Results: Subclavian artery stenosis, with or without poststenotic dilatation (PSD), was found in 26 patients (63%), subclavian artery aneurysms in 12 (29%), chronic subclavian occlusion in 1(2.4%), and axillary artery compression in 2 (5%). Chronic symptoms difficult to discern from neurogenic compression were present in 27 patients (66%; 24 had subclavian stenoses or PSD, or both, 1 had subclavian occlusion, and 2 had axillary artery compression);

13 (32%) presented with acute ischemia (11 had aneurysms and 2 had PSDs), and 1 asymptomatic patient had a subclavian aneurysm. Osteoarticular anomalies were found in 27 patients (66%), including 19 cervical ribs, 4 first rib anomalies, and 4 clavicular or first rib fractures, or both. Among 27 patients with subclavian aneurysms or PSD, 21 (78%) had a bone anomaly. Arterial pathology was deemed significant buy BMS202 in 30 patients (73%) and mild or moderate in 11 (21%). Symptoms in 23 of these patients were compatible with neurogenic compression without clinical suspicion of arterial pathology, but 13 (56%) harbored a significant arterial anomaly.

Conclusions: The incidence of arterial pathology secondary to compression at the TO may be underestimated, and in the absence of obvious ischemia, significant arterial pathology may not be suspected. Two-thirds

of patients with arterial compression have associated bone anomalies. Therefore, routine arterial imaging seems advisable for patients evaluated for TO syndrome in the presence of a bone anomaly at the TO or an examination that shows an arterial abnormality. LY2090314 in vivo In the absence of these signs, however, arterial pathology may be overlooked in patients with symptoms suggestive of neurogenic compression. Further study is needed to elucidate the incidence, natural history, and clinical relevance of arterial compression and PSD at the TO. (J Vasc Surg 2010;52:406-11.)”
“Background: Mineralocorticoid antagonists improve survival among patients with PDK4 chronic, severe systolic

heart failure and heart failure after myocardial infarction. We evaluated the effects of eplerenone in patients with chronic systolic heart failure and mild symptoms.

Methods: In this randomized, double-blind trial, we randomly assigned 2737 patients with New York Heart Association class II heart failure and an ejection fraction of no more than 35% to receive eplerenone (up to 50 mg daily) or placebo, in addition to recommended therapy. The primary outcome was a composite of death from cardiovascular causes or hospitalization for heart failure.

Results: The trial was stopped prematurely, according to prespecified rules, after a median follow-up period of 21 months. The primary outcome occurred in 18.3% of patients in the eplerenone group as compared with 25.9% in the placebo group (hazard ratio, 0.