The effects of sevoflurane on myocardial ischemia and reperfusion injury have not been well studied, especially in in vivo model. The present study aimed to investigate the effect of timing and duration of sevoflurane exposure on the intensity of myocardial response, and ischemia/reperfusion arrhythmias. All anesthetized open-chest rabbits underwent 30 min of left anterior descending coronary artery(LAD) occlusion followed by 3 hrs of reperfusion. In the control group(C), and sevoflurane group(S), rabbits were subjected to 30 min of LAD occlusion and 3 hrs of reperfusion under ketamine/xylazine(k/x) or sevoflurane anesthesia respectively. The ischemia-preconditioned rabbits underwent 5 min of LAD occlusion followed by 10 min of reperfusion under k/x anesthesia(C-IP), or sevoflurane(S-IP). In the sevoflurane-preconditioned group(C-SP), 30 min of sevoflurane exposure at a 1.5% end-tidal concentration was followed by 15 min of washout before 30 min of LAD occlusion and 3 hrs of reperfusion under k/x anesthesia. At the end of 3-hrs reperfusion period, area at risk was delineated by Evans blue and infarct size determined by triphenyltetrazolium chloride(TTC) staining. The rate pressure product did not alter significantly at any point among all the groups. Compared with group C, myocardial protective effect was observed in groups of S, C-IP, S-IP and C-SP. However, infarct size in sevoflurane-preconditioned group was significantly larger than those of S and S-IP groups. Also, infarct limiting effect of S-IP group was significantly intensified compared with C-IP and S. Continuous exposure of sevoflurane reduced arrhythmias during not only ischemia but reperfusion period in rabbit hearts. These results suggested that continuous sevoflurane exposure might confer additive infarct limiting effect on ischemic preconditioning. We found that ischemic preconditioning and sevoflurane preconditioning do not have anti-arrhythmic effect, though sevoflurane exposure has anti-arrhythmic effects against ischemia and reperfusion-induced arrhythmia.
A 56-year-old female was admitted to a hospital due to fever and back pain. She was diagnosed of asthmatic bronchitis and received antibiotic therapy. But two weeks later she complained of back pain again. Her white blood cells and C-reactive protein(CRP) were elevated and computed tomography(CT) revealed aortic arch aneurysm. Two weeks later, she was referred to our hospital. CT revealed rapid enlargement of the aneurysm. She was diagnosed of mycotic descending aortic aneurysm and underwent resection of the aneurysm and in situ prosthetic graft replacement and omentopexy around the graft. She received antibiotic therapy until the day 52 postoperatively. Their postoperative courses were good and no recurrence of infection was seen.
We report a case of late stent thrombosis in the immediate postoperative period of non-cardiac surgery four weeks after a bare metal stent(BMS) implantation. A 77-year old man who was scheduled for thoracoscopic mediastinal lymph node biopsy received preoperatively implantation of BMS for significant stenosis in the proximal left anterior descending coronary artery. The surgery was postponed four weeks after the stent insertion and the dual anti-platelet therapy with aspirin and ticropidine was discontinued one week before the surgery. The surgery was successfully performed under general anesthesia even with episodes of bradycardia and hypotension. Immediately after the surgery, ST-segment elevation in left precordial leads and acute heart failure appeared following a complete atrioventricular block. An emergency coronary angiogram revealed a thrombotic stenosis of the BMS and a restenting restored the stent patency and its hemodynamics. In this case, one of the most important factors causing the stent thrombosis must be discontinuation of antiplatelets. It is very difficult to decide whether to continue antiplatelets or not, because the risk of bleeding or stent thrombosis depends on the type of surgery, stent, and antiplatelets and the time between the stenting and the surgery. Therefore, the issues as stated above should be discussed cautiously among the anesthesiologist, surgeon, and treatment physician.