Spironolactone effect on potassium supplementation in paediatric cardiac intensive care patients.

WHAT IS KNOWN: Spironolactone is used in paediatric patients with heart disease, yet few data are available regarding the impact on potassium supplementation. OBJECTIVE: We sought to determine the effect of spironolactone on potassium supplementation in paediatric cardiac intensive care patients. METHODS: A retrospective, propensity matched cohort study was designed. Patients were included in the study if they received furosemide therapy in the cardiac intensive care unit at our institution. Patients who received spironolactone were matched to patients who did not receive spironolactone. Data collection included patient demographics, diuretic data, potassium monitoring, and total milliequivalents of potassium administered during the cardiac intensive care unit stay. RESULTS AND DISCUSSION: A total of 448 patients met study criteria median age 0.43 (IQR 0.06-3.52) years, 58.9% male. Intensive care unit length of stay was 7 (IQR 3-17) days, cardiovascular surgery occurred in 90.4%. Patients had a mean 4.6±2.6 potassium concentrations assessed per day (29.5%±19.4%<3.5 mmol/L, and 2.9%±6.5%>5.5 mmol/L). Patients received a median of 5.1 mEq/kg (0-323.4 mEq/kg) of potassium. Spironolactone (n=224) was administered for 2 days (IQR 1-4) at mean dose of 0.64±0.54 mg kg-1  d-1 . Median total mEq/kg of potassium administered did not differ between groups (4.6 mEq/kg (IQR 0.66-16.8) vs 6.5 mEq/kg (IQR 1.3-18.3 mEq/kg), P=.13). Potassium laboratory values did not differ in hypokalemia (27.8%±19.1% vs 31.2%±19.5%, P=.06) or hyperkalemia (2.8%±5.4% vs 3.2%±7.5%, P=.49) between groups. WHAT IS NEW: Spironolactone supplementation did not reduce the need for potassium supplementation in paediatric cardiac intensive care patients. CONCLUSION: The routine use of spironolactone in the paediatric cardiac intensive care population may not be more efficacious than potassium supplementation for maintenance of serum potassium concentrations.

A risk assessment scoring system predicts survival following the Norwood procedure.

No one set of characteristics has been consistently predictive of perioperative mortality and morbidity associated with the Norwood procedure. The purpose of the current study is to further validate a scoring system shown to be predictive of mortality following the Norwood procedure. We performed a retrospective review of all infants with the diagnosis of hypoplastic left heart syndrome (HLHS) who underwent the Norwood procedure at St. Louis Children's Hospital from July 1, 1994, to December 31, 2002. A weighted score for each of six factors comprised the scoring system. The factors included ventricular function, tricuspid regurgitation, ascending aortic diameter, atrial septal defect blood flow characteristics, blood type, and age. A score of > or = 7 points indicated lower reconstructive mortality risk, and a total score of < 7 points indicated a higher mortality risk. A total of 57 patients were analyzed. Twenty-five infants (44%) had a low risk score. These infants had a significantly greater survival at 48 hours compared to infants with a score of < 7 (92 vs 75%, p < 0.05). Infants with a high risk score had a significantly greater relative risk of mortality at 48 hours [OR = 2.04; confidence interval (CI) 1.04-4.00; p = 0.036]. The area under the receiver operating characteristic (ROC) curve is 0.8534 (95% CI, 0.78-0.922). This suggests that the scoring system has a very good degree of discriminatory power in selecting children who did not survive. Based on the results of the ROC, a cutoff score of >7 gives the best sensitivity and specificity for survival. When applied retrospectively, the survival outcomes predicted by our scoring system significantly correlated with actual outcomes. This supports the conclusion that a specific population of HLHS patients may have a higher mortality risk independent of surgical technique and postoperative care based on factors that can be assessed preoperatively.

Alterations in the natriuretic hormone system related to cardiopulmonary bypass in infants with congestive heart failure.

This study examined changes in the natriuretic hormone system in five infants with congestive heart failure (CHF) due to intracardiac left-to-right shunting who were exposed to cardiopulmonary bypass (CPB) during surgical repair. Plasma concentrations of three hormones [atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and dendroaspis natriuretic peptide (DNP)] and their secondary messenger, guanosine 3',5'-monophosphate (cGMP), were measured, and the biological activity of the system was quantified. At baseline, BNP and DNP concentrations were normal in our patients, a finding that is strikingly different from that of adult CHF patients, whereas ANP concentrations were elevated. Following CPB, ANP concentrations decreased (median, 175 vs 44 pg/ml; p = 0.043) and BNP concentrations increased (median, 25 vs 66 pg/ ml; p = 0.043), whereas DNP concentrations did not change. Following modified ultrafiltration, BNP concentrations increased (p = 0.043), but other natriuretic peptide concentrations did not change. The calculated biological activity of the natriuretic hormone system decreased following CPB [molar ratio, cGMP / (ANP + BNP + DNP); median, 213 vs 127; p = 0.043)]. Additional studies are needed to expand on these findings and identify patients with other types of congenital heart disease who have perioperative disturbances in the natriuretic hormone system and thus might benefit from pharmacologic intervention.

Circulating cardiac troponin I levels in Kawasaki disease.

