BMP9 (bone morphogenetic protein 9) is a member of the TGF-β (transforming growth factor β) family of cytokines with pleiotropic effects on glucose metabolism, fibrosis, and lymphatic development. However, the role of BMP9 in myocardial infarction (MI) remains elusive.

Higher circulating concentrations of NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity cardiac troponin T (hs-cTnT) and I (hs-cTnI) are associated with left ventricular remodeling and with incident heart failure. The associations of these cardiac biomarkers with changes in cardiac structure and function over time are uncharacterized.

Despite a shortage of potential donors for heart transplant in the United States, most potential donor hearts are discarded. We evaluated predictors of donor heart acceptance in the United States and applied machine learning methods to improve prediction.

An interatrial shunt may provide an autoregulatory mechanism to decrease left atrial pressure and improve heart failure (HF) symptoms and prognosis.

The ISCHEMIA trial (International Study of Comparative Health Effectiveness with Medical and Invasive Approaches) demonstrated greater health status benefits with an initial invasive strategy, as compared with a conservative one, for patients with chronic coronary disease and moderate or severe ischemia. Whether these benefits vary globally is important to understand to support global adoption of the results.

Pursuing initial invasive or conservative management of chronic coronary disease (CCD) is a preference-sensitive decision that should include shared decision-making. Communicating the benefits of either approach is challenging, as individual patients rarely achieve the population-averaged outcomes reported in clinical trials. Our objective was to develop a patient decision aid (PDA) with patient-specific estimates of outcomes for initial invasive versus conservative management of CCD, based on the ISCHEMIA trial (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches).

People who experience out-of-hospital cardiac arrest often require care at a regional center for continued treatment after resuscitation, but many do not initially present to the hospital where they will be admitted. For patients who require interfacility transport after cardiac arrest, the decision to transfer between centers is complex and often based on individual clinical characteristics, resources at the presenting hospital, and available transport resources. Once the decision has been made to transfer a patient after cardiac arrest, there is little direct guidance on how best to provide interfacility transport. Accepting centers depend on transferring emergency departments and emergency medical services professionals to make important and nuanced decisions about postresuscitation care that may determine the efficacy of future treatments. The consequences of early care are greater when transport delays occur, which is common in rural areas or due to inclement weather. Challenges of providing interfacility transfer services for patients who have experienced cardiac arrest include varying expertise of clinicians, differing resources available to them, and nonstandardized communication between transferring and receiving centers. Although many aspects of care are insufficiently studied to determine implications for specific out-of-hospital treatment on outcomes, a general approach of maintaining otherwise recommended postresuscitation care during interfacility transfer is reasonable. This includes close attention to airway, vascular access, ventilator management, sedation, cardiopulmonary monitoring, antiarrhythmic treatments, blood pressure control, temperature control, and metabolic management. Patient stability for transfer, equity and inclusion, and communication also must be considered. Many of these aspects can be delivered by protocol-driven care.

Disparities in guideline-based quality measures likely contribute to differences in heart failure (HF) outcomes. We evaluated between- and within-hospital differences in the quality of care across sex, race, ethnicity, and insurance for patients hospitalized for HF.

Excitation-contraction (E-C) coupling processes become disrupted in heart failure (HF), resulting in abnormal Ca2+ homeostasis, maladaptive structural and transcriptional remodeling, and cardiac dysfunction. Junctophilin-2 (JP2) is an essential component of the E-C coupling apparatus but becomes site-specifically cleaved by calpain, leading to disruption of E-C coupling, plasmalemmal transverse tubule degeneration, abnormal Ca2+ homeostasis, and HF. However, it is not clear whether preventing site-specific calpain cleavage of JP2 is sufficient to protect the heart against stress-induced pathological cardiac remodeling in vivo.