BackgroundOut‐of‐hospital cardiac arrest (OHCA) results in significant morbidity and mortality, primarily from neurologic injury. Predicting neurologic outcome early post‐OHCA remains difficult in patients receiving targeted temperature management.Methods and ResultsRetrospective analysis was performed on consecutive OHCA patients receiving targeted temperature management (32–34°C) for 24 hours at a tertiary‐care center from 2008 to 2012 (development cohort, n=122). The primary outcome was favorable neurologic outcome at hospital discharge, defined as cerebral performance category 1 to 2 (poor 3–5). Patient demographics, pre‐OHCA diagnoses, and initial laboratory studies post‐resuscitation were compared between favorable and poor neurologic outcomes with multivariable logistic regression used to develop a simple scoring system (C‐GRApH). The C‐GRApH score ranges 0 to 5 using equally weighted variables: (C): coronary artery disease, known pre‐OHCA; (G): glucose ≥200 mg/dL; (R): rhythm of arrest not ventricular tachycardia/fibrillation; (A): age >45; (pH): arterial pH ≤7.0. A validation cohort (n=344) included subsequent patients from the initial site (n=72) and an external quaternary‐care health system (n=272) from 2012 to 2014. The c‐statistic for predicting neurologic outcome was 0.82 (0.74–0.90, P<0.001) in the development cohort and 0.81 (0.76–0.87, P<0.001) in the validation cohort. When subdivided by C‐GRApH score, similar rates of favorable neurologic outcome were seen in both cohorts, 70% each for low (0–1, n=60), 22% versus 19% for medium (2–3, n=307), and 0% versus 2% for high (4–5, n=99) C‐GRApH scores in the development and validation cohorts, respectively.Conclusions C‐GRApH stratifies neurologic outcomes following OHCA in patients receiving targeted temperature management (32–34°C) using objective data available at hospital presentation, identifying patient subsets with disproportionally favorable (C‐GRApH ≤1) and poor (C‐GRApH ≥4) prognoses.

Whether assembling proteins onto nanoscale, mesoscopic, or macroscropic material surfaces, maintaining a protein's structure and function when conjugated to a surface is complicated by the high propensity for electrostatic or hydrophobic surface interactions and the possibility of direct metal coordination of protein functional groups. In this study, the assembly of a 1.5 nm CAAKA passivated gold nanoparticle (AuNP) onto FGF1 (human acidic fibroblast growth factor) using an amino terminal His(6) tag is analyzed. The impact of structure and time-dependent changes in the structural elements in FGF1and FGF1-heparin in the presence of the AuNP is probed by a molecular beacon fluorescence assay, circular dichroism, and NMR spectroscopy. Analysis of the results indicates that a time-dependent evolution of the protein structure without loss of FGF1 heparin binding occurs following the formation of the initial FGF1-AuNP complex. The time-dependent changes are believed to reflect protein sampling of the AuNP surface to minimize the free energy of the AuNP-FGF1 complex without impacting FGF1 function.

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Giant cell myocarditis is a rare but often devastating diagnosis. Advances in cardiac imaging and mechanical circulatory support have led to earlier and more frequent diagnoses and successful management. This disease state has wide variation in acuity of presentation, and consequently, optimal treatment ranging from intensity and type of immunosuppression to mechanical circulatory support is not well defined. The following case describes the management of a patient with an unusual presentation of giant cell myocarditis over a 10 year course of advanced heart failure therapies and immunomodulatory support. This case highlights emerging concepts in the management of giant cell myocarditis including sub‐acute presentations, challenges in diagnosis, and treatment modalities in the modern era.

An active 66-year-old diabetic woman presented with a 5-day history of vomiting and abdominal pain, refractory shock and acute kidney injury (AKI). There was concomitant ACE inhibitor (ACEi) use and metformin toxicity with severe lactic acidosis. She suffered a pulseless electrical activity (PEA) cardiac arrest within 30 min of arrival to the Medical Admissions Unit. Despite a serum pH of 6.57 she was successfully resuscitated. She remained haemodynamically unstable even with fluid resuscitation, inotropic support and haemodiafiltration, yet made a full and rapid recovery following the introduction of a methylene blue infusion.