In addition to the vascular findings of Kawasaki disease (KD), clinical, electrocardiographic, and/or echocardiographic signs of myocarditis are recognizable in the acute phase of KD in many patients. The mechanism of myocarditis and an association with the development of subsequent coronary artery abnormalities in KD is unknown. Previous studies of serum cardiac troponin I (cTnI) measurements in pediatric populations have suggested a possible utility of measurements in diagnosis and follow-up of KD. We designed a retrospective study to evaluate cTnI measurements during acute KD and to assess the predictive value of cTnI measurements in acute KD for the subsequent development of coronary artery abnormalities. Twenty-nine children were studied. Group 1 consisted of 15 KD patients who developed coronary artery abnormalities as detected by transthoracic echocardiographic evaluation. Group 2 consisted of 14 KD patients with persistently normal coronary artery findings on echocardiograms. A control group consisted of 11 children, none of whom were known to have had clinical findings of KD or myocarditis. The mean cTnI values for all three groups were lower than the values suggestive of cardiac damage: group 1 = 0.11 +/- 0.16 ng/ml, group 2 = 0.15 +/- 0.34 ng/ml, and control = 0.04 +/- 0.08 ng/ml. The current study demonstrates that there is no significant elevation of cTnI in KD patients. Additionally, there is no correlation between cTnI measurements and the finding of myocarditis, as reflected by decreased cardiac function, or the subsequent development of coronary artery abnormalities.

Myofibrillar disruption in hypocontractile myocardium showing perfusion-contraction matches and mismatches.

Chronically instrumented dogs underwent 2- or 5-h regional reductions in coronary flow that were followed, respectively, by balanced reductions in myocardial contraction and O(2) consumption ("hibernation") and persistently reduced contraction despite normal myocardial O(2) consumption ("stunning"). Previously unidentified myofibrillar disruption developed during flow reduction in both experimental models and persisted throughout the duration of reperfusion (2-24 h). Aberrant perinuclear aggregates that resembled thick filaments and stained positively with a monoclonal myosin antibody were present in 34 +/- 3.8% (SE) and 68 +/- 5.9% of "hibernating" and "stunned" subendocardial myocytes in areas subjected to flow reduction and in 16 +/- 2.5% and 44 +/- 7.4% of subendocardial myocytes in remote areas of the same ventricles. Areas of myofibrillar disruption also showed glycogen accretion and unusual heterochromatin clumping adjacent to the inner nuclear envelope. The degrees of flow reduction employed were sufficient to reduce regional myofibrillar creatine kinase activity by 25-35%, but troponin I degradation was not evident. The observed changes may reflect an early, possibly reversible, phase of the myofibrillar loss characteristic of hypocontractile myocardium in patients undergoing revascularization.

Myocardial injury in children with respiratory syncytial virus infection.

OBJECTIVE: Respiratory syncytial virus (RSV) infection is associated with a number of extrapulmonary manifestations, including a sepsis-like syndrome characterized by any combination of hypothermia, fever, apnea, hypovolemia, and myocardial dysfunction. We hypothesized that RSV can have a direct injurious effect on the myocardium of infants and children that can be detected by the presence of cardiac troponin I (cTnI), a highly sensitive and specific marker of myocardial injury, in the blood of patients infected with the virus. DESIGN: Serial cTnI measurements were obtained from patients admitted with documented RSV infection to the pediatric intensive care unit (PICU). PARTICIPANTS: Data were collected and analyzed from 22 RSV infected patients and 11 control patients. RESULTS: Elevated levels of cTnI were detected in 54.5% (12/22) of the study population during their PICU admission. The average cTnI level was significantly higher in the RSV infected group than in controls. There was a significant association between the presence of a positive troponin assay and the occurrence of a cardiovascular event, the need for inotropic support, and the requirement of mechanical ventilation. Patients who required inotropic support had a significantly higher cTnI level than the rest of the study population. CONCLUSION: A large percentage of children admitted to the PICU with RSV infection have myocardial damage as detected by the use of commercially available troponin assays. Additionally, in a portion of these patients, this damage is clinically significant, leading to cardiovascular instability and the need for inotropic support.

Cardiac transplantation for Kawasaki disease.

OBJECTIVE: Severe cardiac sequelae from Kawasaki disease include coronary ischemia and have been treated with a variety of coronary artery bypass procedures. There is only one published report of a child who underwent cardiac transplantation for severe Kawasaki disease-related cardiac complications. The purpose of this study was to gather the worldwide experience with cardiac transplantation for Kawasaki disease. METHODS: Data were obtained from the United Network for Organ Sharing Registry, the European transplant experience, and a phone survey of many Kawasaki disease investigators. Diagnostic and surgical reports as well as clinical records were reviewed. Results. We identified 13 Kawasaki disease patients who underwent cardiac transplantation and obtained data on 10. In these 10 patients, the timing of transplantation was within 6 months after diagnosis of Kawasaki disease (4 patients), 1 to 5 years after diagnosis (3 patients), and 9 to 12 years after diagnosis (3 patients). Indications for transplantation included severe myocardial dysfunction, severe ventricular arrhythmias including cardiac arrest, and severe distal multivessel occlusive coronary artery disease. Nine of the 10 patients remain alive and healthy, with up to 6 years' posttransplant follow-up. One patient died 10 months posttransplant after severe refractory rejection. In addition, 1 patient required retransplantation at 4 years for severe rejection. CONCLUSIONS: Cardiac transplantation for severe ischemic heart disease as a sequela of Kawasaki disease is feasible and can benefit the small subgroup of patients who are not candidates for revascularization because of distal coronary stenosis or aneurysms and/or those with severe irreversible myocardial dysfunction.