinated coffee drinkers showed that caffeinated coffee decreases the risk of atrial fibrillation occurrence but increases the frequency of premature ventricular contractions. Data are fairly consistent that moderate caffeine consumption, again studied primarily in the setting of coffee consumption, was associated with a lower risk of stroke. Data on high doses of caffeine such as that found in energy drinks are limited and generally suggest cardiovascular harm.

Randomized trials comparing radial and femoral access report access site crossover rates of 3% to 9% for radial access and 1% to 3% for femoral access. However, contemporary real-world crossover rates are not well characterized. The aim was to evaluate contemporary trends and predictors of vascular access site crossover during percutaneous coronary intervention (PCI).

In patients with atrial fibrillation and chronic coronary syndrome beyond 12 months after percutaneous coronary intervention (PCI), oral anticoagulant monotherapy is recommended by the guideline; however, its efficacy and safety in patients with complex PCI remain uncertain.

There is a growing consensus that screening for subclinical preheart failure (HF) may reduce the burden of symptomatic HF by allowing for timely preventive interventions. However, validated screening algorithms are currently lacking. The aim of this study was to evaluate a fully mobile telemedically supervised cardiac magnetic resonance, as a simple standardized, and ubiquitously applicable screening algorithm for subclinical pre-HF in rural and underresourced regions.