Recent studies have highlighted the deleterious role of high phosphate intake in hypertension by means of sympathetic overactivation, yet the underlying mechanisms remain unclear. Dietary phosphate loading triggers physiologic release of FGF23 (fibroblast growth factor-23) from the bone to maintain phosphate homeostasis. Both FGF23 and FGF receptors (FGFRs) are present in the central nervous system, but their role in neural control of blood pressure during phosphate loading is unknown. We investigated central FGF23/FGFR signaling in high-phosphate diet-induced sympathetic dysregulation of blood pressure in rats.

Despite the significant global impact of the COVID-19 pandemic, limited studies have investigated the long-term cardiovascular sequelae of SARS-CoV-2 infection, particularly among Asian populations. This large-scale, population-based binational cohort study with long-term follow-up aimed to investigate the association between SARS-CoV-2 infection and the risk of cardiovascular events.

Severe functional mitral regurgitation (fMR) is a heterogenous disease that exhibits different underlying pathophysiological mechanisms and represents independent entities. The aim of this study was to characterize remodeling patterns defined by the left atrial (LA) to left ventricular (LV) volume ratio in patients with severe fMR and heart failure, and to examine its prognostic implications.

Cardiac amyloidosis is associated with poor outcomes and is caused by the interstitial deposition of misfolded proteins, typically ATTR (transthyretin) or AL (light chains). Although specific therapies during early disease stages exist, the diagnosis is often only established at an advanced stage. Cardiovascular magnetic resonance (CMR) is the gold standard for imaging suspected myocardial disease. However, differentiating cardiac amyloidosis from hypertrophic cardiomyopathy may be challenging, and a reliable method for an image-based classification of amyloidosis subtypes is lacking. This study sought to investigate a CMR machine learning (ML) algorithm to identify and distinguish cardiac amyloidosis.

The somatic JAK2V617F sequence variation, a key driver of myeloproliferative neoplasms, has been associated with increased risk of aortic aneurysms. This study aimed to explore associations between the JAK2V617F variant allele frequency (VAF) and ascending, descending, and abdominal aortic aneurysms.

Previous research suggests that exposures to air pollution and nonoptimal temperatures are associated with a higher risk of acute myocardial infarction (AMI), but few studies examined the exposures jointly. Furthermore, moderate exposures were often overlooked. We evaluated short-term exposure to ambient ozone pollution and ambient temperature jointly and over the entire range of exposures, with the occurrence of AMI among adults aged 18 to 64 years (an understudied population) in the contiguous United States.

The win ratio is a method for analyzing a hierarchical composite outcome. It has been most widely used in randomized clinical trials (RCTs) in cardiovascular disease. We performed a review of cardiovascular RCTs using the win ratio published between January 2022 and July 2024. The aims were to summarize current use and to provide examples to illustrate effective use and communication. We identified 36 eligible RCTs, mainly in heart failure and ischemic heart disease. Intervention was pharmaceutical in 26, a procedure in 7, and treatment strategy in 3 trials. When outcomes were analyzed with both conventional composite end points or hierarchical analysis, the conclusions tended to be similar. The win ratio was often used to combine evidence from event outcomes and quantitative measures together in a hierarchical composite, as was done in 23 RCTs. It was also used to create a clinically more relevant measure in RCTs by recognizing the clinical priorities among event outcomes. Selected example RCTs illustrate how the clarity of win ratio findings can be improved by (1) complementing the win ratio (a relative measure) with the win difference, (2) identifying which components of a hierarchical composite drive the overall results, and (3) clearly prespecifying the outcomes and win ratio analysis to be used. We conclude with a set of recommendations for future use of hierarchical composite outcomes and the win ratio. When used wisely, the win ratio is a valuable tool in the analysis of RCTs.

The efficacy of extensive linear ablation strategies, in addition to pulmonary vein (PV) isolation, remains controversial in persistent atrial fibrillation (AF) ablation. Gaps in previously ablated lesions can induce arrhythmias and potentially decrease the effectiveness of extensive ablation. This study evaluated the incidence of conduction gaps, gap-related reentry, and subsequent recurrence following redo AF ablation in the EARNEST-PVI trial (Efficacy of Pulmonary Vein Isolation Alone in Patients With Persistent Atrial Fibrillation; REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03514693).

The pulsatile nature of blood flow and the hydrostatic effect of pulmonary capillary wedge pressure are 2 fundamental, yet often overlooked features of right ventricular-pulmonary arterial interactions in advanced heart failure and cardiogenic shock. These 2 features (above all others) define both the mechanical forces experienced by the pulmonary arteries, and in turn, the vascular afterload imposed by the pulmonary circulation on the right ventricular. For over half a century, it has been assumed that the pulsatile components of the pulmonary circulation exist in predictable and constant proportion to resistive afterload. In other words, that the vascular afterload can be estimated from mean pulmonary arterial pressure and pulmonary vascular resistance alone. While this tenet holds true for most forms of pulmonary hypertension, pulmonary hypertension resulting from the passive transmission of elevated left atrial pressure is a notable exception. In these cases, arterial compliance decreases proportionally more than any increase in pulmonary vascular resistance and is highly dependent upon recruitment and distensibility of the pulmonary circulation. As questions regarding the optimal method to predict right ventricular failure resurface, along with a modern armamentarium of techniques to assess pulsatile pressure-flow relations, it serves as a timely reminder that, in those with normal or near-normal pulmonary arterial pressures, the pulsatile component of pulmonary vascular afterload may account for anywhere between one-quarter and half of the total power of the right ventricular. In this State-of-the-Art Review, we address the role of pulmonary circulation in those with advanced heart failure and cardiogenic shock. Unlike previous discussions on this topic, we set aside considerations of established precapillary disease, focusing specifically on the process by which an acute or chronic elevation of pulmonary capillary wedge pressure results in pulmonary hypertension from left-sided heart failure. In doing so, we create a framework to assess pulmonary vascular afterload in an era of advanced therapeutics and device technologies to treat advanced heart failure and cardiogenic shock.

