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.

Neisseria gonorrhoeae, a gram-negative coccus, is a major cause of morbidity among sexually active individuals. Hematogenous spread of N gonorrhoeae from the initial site of infection is thought to occur in only 0.5% to 3% of infected patients. Disseminated gonococcal infections can rarely lead to serious sequelae, such as endocarditis or meningitis. In this article, we present a case that demonstrates a rare finding of disseminated gonococcal infection leading to N gonorrhoeae meningitis, complicated by hydrocephalus. The patient in this case initially presented with intermittent polyarthralgias for two years and later developed a rash. Cultures from blood and joint aspirate were negative. Urine nucleic acid amplification test for N gonorrhoeae was also negative. He was initially started on steroids for what was believed at first to be an autoimmune polyarthritis. The patient later developed acute encephalopathy. Head imaging revealed hydrocephalus. Cerebrospinal fluid analysis was consistent with bacterial meningitis. Blood, joint, and mucosal membrane studies failed to isolate the causative organism, but his cerebrospinal fluid grew N gonorrhoeae. He was treated with high-dose intravenous ceftriaxone for two weeks with rapid improvement in his mental status and resolution of his joint pains and rash.

Penicillin G and tetracycline should be given only in cases of proven sensibility. Resistance against ciprofloxacin may occur, especially in isolates acquired in south-east Asia. Ceftriaxone, spectinomycin and azithromycin were active against all isolates. The actual resistance situation should be monitored.

Multiple myeloma is a relatively common clonal plasma cell disorder, comprising 17% of hematologic malignancies. One of the hallmark features of this disease is immunoparesis, which is characterized by the suppression of immunoglobulin polyclonality. Though not entirely elucidated, the mechanism behind this process can be attributed to the changes in the tumor microenvironment. All treating clinicians must consider potential complications related to immunoparesis in the management of multiple myeloma. Though not explicitly described in large data series, the increased risk of infection in multiple myeloma is likely, at least in part, due to immunoglobulin suppression. Additionally, the presence of immunoparesis serves as a prognostic factor, conveying poorer survival and a higher risk of relapse. Even in the era of novel agents, these findings are preserved, and immunoglobulin recovery also serves as a sign of improved outcome following autologous HSCT. Though not within the diagnostic criteria for multiple myeloma, the presence and degree of immunoparesis should be at diagnosis for prognostication, and immunoglobulin recovery should be tracked following myeloablative therapy and autologous HSCT.