Inherited thoracic aortopathies denote a group of congenital conditions that predispose to disease of the thoracic aorta. Aortic wall weakness and abnormal aortic hemodynamic profiles predispose these patients to dilatation of the thoracic aorta, which is generally silent but can precipitate aortic dissection or rupture with devastating and often fatal consequences. Current strategies to assess the future risk of aortic dissection or rupture are based primarily on monitoring aortic diameter. However, diameter alone is a poor predictor of risk, with many patients experiencing dissection or rupture below current intervention thresholds. Developing tools that improve the risk assessment of those with aortopathy is internationally regarded as a research priority. A robust understanding of the molecular pathways that lead to aortic wall weakness is required to identify biomarkers and therapeutic targets that could improve patient management. Here, we summarize the current understanding of the genetically determined mechanisms underlying inherited aortopathies and critically appraise the available blood biomarkers, imaging techniques, and therapeutic targets that have shown promise for improving the management of patients with these important and potentially fatal conditions.

The tissue selectivity of pulsed field ablation (PFA) provides safety advantages over radiofrequency ablation in treating atrial fibrillation. One-shot PFA catheters have been shown capable of performing pulmonary vein isolation, but not flexible lesion sets such as linear lesions. A novel lattice-tip ablation catheter with a compressible 9-mm nitinol tip is able to deliver either focal radiofrequency ablation or PFA lesions, each in 2 to 5 s.

Endovascular repair (EVR) has replaced open surgery as the procedure of choice for patients requiring elective abdominal aortic aneurysm (AAA) repair. Long-term outcomes of the 2 approaches are similar, making the relative cost of caring for these patients over time an important consideration.

Venous thromboembolism (VTE) is a major preventable disease that affects hospitalized inpatients. Risk stratification and prophylactic measures have good evidence supporting their use, but multiple reasons exist that prevent full adoption, compliance, and efficacy that may underlie the persistence of VTE over the past several decades. This policy statement provides a focused review of VTE, risk scoring systems, prophylaxis, and tracking methods. From this summary, 5 major areas of policy guidance are presented that the American Heart Association believes will lead to better implementation, tracking, and prevention of VTE events. They include performing VTE risk assessment and reporting the level of VTE risk in all hospitalized patients, integrating preventable VTE as a benchmark for hospital comparison and pay-for-performance programs, supporting appropriations to improve public awareness of VTE, tracking VTE nationwide with the use of standardized definitions, and developing a centralized data steward for data tracking on VTE risk assessment, prophylaxis, and rates.

Pulsed field ablation (PFA) is a nonthermal energy that may provide safety advantages over radiofrequency ablation (RFA). One-shot PFA catheters have been developed for pulmonary vein isolation, but they do not permit flexible lesion sets. This study investigated a novel lattice-tip catheter designed for focal RFA or PFA ablation.

Mutations in desmoplakin (DSP), the primary force transducer between cardiac desmosomes and intermediate filaments, cause an arrhythmogenic form of cardiomyopathy that has been variably associated with arrhythmogenic right ventricular cardiomyopathy. Clinical correlates of DSP cardiomyopathy have been limited to small case series.

The optimal method to identify the arrhythmogenic substrate of scar-related ventricular tachycardia (VT) is unknown. Sites of activation slowing during sinus rhythm (SR) often colocalize with the VT circuit. However, the utility and limitations of such approach for guiding ablation are unknown.

The objective of this review is to provide an overview of the role of cardiac magnetic resonance (CMR) in aortic stenosis (AS). Although CMR is undeniably the gold standard for assessing left ventricular volume, mass, and function, the assessment of the left ventricular repercussions of AS by CMR is not routinely performed in clinical practice, and its role in evaluating and quantifying AS is not yet well established. CMR is an imaging modality integrating myocardial function and disease, which could be particularly useful in a pathology like AS that should be considered as a global myocardial disease rather than an isolated valve disease. In this review, we discuss the emerging potential of CMR for the diagnosis and prognosis of AS. We detail its utility for studying all aspects of AS, including valve anatomy, flow quantification, left ventricular volumes, mass, remodeling, and function, tissue mapping, and 4-dimensional flow magnetic resonance imaging. We also discuss different clinical situations where CMR could be useful in AS, for example, in low-flow low-gradient AS to confirm the low-flow state and to understand the reason for the left ventricular dysfunction or when there is a suspicion of associated cardiac amyloidosis.

Paclitaxel-containing devices (PTXDs) significantly reduce reintervention in patients with symptomatic femoropopliteal peripheral artery disease. A recent aggregate-data meta-analysis reported increased late mortality in patients with peripheral artery disease treated with PTXDs. We performed an individual patient data meta-analysis to evaluate mortality.

Prescribed dosages of heart failure (HF) therapy in patients with a reduced left ventricular ejection fraction remain lower than guideline recommended. It remains unclear whether systolic blood pressure (BP) influences prescription of HF drugs to HF patients with a reduced left ventricular ejection fraction in a European setting. This study aimed to investigate the role of systolic BP on the prescription rate and actual dose of guideline-recommended HF therapy.