The treatment of calcified coronary lesions requires optimal lesion preparation to achieve a larger minimal stent area (MSA), the strongest predictor of long-term outcomes. The comparative mechanisms of action of calcium-modifying therapies have not been well defined.

Cardiac resynchronization therapy (CRT) is an important therapeutic option in selected pediatric patients and patients with congenital heart disease with reduced systemic ventricular ejection fraction (SVEF). However, the identification of optimal responders is challenging. This study aimed to identify predictors of response to CRT in children and patients with congenital heart disease at 5 large quaternary referral centers.

Hemolysis is a recognized side effect of pulsed field ablation (PFA). Severe hemolysis can lead to acute kidney injury, affecting the morbidity of patients undergoing PFA for atrial fibrillation. Here, we aimed to characterize the degree of hemolysis across different PFA technologies.

Retrograde ethanolization of the vein of Marshall (VOM) has been identified as an adjunct technique in the treatment of persistent atrial fibrillation (AF) and left atrial tachycardia, as stated in the last consensus statement on ablation of AF. However, there is a lack of high-volume data on the technique.

Horses are one of the few animals that spontaneously develop atrial fibrillation (AF), making them a powerful model for studying AF mechanisms and treatment effects. Despite the initial effectiveness of treatment in horses and humans, AF-induced atrial remodeling compromises its long-term success. Observational studies have suggested that metformin may reduce the risk of AF, but its effects on progressive AF-induced atrial remodeling have yet to be evaluated in a high-fidelity large animal model.

Cavotricuspid isthmus (CTI) ablation is frequently performed either as a standalone procedure or in combination with pulmonary vein isolation. With the rapid adoption of pulsed field ablation for atrial fibrillation, it is essential to delineate the utility of this modality in treating CTI-dependent atrial flutter (AFL). This study aims to evaluate the procedural and clinical outcomes of CTI ablation using pulsed field energy.

In a previous study, on pulsed-field ablation (PFA) in the swine ventricle, we found that lesion depth was described (±1 mm accuracy) by a logarithmic function of contact force (CF) and the number of PFA pulses (PF-ablation index). This study was designed to validate prospectively whether the novel PF-ablation index would allow PFA lesions to be created at depths of 3.5, 4.5, 5.5, and 6.5 mm with high prediction accuracy in a swine-beating heart model.

Long QT syndrome (LQTS) is primarily an inherited condition associated with the risk of sudden cardiac death. Due to variable phenotypic expression, a prolonged QT interval on a 12-lead ECG is not always present. LQTS may present in the fetus with persistent bradycardia, including sinus bradycardia or functional 2:1 atrioventricular block. We report our experience of persistent fetal bradycardia prompting parental assessment for congenital LQTS.

Activation recovery interval (ARI), extracted from unipolar electrograms, serves as a practical surrogate for repolarization during experimental studies in vivo. Far-field signal contamination and low spatial resolution obscure regional repolarization gradients and duration alternans detection using unipolar ARI. We hypothesized that the attenuation of far-field contamination with the principal component-referenced unipole will allow for a more accurate assessment of true local repolarization gradients and spatially assess action potential duration alternans.

Metabolic and genetic abnormalities have long been noted in cardiovascular diseases, but the contribution of mitochondrial genetic (mitochondrial DNA [mtDNA]) variation is understudied. Mitochondrial genetics is complex in that each mitochondrion contains multiple mtDNA copies that may carry different variants, which is called heteroplasmy. Heteroplasmic variation is dynamic, increases with advancing age, and may contribute to aging-related cardiovascular diseases. Pathogenic variants in mitochondrial genes of the mtDNA or nuclear genome cause mitochondrial diseases, often with cardiac involvement, particularly in patients with adult-onset disease. Population-level studies have identified mtDNA variants associated with cardiovascular risk factors and disease, but evaluation of mtDNA genetic variation is often limited to only a handful of variants and small sample sizes. Studies in animal models have linked several mtDNA variants to cardiac remodeling and dysfunction and suggest a role for mitochondrial-nuclear genetic interactions in disease penetrance. The objective of this scientific statement is to outline the current state of understanding of the role of mitochondrial genetics in cardiovascular pathobiology and highlight important gaps in knowledge. The intended audience of this scientific statement is meant to be broad, spanning clinical, translational, and basic researchers and health care professionals. Despite remaining limitations and barriers, recent advances in genomic sequencing, mtDNA gene editing modalities, and the directed differentiation of stem cells to cardiovascular cell types are creating new opportunities to advance understanding of mitochondrial genetics in cardiovascular pathophysiology.