[A preliminary investigation of relationship between serum apelin level and pulmonary artery pressure in children with congenital heart disease].

OBJECTIVE: To preliminarily investigate the relationship between serum apelin level and pulmonary artery pressure in children with congenital heart disease. METHODS: One hundred and twenty-six children with congenital heart disease undergoing surgical treatment were enrolled as subjects. The serum level of apelin was determined before surgery and at 7 days after surgery. The ratio of pulmonary artery systolic pressure to aortic systolic pressure (Pp/Ps) was calculated before extracorporeal circulation. According to the Pp/Ps value, patients were classified into non-pulmonary arterial hypertension (PAH) group, mild PAH group, moderate PAH group, and severe PAH group. Pulmonary artery mean pressure was estimated by echocardiography at 7 days after surgery. RESULTS: The non-PAH group had the highest serum level of apelin before and after surgery, followed by the mild PAH group, moderate PAH group, and severe PAH group (P<0.05). All groups had significantly increased serum levels of apelin at 7 days after surgery (P<0.05). The serum level of apelin was negatively correlated with pulmonary artery pressure before surgery (r=-0.51, P<0.05) and at 7 days after surgery (r=-0.54, P<0.05). CONCLUSIONS: The decrease in serum apelin level is associated with the development of pulmonary hypertension in children with congenital heart disease. The significance of serum apelin in predicting the development and degree of pulmonary hypertension in children with congenital heart disease deserves further studies.

[Effects of different arterial oxygen partial pressures on serum protein S100ß and neuron specific enolase during cardiopulmonary bypass in infants with cyanotic congenital heart disease].

OBJECTIVE: A prospective study was conducted to probe into the relationship between arterial oxygen partial pressure (PaO2) and brain injury during cardiopulmonary bypass (CPB) in infants with cyanotic congenital heart disease (CHD). METHOD: Enrolled in the study were 45 cyanotic infants, who were less than three years old and underwent corrective cardiac surgery from August 1(st), 2010 to January 31(st), 2011 at Guangdong General Hospital. All the infants had a pulse oxygen saturation (SpO2) lower than 85% and were randomly allocated into three groups by a specific computer program. In controlled group 1 (G1 group), PaO2 levels were controlled at 80 - 120 mm Hg (1 mm Hg = 0.133 kPa) during CPB; in controlled group 2 (G2 group), PaO2 levels at 120 - 200 mm Hg during CPB; while in uncontrolled group (G3 group), PaO2 levels were at 200 - 400 mm Hg during CPB. Blood samples were collected just before starting CPB, at the end of CPB, and at 3 h, 5 h, and 24 h after CPB (T1, T2, T3, T4, T5) for the determination of serum concentrations of protein S100ß, neuron specific enolase (NSE), and adrenomedullin (ADM) by ELISA. RESULT: Protein S100ß rose significantly after starting CPB. In group G3, it reached a peak of (699 ± 139) ng/L by the end of CPB, significantly higher than those in groups G1 and G2 [(528 ± 163) ng/L and (585 ± 155) ng/L], and was positively correlated with PaO2 levels (r = 0.526, P < 0.01). NSE levels of group G1 were continuously rising after starting CPB and reached significantly high levels at 3 h or 5 h after CPB [(12.2 ± 3.4) µg/L and (12.3 ± 3.7) µg/L], while those of group G2 rose significantly during CPB [(10.9 ± 4.8) µg/L] and even higher at 3 h or 5 h after CPB [(12.6 ± 5.1) µg/L and (13.2 ± 5.4) µg/L]. NSE levels of group G3 rose significantly during CPB and maintained at a high level [(12.2 ± 5.7) µg/L] afterwards. There was no significant difference in serum ADM concentrations among different time points in each group and among these three groups. All the infants were discharged from the hospital without any obvious nervous symptom and sign. CONCLUSION: High PaO2 during CPB in infants with CHD might cause an increase of serum protein S100ß and NSE, indicating that brain injury might become worse with a higher PaO2 and might be positively correlated with PaO2 during CPB.

Palliative arterial switch for transposition of the great arteries, ventricular septal defect, and pulmonary vascular obstructive disease: midterm outcomes.

OBJECTIVE: Our objective was to evaluate the early and midterm outcomes of palliative arterial switch operation in which a ventricular septal defect was not closed or repaired with a fenestrated patch in patients with transposition of the great arteries, ventricular septal defect, and severe pulmonary vascular obstructive disease. METHODS: Between March 2000 and September 2009, the palliative arterial switch operation was performed in 21 patients with a mean age of 3.7 years (range, 0.5-15). Mean preoperative values for systolic pulmonary arterial pressure and systemic arterial oxygen saturation were 91 mm Hg and 69%, respectively. Eighty-one percent of the patients were in New York Heart Association functional class III or IV preoperatively. RESULTS: Early mortality was 14.3%. Mean follow-up was 4.0 years (maximum 9.5 years). Regression of pulmonary arterial pressure occurred in 8 patients (44% of the early survivors). Three of the 8 fenestrations were closed interventionally. Mean postoperative systemic arterial oxygen saturation increased significantly to 93% (P < .001). One late death occurred 3 months after surgery. All the long-term survivors (n = 17) were in New York Heart Association functional class I or II (P < .001). CONCLUSIONS: The palliative arterial switch operation significantly improved the quality of life and possibly life expectancy in patients with transposition of the great arteries, ventricular septal defect, and severe pulmonary vascular obstructive disease. Postoperative pulmonary vascular resistance might be reversible in some patients. Closing the ventricular septal defect with a fenestrated patch, which can be easily closed nonsurgically later on, might contribute to a safer postoperative recovery.