Results of several short-term studies suggest that tolvaptan, an oral vasopressin V2 receptor blocker, improves fluid management and hemodynamics in patients with acute decompensated heart failure. In the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST) trial, patients hospitalized with worsening heart failure were randomly assigned to receive either tolvaptan or placebo in addition to standard therapy. The trial results are reported in 2 articles in this issue. In the first article, Konstam and colleaguesArticle report that after a median follow-up of 9.9 months, tolvaptan, which was initiated for in-hospital treatment of acute heart failure and continued for a minimum of 60 days, had no effect on long-term mortality or heart failure–related morbidity compared with placebo. In the second article, Gheorghiade and colleaguesArticle report that compared with placebo, adding tolvaptan to standard therapy, including diuretics, improved many, but not all, of the signs and symptoms of heart failure and reduced body weight at day 7 or at discharge if earlier during hospitalization without evidence of serious adverse effects. In an editorial, YancyArticle discusses implications of these findings for patients with acute decompensated heart failure.
In the randomized, double-blind, placebo-controlled trial Measuring Effects on Intima-Media Thickness: an Evaluation of Rosuvastatin (METEOR), Crouse and colleaguesArticle investigated whether rosuvastatin therapy (40 mg/d for 2 years) could slow progression and/or cause regression of carotid intima-media thickness (CIMT) in patients with low Framingham risk scores (<10%) and mild to moderate subclinical atherosclerosis. The authors report that compared with placebo, treatment with rosuvastatin was associated with a statistically significant reduction in the rate of progression but not regression of CIMT. In an editorial, LauerArticle discusses primary prevention of atherosclerotic disease.
Fibrates, widely used to treat lipid disorders, are weak and relatively nonspecific agonists of the peroxisome proliferator–activated receptor α (PPAR-α). A number of potent and selective PPAR-α agonists have been developed, but little is known about their safety and efficacy. Nissen and colleagues report the safety and efficacy of a PPAR-α agonist, LY518674, assessed in 2 separate randomized clinical trials: one involving patients with atherogenic dyslipidemia and the other, patients with hypercholesterolemia. In both trials, the authors found that LY518674 decreased triglyceride levels and increased high-density lipoprotein cholesterol levels relative to placebo. In the dyslipidemia trial, patients receiving LY518674 experienced an increase in low-density lipoprotein cholesterol (LDL-C) levels. In the hypercholesterolemia trial, LY518674 as monotherapy reduced LDL-C levels, but there was no further reduction in LDL-C levels when LY518674 was added to atorvastatin. Overall, patient outcomes with LY518674 were similar to those with fenofibrate, and both LY518674 and fenofibrate were associated with potential oncogenesis, renal dysfunction, rhabdomyolysis, and cardiovascular toxicity.
“In this tiny bit of shared space and time, I got a small but powerful look into the world of addiction and its physical and emotional manifestations, all magnified in the confines of the elevator.” From “Going Up?”
Results from a scan of the largest collection of DNA samples from families affected by autism provide clues to genes that may convey risk for developing the disorder.
Prevalence, clinical characteristics, and outcomes of prosthetic valve endocarditis.
Join Peter B. Bach, MD, MAPP, April 21, 2007, from 2 to 3 PM eastern time to discuss the effect of computed tomography screening on lung cancer diagnoses. To register, go to http://www.ihi.org/AuthorintheRoom.
Dr DeAngelis summarizes and comments on this week's issue. Go to http://jama.ama-assn.org/misc/audiocommentary.dtl.
For your patients: Information about heart valve infections.
This Week in JAMA . JAMA. 2007;297(12):1289. doi:10.1001/jama.297.12.1289