Cardiac troponin provides diagnostic and prognostic information in acute coronary syndromes, but its role in acute decompensated heart failure is unclear. The purpose of our study was to describe the association between elevated cardiac troponin levels and adverse events in hospitalized patients with acute decompensated heart failure. We analyzed hospitalizations for acute decompensated heart failure between October 2001 and January 2004 that were recorded in the Acute Decompensated Heart Failure National Registry (ADHERE). Entry criteria included a troponin level that was obtained at the time of hospitalization in patients with a serum creatinine level of less than 2.0 mg per deciliter (177 μmol per liter). A positive troponin test was defined as a cardiac troponin I level of 1.0 μg per liter or higher or a cardiac troponin T level of 0.1 μg per liter or higher. Troponin was measured at the time of admission in 84,872 of 105,388 patients (80.5%) who were hospitalized for acute decompensated heart failure. Of these patients, 67,924 had a creatinine level of less than 2.0 mg per deciliter. Cardiac troponin I was measured in 61,379 patients, and cardiac troponin T in 7880 patients (both proteins were measured in 1335 patients). Overall, 4240 patients (6.2%) were positive for troponin. Patients who were positive for troponin had lower systolic blood pressure on admission, a lower ejection fraction, and higher in-hospital mortality (8.0% vs. 2.7%, P<0.001) than those who were negative for troponin. The adjusted odds ratio for death in the group of patients with a positive troponin test was 2.55 (95% confidence interval, 2.24 to 2.89; P<0.001 by the Wald test). In patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality, independently of other predictive variables. (ClinicalTrials.gov number, NCT00366639.)

Objective: Morphine is a long-standing therapy in acute decompensated heart failure (ADHF), despite few supporting data. A study was undertaken to compare the outcomes of patients who did and did not receive morphine for ADHF. Methods: The study was a retrospective analysis of the Acute Decompensated Heart Failure National Registry (ADHERE) which enrols hospitalised patients with treatment for, or a primary discharge diagnosis of, ADHF. Patients were stratified into cohorts based on whether or not they received intravenous morphine. ANOVA, Wilcoxon and χ² tests were used in univariate analysis, followed by multivariate analysis controlling for parameters previously associated with mortality. Analyses were repeated for ejection fraction subgroups and in patients not on mechanical ventilation. Results: There were 147 362 hospitalisations in ADHERE at December 2004, 20 782 of whom (14.1%) received morphine and 126 580 (85.9%) did not. There were no clinically relevant differences between the groups in the initial age, heart rate, blood pressure, blood urea nitrogen, creatinine, haemoglobin, ejection fraction or atrial fibrillation. A higher prevalence of rest dyspnoea, congestion on chest radiography, rales and raised troponin occurred in the morphine group. Patients on morphine received more inotropes and vasodilators, were more likely to require mechanical ventilation (15.4% vs 2.8%), had a longer median hospitalisation (5.6 vs 4.2 days), more ICU admissions (38.7% vs 14.4%), and had greater mortality (13.0% vs 2.4%) (all p<0.001). Even after risk adjustment and exclusion of ventilated patients, morphine was an independent predictor of mortality (OR 4.84 (95% CI 4.52 to 5.18), p<0.001). Conclusions: Morphine is associated with increased adverse events in ADHF which includes a greater frequency of mechanical ventilation, prolonged hospitalisation, more ICU admissions and higher mortality.

