Explore the vast range of titles available.

Among patients hospitalized for acute myocardial infarction and at risk for heart failure, empagliflozin did not lead to a significantly lower risk of a first heart-failure hospitalization or death from any cause than placebo.

Patients with acute myocardial infarction (MI) are at risk for developing heart failure (HF) and subsequently are at an increased risk of mortality. Sodium-glucose cotransporter-2 inhibitors have been proven to improve outcomes in patients with HF with reduced ejection fraction, and, in the case of empagliflozin, in HF with preserved ejection fraction even without diabetes, but their efficacy and safety in the post-MI population has not yet been evaluated. The EMPACT-MI trial will evaluate the safety and efficacy of empagliflozin compared with placebo in patients hospitalized for MI with or at high risk of new onset HF, in addition to standard care. EMPACT-MI is a streamlined, multinational, randomized, double-blind, placebo-controlled trial randomizing 5,000 participants at approximately 480 centers in 22 countries. Eligible patients presenting with spontaneous MI must have new signs or symptoms of pulmonary congestion requiring treatment or new left ventricular dysfunction (LVEF<45%), and at least 1 additional risk factor for development of future HF. Eligible and consenting patients are randomized to empagliflozin 10mg or placebo daily in addition to standard of care within 14 days of hospital admission for MI. The primary composite end point is time to first hospitalization for HF or all-cause mortality. EMPACT-MI will inform clinical practice regarding the role of empagliflozin in patients after an MI with high-risk for the development of future HF and mortality.

Background In the EMPACT‐MI trial, empagliflozin did not reduce the primary endpoint of all‐cause mortality or hospitalization for heart failure (HHF) following acute myocardial infarction (AMI) but was associated with a risk reduction for HF events. Objectives This study aimed to evaluate whether the effect of empagliflozin on HF events is consistent in patients with and without type 2 diabetes and/or chronic kidney disease enrolled in the EMPACT‐MI trial. Methods Post hoc analysis assessing the effect of empagliflozin on the primary endpoint and on HF events in AMI patients with and without an established recommendation for a sodium–glucose cotransporter‐2 inhibitor (SGLT2i) (type 2 diabetes or chronic kidney disease). Results Of 6522 participants, 3489 (53%) did not have type 2 diabetes and/or chronic kidney disease. Those without these conditions were younger and with fewer comorbidities. No differences were observed for the primary endpoint. Empagliflozin reduced time to first HHF, total HHF, time to adverse event (AE) of HF (including outpatient HF events) and total AEs of HF similarly in patients with and without type 2 diabetes or chronic kidney disease. Total HHFs were 50 and 63 [adjusted event rate 1.74 and 2.31 events per 100 patient‐years; rate ratio (RR) 0.75; 95% confidence interval (CI) 0.48, 1.18] in patients without and 98 and 144 (adjusted event rate 3.91 and 6.04 events per 100 patient‐years; RR 0.65; 95% CI 0.45, 0.94; P for interaction = 0.61) in those with type 2 diabetes or chronic kidney disease in the empagliflozin and placebo arms, respectively. Any AEs, serious AEs and AEs leading to permanent study drug discontinuation were similar between treatment groups in both subgroups. Conclusions Empagliflozin improved HF outcomes similarly in patients after AMI with or without type 2 diabetes or chronic kidney disease. Impact of empagliflozin in patients with and without T2D or CKD in the EMPACT‐MI trial. Baseline characteristics, HF outcomes and subgroup analysis of efficacy endpoints are shown. # Hazard ratios estimated via Cox proportional hazard model (unless indicated otherwise). ^ Rate ratios via negative binomial regression. ACM = all‐cause mortality, AE = adverse event, BMI = body mass index, eGFR = estimated glomerular filtration rate, HHF = hospitalization for heart failure, SGLT2 = sodium glucose cotransporter‐2.

The realization of effective quantum error correction protocols remains a central challenge in the development of scalable quantum computers. Protocols employing redundancy over multiple physical qubits to encode a single error-protected logical qubit are theoretically effective, but imply a large resource overhead. Alternative, more hardware-efficient, approaches seek to deploy higher-dimensional quantum systems known as qudits. Recently, proposals have emerged for exploiting high-spin magnetic nuclei coupled to condensed matter electron spin qubits to implement fault-tolerant memories. Here, we explore experimentally the simplest of these proposals, a logical qubit encoded on the four states of a I=3/2 nuclear spin hyperfine-coupled to a S=1/2 electron spin qubit; the encoding protects against the dominant decoherence mechanism in such systems, fluctuations of the quantizing magnetic field. We implement the encoding using electron-nuclear double resonance within a subspace of the spin levels in an ensemble of highly coherent manganese defects in zinc oxide. We explore the dynamics of the encoded state both under a controlled application of the fluctuation and under natural decoherence processes. Our results confirm the potential of these proposals for practical, implementable, fault tolerant quantum memories.