2%) or bleeding (10 2%) complications, pulmonary reperfusion edem

2%) or bleeding (10.2%) complications, pulmonary reperfusion edema (9.6%), pericardial effusion (8.3%), need for extracorporeal membrane oxygenation (3.1%), and in-hospital mortality due to perioperative complications (4.7%). Documented 1-year mortality was 7%. Preoperative exercise capacity was predictive of 1-year mortality. Postoperative pulmonary vascular resistance predicted in-hospital and 1-year

mortality. In patients evaluated within 1 year after surgery, the median pulmonary vascular resistance had decreased from 698 to 235 dyn.s.cm(-5) (95% confidence limit, 640-874 and 211-255, respectively, n – 70) and the median 6-minute walk MRT67307 distance had increased from 362 to 459 m (95% confidence limit, 340-399 and 440-473, respectively, n – 168). New York Heart Association functional class improved with most patients progressing from class III/IV to class I/II.

Conclusions: Pulmonary endarterectomy is associated with a low in-hospital mortality rate and improvements in hemodynamics and exercise capacity. (J Thorac Cardiovasc Surg 2011;141:702-10)”
“Brain ischemia is often a consequence of cardiac or neurologic surgery. Prophylactic pharmacological LY2109761 purchase neuroprotection would be beneficial for patients undergoing surgery to reduce brain damage due to ischemia. We examined the effects of two antiarrhythmic doses of lidocaine (2

or 4 mg/kg) on rats in a model of transient global cerebral ischemia. The occlusion of both common carotid arteries combined with hypotension for 10 min induced neuronal loss in the CA1 region of the hippocampus (18 +/- 12 vs. 31 +/- 4 neurons/200 mu m linear distance of the cell body layer, X +/- SD; P<0.01). Lidocaine (4 mg/kg) 30 min before, during and 60 min after ischemia increased dorsal hippocampal CA1 neuronal survival 4 weeks after global cerebral ischemia

(30 +/- 9 vs. 18 +/- 12 neurons/200 mu m; P<0.01). There was no significant cell loss after 10 min of ischemia in the CA3 region, the dentate region or the amygdalae; these regions were less sensitive than the CA1 region to ischemic damage. Lidocaine not only increased hippocampal CA1 neuronal survival, but also preserved cognitive function associated with the CA1 region. Using secondly an active place avoidance task, there were fewer entrances into an avoidance zone, defined by relevant distal room-bound cues, in the lidocaine groups. The untreated ischemic group had an average, over the nine sessions, of 21 +/- 12 (X +/- SD) entrances into the avoidance zone per session; the 4 mg/kg lidocaine group had 7 +/- 8 entrances (P<0.05 vs. untreated ischemic) and the non-ischemic control group 7 +/- 5 entrances (P<0.01 vs. untreated ischemic). Thus, a clinical antiarrhythmic dose of lidocaine increased the number of surviving CA1 pyramidal neurons and preserved cognitive function; this indicates that lidocaine is a good candidate for clinical brain protection. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

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