Background: In nonvalvular atrial fibrillation (NVAF), rivaroxaban is used to prevent stroke and systemic embolism.Objective: To evaluate major bleeding (MB) in NVAF patients treated with rivaroxaban in a real‐world clinical setting.Methods: From January 1, 2013, to March 31, 2014, US Department of Defense electronic health care records were queried to describe MB rates and demographics. Major bleeding was identified using a validated algorithm.Results: Of 27 467 patients receiving rivaroxaban, 496 MB events occurred in 478 patients, an incidence of 2.86 per 100 person‐years (95% confidence interval: 2.61‐3.13). The MB patients were older, mean (SD) age of 78.4 (7.7) vs 75.7 (9.7) years, compared with non‐MB patients. Patients with MB had higher rates of hypertension (95.6% vs 75.8%), coronary artery disease (64.2% vs 36.7%), heart failure (48.5% vs 23.7%), and renal disease (38.7% vs 16.7%). Of MB patients, 63.2% were taking 20 mg, 32.2% 15 mg, and 4.6% 10 mg of rivaroxaban. Four percent of MB patients took warfarin within the prior 30 days. Major bleeding was most commonly gastrointestinal (88.5%) or intracranial (7.5%). Although 46.7% of MB patients received a transfusion, none had sufficient evidence of receiving any type of clotting factor. Fourteen died during their MB hospitalization, yielding a fatal bleeding incidence rate of 0.08 per 100 person‐years (95% confidence interval: 0.05‐0.14). Mean age at death was 82.4 years.Conclusions: In this large observational study, the MB rate was generally consistent with the registration trial results, and fatal bleeds were rare.

Vasoactive therapy is often used to treat acute decompensated heart failure (ADHF). The authors sought to determine whether clinical outcomes are temporally associated with time to vasoactive therapy (vasoactive time) in ADHF. Using the Acute Decompensated Heart Failure (ADHERE) Registry, the authors examined the relationship between vasoactive time and inpatient mortality within 48 hours of hospitalization. Vasoactive agents were used early (defined as <6 hours) in 22,788 (63.8%) patients and late in 12,912 (36.2%). Median vasoactive time was 1.7 and 14.7 hours in the early and late groups, respectively. In‐hospital mortality was significantly lower in the early group (odds ratio, 0.87; 95% confidence interval, 0.79–0.96; P=.006), and the adjusted odds of death increased 6.8% for every 6 hours of treatment delay (95% confidence interval, 4.2–9.6; P<.0001). Early vasoactive initiation is associated with improved outcomes in patients hospitalized for ADHF.

To review the mechanisms of action, expected efficacy and side effects of strategies to control hyperkalemia in acutely ill patients. We searched MEDLINE and EMBASE for relevant papers published in English between Jan 1, 1938, and July 1, 2018, in accordance with the PRISMA Statement using the following terms: “hyperkalemia,” “intensive care,” “acute kidney injury,” “acute kidney failure,” “hyperkalemia treatment,” “renal replacement therapy,” “dialysis,” “sodium bicarbonate,” “emergency,” “acute.” Reports from within the past 10 years were selected preferentially, together with highly relevant older publications. Hyperkalemia is a potentially life-threatening electrolyte abnormality and may cause cardiac electrophysiological disturbances in the acutely ill patient. Frequently used therapies for hyperkalemia may, however, also be associated with morbidity. Therapeutics may include the simultaneous administration of insulin and glucose (associated with frequent dysglycemic complications), β-2 agonists (associated with potential cardiac ischemia and arrhythmias), hypertonic sodium bicarbonate infusion in the acidotic patient (representing a large hypertonic sodium load) and renal replacement therapy (effective but invasive). Potassium-lowering drugs can cause rapid decrease in serum potassium level leading to cardiac hyperexcitability and rhythm disorders. Treatment of hyperkalemia should not only focus on the ability of specific therapies to lower serum potassium level but also on their potential side effects. Tailoring treatment to the patient condition and situation may limit the risks.

More than 7 million patients annually present to US emergency departments (EDs) with symptoms suggestive of acute coronary syndrome (ACS).¹ Many of these individuals (approximately 90%) will not have an acute myocardial infarction (AMI) and will have no major adverse cardiac events (ACEs), defined as MI, urgent revascularization, or cardiac death, within the next 30 days. However, these patients are commonly hospitalized or kept under observation for an evaluation that is often negative.² In fact, rule-in rates in some studies approach zero.^3-6 This high rate of negative evaluation occurs because of the nonspecific presentation of ACS and the potential for ACE with inappropriate discharge. There is general consensus that an acceptable ACS risk-stratification strategy for discharge from the ED should identify a cohort with 30-day ACE rates less than 1%.^7-9 This 1% rate represents the breakpoint between the risk of unnecessary hospitalization resulting in morbidity from a hospital-acquired condition and the potential harm from an inappropriate ED discharge.