Faculty Bibliography

This report presents a case of pulmonary atresia/intact ventricular septum with right ventricular-dependent coronary circulation. At 7 months of age, the infant underwent coil embolization of the connection between the right ventricle and the coronary circulation. The child is currently well following surgical decompression of the right ventricle

BACKGROUND: Optimal antimicrobial prophylaxis for the pediatric cardiac surgical patient is unknown. We have reviewed our experience with more than 4,000 pediatric cardiac surgical patients at the University of Michigan to evaluate antibiotic prophylaxis regimens. METHODS: Three antibiotic prophylaxis protocols were serially used during a 6-year period: Protocol 1 (n = 786): cefazolin was administered before operation and continued as long as thoracostomy tubes or central venous catheters were present; Protocol 2 (n = 1095): cefazolin was discontinued 48 hours postoperatively, regardless of the presence of tubes or catheters; Protocol 3 (n = 2039): cefazolin was continued as long as thoracostomy tubes were present, but not for central venous catheters. Patients with an open chest postoperatively received vancomycin and gentamicin until chest closure. This was identical during all three protocols. We retrospectively determined the rate of surgical site infections and unrelated bloodstream infections (the latter for both cardiac medical and surgical patients) for the three protocols. RESULTS: Surgical site infections per 100 operations for protocols 1, 2, and 3 was 2.04, 6.58, and 1.67, respectively (p < 0.05 for protocol 2 versus protocols 1 and 3). The mean age of patients with a surgical site infection ranged from 12 to 15.4 months. Patients with an open chest had a higher rate of surgical site infection (18.8% for protocol 2 and 9.3% for protocol 3). Bloodstream infections per 1,000 patient days for protocols 1, 2, and 3 were 2.18, 6.51, and 5.02, respectively (p < 0.05 protocol 1 versus protocols 2 and 3). CONCLUSIONS: These data suggest that pediatric cardiac surgical patients may benefit from prophylactic antibiotics as long as thoracostomy tubes are in place

BACKGROUND: Apoptosis contributes to ventricular remodeling in heart failure (HF). Nitric oxide (NO) inhibits caspase 3, a key effector apoptotic enzyme. We hypothesized that reduced endogenous NO in HF disinhibits cardiac caspase 3 to promote apoptosis. METHODS: Caspase 3 activity was measured colorimetrically in myocardial cell lysates from endothelial NO synthase (eNOS)-deficient mice (eNOS -/-; n = 18), cardiomyopathic (CMP) hamsters (n = 8), and explanted failing human hearts (n = 10). We stimulated myocardial caspase 3 activity by adding upstream caspase 8 or 9. Cell lysates were incubated with 10(-4) mol/liter NO donor, S-nitroso-N-acetyl penicillamine; NOS inhibitor, nitro-L-arginine-methyl ester (L-NAME); or angiotensin-converting enzyme (ACE) inhibitor, enalaprilat. Hamsters underwent echocardiography so we could study the progression of ventricular dysfunction. RESULTS: Stimulated caspase 3 activity was lower in myocardium of eNOS +/+ compared with eNOS -/- mouse hearts (5.1 +/- 0.5 vs 7.6 +/- 1.0 pmol/10 microg/min, p < 0.05). L-NAME increased enzyme activity only in eNOS +/+ mice, indicating that endogenous NO inhibits caspase 3. Stimulated caspase 3 activity was lower in control hamsters, 3.3 +/- 0.3 pmol/10 microg/min, compared with CMP hamsters, 9.6 +/- 0.7 and 6.9 +/- 0.4 pmol/10 microg/min at 4 and 9 months, respectively. This was associated with progressive ventricular dysfunction, thinning, and dilatation. L-NAME increased enzyme activity in normal but not in CMP hamsters. In failing human myocardium, L-NAME failed to alter caspase activity, indicating reduced NO availability. Enalaprilat inhibited caspase 3, which was reversed by L-NAME. S-nitroso-N-acetyl penicillamine reversed caspase 3 activation in all groups. CONCLUSIONS: Nitric oxide reversibly inhibits myocardial caspase 3 independent of the apoptotic signaling pathway. Reduced NO in HF increases myocardial caspase 3 activity. Agents that promote NO synthesis, including ACE inhibitors, may prevent caspase activation in HF

Aortic atresia is the most severe variant of hypoplastic left heart syndrome (HLHS), and has been associated with significant mortality after stage I palliation. Coronary artery abnormalities are more prominent in this group of patients, especially in the presence of a patent mitral valve. Herein, we describe a case of isolated left ventricular ischemia after the Norwood procedure in a neonate with hypoplastic left heart syndrome, left ventricular hypertrophy, mitral stenosis, aortic atresia, and anomalous left coronary artery

Hemodynamics after Norwood palliation for hypoplastic left heart syndrome (HLHS) have been incompletely characterized, although emphasis has been placed on the role that an excess pulmonary-to-systemic blood flow ratio (Qp/Qs) may play in causing hemodynamic instability. Studies suggest that maximal oxygen delivery occurs at a Qp/Qs < 1. However, it remains unclear to what extent cardiac output can increase with increasing pulmonary perfusion. One approach is to use the oxygen excess factor omega, an index of systemic oxygen delivery, and compare omega with measured Qp/Qs. We measured Qp/Qs and omega in neonates after Norwood palliation for HLHS, and determined how they were related. In addition, we determined the temporal course of surrogate indexes of systemic perfusion in the early postoperative period. Arteriovenous oxygen saturation difference, blood lactate, and omega were recorded on admission and every 3 to 12 hours for 2 days in 18 consecutive infants with HLHS or variant after Norwood palliation. Three infants required extracorporeal membrane oxygenation (ECMO) 6 to 9 hours after admission. These infants had higher Qp/Qs, blood lactate, arteriovenous oxygen saturation difference, and lower omega than non-ECMO patients. In non-ECMO patients between admission and 6 hours, omega decreased significantly despite no appreciable change in Qp/Qs. We conclude that: (1) Oxygen delivery is significantly decreased at 6 postoperative hours unrelated to Qp/Qs. This modest decline in oxygen delivery is insufficient to compromise tissue oxygenation. (2) Patients requiring ECMO have significant derangements in oxygen delivery