Magnesium Lowers the Incidence of Postoperative Junctional Ectopic Tachycardia in Congenital Heart Surgical Patients: Is There a Relationship to Surgical Procedure Complexity?

Magnesium sulfate was given to pediatric cardiac surgical patients during cardiopulmonary bypass period in an attempt to reduce the occurrence of postoperative junctional ectopic tachycardia (PO JET). We reviewed our data to evaluate the effect of magnesium on the occurrence of JET and assess a possible relationship between PO JET and procedure complexity. A total of 1088 congenital heart surgeries (CHS), performed from 2005 to 2010, were reviewed. A total of 750 cases did not receive magnesium, and 338 cases received magnesium (25 mg/kg). All procedures were classified according to Aristotle score from 1 to 4. Overall, there was a statistically significant decrease in PO JET occurrence between the two groups regardless of the Aristotle score, 15.3 % (115/750) in non-magnesium group versus 7.1 % (24/338) in magnesium group, P < 0.001. In the absence of magnesium, the risk of JET increased with increasing Aristotle score, P = 0.01. Following magnesium administration and controlling for body weight, surgical and aortic cross-clamp times in the analyses, reduction in adjusted risk of JET was significantly greater with increasing Aristotle level of complexity (JET in non-magnesium vs. magnesium group, Aristotle level 1: 9.8 vs. 14.3 %, level 4: 11.5 vs. 3.2 %; odds ratio 0.54, 95 % CI 0.31–0.94, P = 0.028). Our data confirmed that intra-operative usage of magnesium reduced the occurrence of PO JET in a larger number and more diverse group of CHS patients than has previously been reported. Further, our data suggest that magnesium’s effect on PO JET occurrence seemed more effective in CHS with higher levels of Aristotle complexity

Characterizing the angiogenic activity of patients with single ventricle physiology and aortopulmonary collateral vessels.

OBJECTIVE: Single ventricle (SV) congenital heart disease patients often form aortopulmonary collateral (APC) vessels via an unclear mechanism. To gain insights into APC pathogenesis, we correlated angiogenic factor levels with in vitro activity and angiographic APC assessment and examined whether SV patients have increased angiogenic factors that can stimulate endothelial cell sprouting in vitro. METHODS: In single ventricle (n=27) and biventricular acyanotic control patients (n=21), hypoxia inducible angiogenic factor levels were measured in femoral venous and arterial plasma at cardiac catheterization. To assess plasma angiogenic activity, we utilized a 3-D in vitro cell sprouting assay that recapitulates angiogenic sprouting. APC angiograms were graded using a 4-point scale. RESULTS: Compared to controls, SV patients had increased vascular endothelial growth factor (VEGF) (artery: 58.7 ± 1.2 vs. 35.3 ± 1.1 pg/mL, p<0.01; vein: 34.8 ± 1.1 vs. 21 ± 1.2, p<0.03), stromal derived factor (SDF-1a) (artery: 1901.6 ± 1.1 vs. 1542.6 ± 1.1 pg/mL, p<0.03; vein: 2092.8 ± 1.1 vs. 1752.9 ± 1.1, p<0.02), and increased arterial soluble fms-like tyrosine kinase-1 (sFlt-1), a regulatory VEGF receptor (612.3 ± 1.2 vs. 243.1 ± 1.2 pg/mL, p<0.003). Plasma factors and sprout formation correlated poorly with APC severity. CONCLUSIONS: We are the first to correlate plasma angiogenic factor levels with angiography and in vitro angiogenic activity in SV patients with APCs. SV patients have increased SDF-1a and sFlt-1 and their roles in APC formation require further investigation. Plasma factors and angiogenic activity correlate poorly with APC severity in SV patients suggesting complex mechanisms of angiogenesis