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Acute right ventricular (RV) failure is a frequent and serious clinical challenge in the intensive care unit. It is usually seen as a consequence of left ventricular failure, pulmonary embolism, pulmonary hypertension, sepsis, acute lung injury or after cardiothoracic surgery. The presence of acute RV failure not only carries substantial morbidity and mortality, but also complicates the use of commonly used treatment strategies in critically ill patients. In contrast to the left ventricle, the RV remains relatively understudied, and investigations of the treatment of isolated RV failure are rare and usually limited to nonrandomized observations. We searched PubMed for papers in the English language by using the search words right ventricle, right ventricular failure, pulmonary hypertension, sepsis, shock, acute lung injury, cardiothoracic surgery, mechanical ventilation, vasopressors, inotropes, and pulmonary vasodilators. These were used in various combinations. We read the abstracts of the relevant titles to confirm their relevance, and the full papers were then extracted. References from extracted papers were checked for any additional relevant papers. This review summarizes the general measures, ventilation strategies, vasoactive substances, and surgical as well as mechanical approaches that are currently used or actively investigated in the treatment of the acutely failing RV.

1. Of the inflammatory markers identified, C-reactive protein (CRP) has the analyte and assay characteristics that are the most conducive for use in practice. 2. To obtain a CRP concentration in metabolically stable patients, 2 measurements, fasting or nonfasting, should be made (optimally 2 weeks apart) and the results averaged. If the CRP level is Ͼ10 mg/L, then the test should be repeated and the patient examined for sources of infection or inflammation. 3. CRP results should be expressed only as milligrams per liter and expressed to 1 decimal point. 4. Risk assessment should be modeled after the lipids approach via 3 risk categories: low risk, average risk, and high risk. On the basis of the CRP population distributions, the following tertiles are recommended for categorizing patients: low risk, Ͻ1.0 mg/L; average risk, 1.0 to 3.0 mg/L; and high risk, Ͼ3.0 mg/L. It should be recognized that other acute inflammatory conditions may result in mildly to moderately increased CRP levels, such as inflammatory bowel disease, 2 rheumatoid arthritis, 3 and long-term alcoholism. 4 5. Performance goals for CRP measurement, similar to those developed for total cholesterol, HDL and LDL cholesterol, and triglycerides, need to be developed with a view toward better characterization of the total allowable error required to measure CRP reliably. DiscussionThe Laboratory Science Discussion Group was charged with reviewing the available analytical data on inflammatory markers and recommending those, if any, that were ready to move from the research setting into the routine clinical laboratory. The markers were divided into 3 groups of molecules: cytokines and chemokines, soluble adhesion molecules, and acute-phase reactants. The laboratory group primarily focused on the availability of commercial assays, their limitations and strengths, ability to standardize assay results, assay performance, and how results should be interpreted for assessing the risk of future CVD. As our knowledge of the atherosclerotic process has improved in recent years, evidence suggests that after initiation, inflammation plays a significant role in the development of this disease. A variety of markers associated with inflamThis paper represents a summary of a scientific conference sponsored

BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.