Persistent thoracic false lumen flow and subsequent aortic expansion are common complications following thoracic endovascular aortic repair for type B aortic dissection, as well as aortic arch replacement with the elephant trunk technique for type A aortic dissection. Although thoracic false lumen-perfused branches are known to contribute to thoracic false lumen backflow, robust imaging evidence is still lacking. This review illustrates how these branches perpetuate thoracic false lumen flow through detailed imaging analysis, emphasizing the critical need for advancing rapid, accurate, and minimally invasive imaging techniques and novel therapeutic devices to address this persistent clinical challenge.

Although survival for out-of-hospital cardiac arrest (OHCA) is lower at emergency medical service (EMS) agencies serving Black/Hispanic communities, it is unknown whether this is due to practice differences.

The accuracy of contemporary administrative claims codes to discriminate between different phenotypes of peripheral artery disease is not well defined. We aimed to validate a predefined set of International Classification of Diseases, Tenth Revision, codes used to distinguish between claudication and chronic limb-threatening ischemia (CLTI) and to optimize their diagnostic accuracy using a supervised machine-learning approach.

Patients with lung disease, sleep apnea, and chronic thromboemboli can develop pulmonary hypertension, currently classified as group 3 or 4. Many of these patients also have risk factors for heart failure with preserved ejection fraction (HFpEF), but the optimal approach to identify the disease overlap remains unclear.

Access-related vascular and bleeding complications during transcatheter aortic valve implantation (TAVI) are associated with significant morbidity and mortality. Ultrasound-guided (USG) puncture may reduce the incidence of these adverse events, particularly in large-bore arterial access. However, large-scale data on this approach are limited, and it has not yet been fully implemented into standard clinical practice. We compared access-related vascular and bleeding complications in USG versus fluoroscopy-guided access from a large multicenter TAVI registry.

Ventricular arrhythmias (VAs) are a major concern in athletes. We sought to determine the prognostic role of noninvasive and invasive assessments in athletes with complex VAs.

This study aimed to evaluate the prevalence of pathogenic/likely pathogenic cardiomyopathy variant carriers in a multiancestry US population and examine the risk of adverse clinical outcomes.

Obtaining informed consent for clinical trial participation in acute myocardial infarction presents unique ethical and logistical challenges because of the patient distress, sedation, and the urgency of treatment. Traditional consent procedures often conflict with the narrow enrollment windows, prompting the use of legally authorized representatives and short- and long-form consent models. Although these approaches enable faster trial enrollment, they may compromise patient autonomy, introduce selection bias, or create postenrollment ethical dilemmas. This review explores the complexities of informed consent in acute myocardial infarction research, evaluating the advantages and limitations of existing strategies, including legally authorized representative consent, 2-step consent processes, and alternatives such as deferred and verbal consent. It also examines international variations in regulatory oversight and presents emerging solutions, such as preemptive consent, opt-out models, electronic platforms, and registry-based trials, to streamline the enrollment without delaying care. Ultimately, consent regulations should be re-evaluated and potentially relaxed to better support timely research. A thoughtful reassessment of consent frameworks is essential to ethically and effectively advance acute myocardial infarction research in time-sensitive settings.

There is heterogeneity in coronary artery disease (CAD) severity among individuals with severe aortic stenosis (AS), but whether this differentially influences prognosis is unknown.

Sinoatrial node (SAN) dysfunction is commonly associated with atrial dysrhythmia (tachy-brady syndrome) and is a particularly important feature of inherited atrial cardiomyopathies leading to artificial pacemaker implantation. Essential MYL4 (myosin light chain-4) is an atrial-selective protein that associates with the myosin light chain and participates importantly in cardiacmuscle contraction. MYL4 gene variants encoding dysfunctional versions of MYL4 cause familial atrial cardiomyopathy with a high incidence of early SAN dysfunction (SND) and pacemaker requirement. In this study, we used a rat line, genetically modified to express an E11K gene mutation responsible for familial atrial cardiomyopathy, to address the mechanisms underlying SND.

Dilated cardiomyopathy (DCM) is substantially influenced by genetic factors. Sarcomere function is intricately associated with other organelles, particularly the reciprocal regulation between sarcomeres and mitochondria. Mitochondrial stress dysregulation is linked to DCM progression, yet mechanisms remain unclear. In this study, we investigated the effects of cTnT (cardiac troponin T) dysregulation on sarcomere-mitochondrial communication in DCM.