In hypertrophic obstructive cardiomyopathy, left ventricular mass index (LVMi) regresses following septal myectomy, but the specific dynamics, mechanisms (involving cellular and extracellular compartments), and related factors remain unclear.

Randomized trials have clearly demonstrated the benefits of anticoagulant therapy in patients with atrial fibrillation who are at high risk of ischemic stroke. However, less is known about the benefit of anticoagulation in low-risk patients, and exactly how low baseline stroke risk justifies further attempts to reduce it with direct oral anticoagulants (DOACs) remains unclear.

The benefits of switching from warfarin to direct oral anticoagulants in atrial fibrillation remain unclear.

Racial differences in the use and outcomes of intravascular imaging (IVI) and invasive physiology (IP) during percutaneous coronary intervention (PCI) are underreported in the United States.

Congenital heart disease (CHD) is the most common heterogeneous birth defect, with prevalence varying across populations. A comprehensive meta-analysis could refine the genetic risk estimates and enhance our understanding of CHD susceptibility.

The purpose of this study was to assess the feasibility and prognostic value of cardiac output (CO) reserve assessment using exercise echocardiography in Fontan patients. We hypothesized that adults with Fontan palliation had lower CO reserve compared with controls, and impaired CO reserve was associated with greater congestion (NT-proBNP [N-terminal pro-B-type natriuretic peptide]) and cardiovascular events (death/transplant/heart failure hospitalization) in Fontan patients.

Bradyarrhythmia is a common and potentially serious cause of syncope, often difficult to detect due to its intermittent nature. Traditional ECG monitoring methods either provide low diagnostic accuracy or delay diagnosis, increasing the risk of recurrence. We hypothesized that a deep learning-enabled, 24-hour, single-lead ECG could detect past episodes of bradyarrhythmia.

Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome characterized by left ventricular diastolic dysfunction, elevated filling pressures, and normal ejection fraction (left ventricular ejection fraction ≥50%) in the absence of an underlying disease process. Its prevalence is increasing, driven by an aging population and rising comorbidities including obesity, diabetes, and hypertension. Given the benefit of emerging HFpEF therapies, such as glucagon-like peptide-1 inhibitors, early and accurate diagnosis is critical to improve outcomes. The diagnosis of HFpEF, however, can be challenging to make, and clinical practice relies heavily on echocardiographic evidence of diastolic dysfunction. There is a need for additional noninvasive diagnostic strategies to facilitate earlier HFpEF diagnosis to improve clinical outcomes. Emerging evidence suggests that cardiac magnetic resonance (CMR) imaging may have clinical value in enhancing HFpEF diagnosis and prognosis. Moreover, CMR tissue characterization by parametric mapping sequences (T1/T2 mapping and extracellular volume quantification) makes CMR a powerful tool for evaluating HFpEF mimickers, specific diseases that cause the clinical syndrome of heart failure in the setting of normal ejection fraction, which may confound HFpEF diagnosis. Finally, novel imaging sequences, such as magnetic resonance spectroscopy, diffusion tensor imaging, and elastography, are being developed to characterize metabolism and hemodynamics in vivo and may provide insight into HFpEF pathophysiology. The diagnostic and prognostic values of CMR-derived indices of diastolic dysfunction and the use of CMR to distinguish between HFpEF and its mimickers, as well as the use of novel CMR sequences in HFpEF, are reviewed herein.

Hypertrophic cardiomyopathy (HCM) is a naturally occurring cardiac disorder afflicting humans, cats, rhesus macaques, pigs, and rarely dogs. The disease is characterized by maladaptive left ventricular wall thickening. Over 1500 sarcomere-coding mutations explain HCM in humans, whereas only 3 have been reported in cat breeds. To date, no mutations have been described in dogs. HCM in a nuclear family of Golden Retrievers was identified following the sudden cardiac death of 3 related puppies <2 years of age from 2 dam-offspring repeat matings.