N,N,N-trimethylsphingosine (TMS), a stable synthetic sphingosine derivative, was investigated in a feline model of myocardial ischemia (90 min) and reperfusion (270 min) injury. TMS (60 micrograms/kg), administered intravenously 10 min before reperfusion, significantly attenuated myocardial necrosis (15 +/- 3 vs. 31 +/- 4% necrosis of area at risk, P < 0.01) and cardiac myeloperoxidase activities, a marker of neutrophil accumulation, compared with vehicle-treated cats. Endothelium-dependent relaxation to acetylcholine in ischemic-reperfused coronary artery rings treated with TMS was also significantly preserved compared with vehicle (73 +/- 4 vs. 34 +/- 4% vasorelaxation, P < 0.01). Polymorphonuclear neutrophil (PMN) adherence to coronary endothelium 270 min after reperfusion was markedly attenuated in the TMS group compared with vehicle-treated cats (37 +/- 5 vs. 76 +/- 5 PMN/mm2, P < 0.01). TMS also attenuated upregulation of P-selectin on coronary venular endothelium by immunohistochemistry. This was consistent with in vitro findings that TMS attenuates PMN adherence to thrombin-stimulated coronary endothelium and P-selectin upregulation on thrombin-stimulated cat platelets. A sphingolipid derivative, TMS at physiological concentrations exerts cardioprotective actions and preserves coronary endothelial function following myocardial ischemia and reperfusion in vivo. The effects appear to be mediated by the inhibition of PMN-endothelial interaction and subsequent accumulation into the ischemic myocardium. Thus TMS may be a useful agent in attenuating myocardial reperfusion injury.

In recent years, peripheral nerve injury is a relatively few complication after cardiac surgery. We investigated that peripheral nerve injuries were retrospectively assessed in the results of the patients who underwent open heart surgery during a 36-month period. Peripheral nerve injuries was reported in 11 cases (1.9%) of 581 patients who underwent correction of congenital heart surgery, valve operation and coronary artery bypass grafting with median sternotomy. The main symptoms were continuous pain, and motor and sensory disturbances at the affected upper or lower extremity. The majority of patients recovered without further treatment. This article introduces the basic anatomy and physiology of peripheral nerves and nerve injuries. A clear understanding of these mechanisms is important in order to modify surgical and nursing managements to prevent this neglected complication of cardiac surgery.

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The objective is to summarize initial experience in the management of acute aortic dissections. From January 2010 to July 2014, we had Debakey I aortic dissection 17 (39.5), Debakey II 4 (9.3%) and Debakey III 22(51.2%). Surgery was performed in 10 patients. Thoracic endovascular repair was performed in 15 patients. The other 10 patients received medical therapy. Aortic remodeling was evaluated comparing preoperative and most recent computed tomography scans during their follow up. In surgical treatment of 10 cases, the mean cardiopulmonary bypass time was 203.50 ± 109.64 min, mean myocardial ischemia time was 82.20 ± 49.68 min, and mean time of selective cerebral perfusion at 25°C was 36.24 ± 15.48 min. Main complications were bleeding (10%), low cardiac output syndrome(10%), stroke (10%), prolonged mechanical ventilation (20%) and acute renal failure (20%). In-hospital mortality of 10.0%. There was no need for second-stage operation. Thoracic endovascular repair was successfully performed in 10 cases. False-lumen thrombosis was obtained in 80%. Follow up duration ranged from 20-60 months. There was no death, reoperation or no rupture during the follow up. Timely and accurate diagnosis in early stage and individualized treatment can improve the survival of aortic dissections and reduce the incidence of serious complication. The severity of the underlying disease justifies high mortality rates. The learning curve is a reality.

Hypoglycemia remains an infrequently and potentially dangerous complication in all patients. Patients who are suspected of having hypoglycemia should be questionable until confirmed by appropriate tests. Herein, we report clinical findings of three cyanotic congenital heart disease cases diagnosed artifactual hypoglycaemia, including an updated review of literature of artifactual hypoglycaemia. The cyanotic congenital heart disease led to secondary erythrocytosis, which provided the high levels of erythrocytes that we believe caused the artifactual hypoglycemia in combination with delayed processing of the sample. Currently, there are few specific studies on cyanotic congenital heart disease cases diagnosed artifactual hypoglycaemia. The report of our cases and the literature review underline the unnecessary of a detailed work-up for artifactual hypoglycaemia can be avoided if it is suspected in patients with cyanotic congenital heart disease. Clinicians should consider potential discrepancy in asymptomatic individuals before initiating costly examination. Our paper may represent the tip of the iceberg and raises concerns about the proper management of individuals with artifactual hypoglycaemia in cyanotic congenital heart disease.