Pediatric heart failure-related cardiogenic shock carries high morbidity and mortality but is understudied. Improving outcomes in pediatric cardiogenic shock hinges on timely diagnosis and appropriate triage, medical management tailored to the cause and phenotype of cardiogenic shock, and optimal timing of escalation to appropriate mechanical circulatory support. This scientific statement provides a diagnostic framework for the bedside clinician, in addition to proposing a pediatric cardiogenic shock definition and severity staging aligned with systems previously validated in other studies. It outlines the initial approach to diagnosis and stabilization of a child with suspected cardiogenic shock and offers guidance on optimal noninvasive and invasive monitoring strategies to determine clinical trajectory because a significant proportion of children with cardiogenic shock will continue to deteriorate in the first 24 hours. Last, it identifies future directions for the field, including educational interventions for the frontline clinicians seeing these patients, studying the role of a multidisciplinary shock team, evaluating the prognostic and clinical relevance of known and novel biomarkers, and leveraging all these to develop clinical decision tools or algorithms to guide nuanced management of these patients.

Heart failure (HF) involves complex metabolic and lipid-related disturbances. While prior studies have shown that static lipid and metabolic profiles are associated with poor prognosis in chronic stable HF, it remains unclear whether serially measured lipid and metabolic biomarkers are associated with adverse outcomes.

Fee-for-service (FFS) Medicare linkage to clinical registries has been used to assess medical device performance, quality improvement, and postmarket surveillance, but have excluded Medicare Advantage (MA). We assessed the accuracy and implications of linking registry data to combined Medicare FFS and MA claims.

Predictors of target lesion failure (TLF) after percutaneous coronary intervention with drug-coated balloon therapy in patients with in-stent restenosis, as opposed to de novo disease, are limited. This post hoc analysis of the AGENT IDE trial (Agent Paclitaxel-Coated PTCA Balloon Catheter for the Treatment of Subjects With In-Stent Restenosis) aimed to identify predictors of TLF in patients with in-stent restenosis treated with a paclitaxel-coated balloon.

Isthmus conduction velocity (CV) predicts ventricular tachycardia risk in tetralogy of Fallot and traditionally is calculated using electrogram-based methods (electrogram CV index [EGM-CVi]). Isochronal activation mapping approximates CV in adults with ischemic and nonischemic cardiomyopathy but has never been tested in congenital heart disease populations. Our objectives were to (1) investigate the diagnostic performance of isochronal CV index (ISO-CVi) in predicting inducible ventricular tachycardia and (2) compare it to traditional EGM-CVi in a population of patients with repaired tetralogy of Fallot undergoing electrophysiology study before transcatheter pulmonary valve replacement.

Static cold storage of cardiac allografts at 4-8 °C or 10 °C has yielded promising heart transplant outcomes compared with ice storage. However, direct comparisons between these 2 preservation temperatures are lacking. This dual-center study is the first to compare adult heart transplant outcomes using allografts preserved at 10 °C versus 4-8 °C static cold storage.

Among 508 patients randomized to interatrial shunt implantation versus a placebo procedure in the RELIEVE-HF trial (Reducing Lung Congestion Symptoms Using the V-Wave Shunt in Advanced Heart Failure), 2-year clinical outcomes were improved in heart failure with reduced ejection fraction (HFrEF, n=206) and worsened in heart failure with preserved ejection fraction (HFpEF, n=302). However, randomized trials typically include therapeutic responders and nonresponders. We sought to determine the independent predictors of outcomes and model individual patient risk after atrial shunt implantation in HFrEF and HFpEF.

Extracranial bleeding is the most common complication of oral anticoagulant (OAC) therapy for atrial fibrillation (AF), but its clinical importance for patients may be underrecognized. We sought to characterize extracranial bleeding events according to standardized severity definitions, identify baseline risk factors for bleeding, and quantify their population attributable fraction in patients with AF receiving OACs.

Myocardial ischemia-reperfusion (MIR) injury compromises therapeutic effects of revascularization and leads to functional impairment and exacerbation of structural damage in the heart. Limiting the damage caused by MIR is crucial but is still an unmet clinical need because of the complexity of the underlying mechanisms. Increasing evidence suggests that lysosomal autophagy plays a significant regulatory role in MIR injury. The specific mechanisms involved remain to be fully understood.

Chronic transplant arteriosclerosis is the primary cause of long-term graft failure. Selectively targeting specific inflammatory macrophage subpopulations is essential for inhibiting the primary triggers of inflammatory and immune responses. Therefore, elucidating the origins and regulatory mechanisms of these macrophages in allograft arteriosclerosis is key for the development of targeted therapies.

Mitral valve prolapse (MVP) is a common cardiac condition that is generally benign, yet a subset of affected patients develop malignant ventricular arrhythmias and sudden cardiac death. Female sex and myocardial fibrosis detected by late gadolinium enhancement on cardiovascular magnetic resonance imaging have been proposed as risk factors though their independent contributions to arrhythmic risk remain uncertain.

Atherosclerosis is the primary underlying cause of coronary artery disease. LMOD1 is a coronary artery disease risk gene whose role in coronary artery pathophysiology is unknown. Whole-body loss of Lmod1 causes a lethal neonatal visceral myopathy in mice, necessitating unique approaches for the study of vascular smooth muscle cell (VSMC) phenotypes.