Cardioprotective effects of adenosine during surgical correction of congenital heart diseases

Objective: To evaluate cardioprotective effects of adenosine on myocardial recovery during repair of CHD using CPB and included 40 pediatric patients ASA II and III

Patients and Methods: Patients were allocated into 2 equal groups [n=20]: Control group [group C] and Adenosine group [group A]. In group A, 3 minutes after starting the CPB, adenosine 150 micro g/kg/minute was infused for 6 minute and was added to the cardioplegia in a concentration of 200 micro mol/L. In group C, 3 minutes after starting CPB, equal volume of saline infused for the same period of time. Ischemic time, duration of CPB, total duration of mechanical ventilation and PICU stay were recorded. Cardiac indices were obtained using trans-esophageal Doppler probe. Hemodynamic parameters were recorded at different times. Blood levels of CK-MB isoenzyme and neutrophil count were measured before and after CPB

Results: Adenosine administrations improved the cardiac indices and significantly induced elevation of SVI, CI and PVI at 15-min and 1-hr after CPB and till 6-hrs after admission to PICU in comparison to group C. The sum of epinephrine doses was significantly higher in group C than in group A from 6-hrs till 36-hrs, and also its duration of infusion was significantly higher in group C than in group A at 24,36, and 48-hrs. The total duration of mechanical ventilation, and ICU stay were higher in group C than in group A nevertheless this difference did not reach a statistical significance. There was a non-significant difference between both groups as regards changes of HR, SBP, DBP and CVP. There was a non-significant difference between both groups as regards the mean ischemia time and CPB duration. Mean of estimated levels of CK-MB were significantly elevated at 24, 48hrs after admission to PICU in both groups compared to their baseline levels and significantly decreased at 48-hrs compared to levels estimated at 24-hrs hours after admission to PICU with a non-significant difference between both groups. Neutrophil count was non-significantly elevated in group C but decreased in group A compared to their baseline levels, with a significantly higher count in group C compared to group A

Conclusion: Use of Adenosine resulted in improvement of postoperative cardiac performance in terms of CI, PVI and SVI in patients undergoing surgical correction of CHD. It also decreased the sum of epinephrine doses, the total duration of epinephrine use and the number of patients needed inotropic support

Abbreviation: SV: Stroke volume; Cardiac index; SVI: Stroke volume index; SVRI: Systemic vascular resistance index; FTc: Time of systolic flow corrected for heart rate determines the preload; PVI: Peak velocity index to determine myocardial contractility [It is the maximum velocity of blood measured during systole normalized for body surface area]; CK-MB: creatinine kinase isoenzyme; HR: Heart rate; SBP: Systolic BP; DBP: Diastolic BP, CVP:Central venous pressure; CPB: Cardiopulmonary bypass; PICU: Pediatric ICU; CHD: Congenital heart disease; BIS: Bispectral index; ACT: Activated clotting time; CO=SV*HR [L/min]; SVI = SV/BSA [ml/m2]; CI=CO/BSA [L/min/m2]; SVR=[MAP-CVP]/CO*79.7 [dyne.sec.cm-5]; SVRI =SVR/BSA [dyne.sec.cm-5.m2]; PVI=PV/BSA [dyne/sec/m2]

Total anomalous pulmonary venous connection: outcome of surgical correction and long term follow up

We report a prospective analysis of the demographic and clinical profiles of patients in order to assess the results of operative repair for total anomalous pulmonary venous connection [TAPVC] and the long term follow up. Methods: In the period between January 1998 and September 2006, 28 patients [16 boys, 12 girls] underwent repair for total anomalous pulmonary venous connection. Their ages ranged from 2 weeks to 1.2 years [mean 4 months]. The patients weight ranged from 3 to 7.5 kg [mean 5 kg]. About 80% of patients [n=22] were less than the 50th percentile of predicted weight for age and sex. The anomalous connection was supracardiac in 23 [82%], cardiac in 3 [11%], infracardiac in 1[3.6%] and mixed in 1[3.6%] patient. Six [21%] patients had obstructed drainage and 9 patients [32%] had moderate or severe pulmonary arterial hypertension. Five patients [18%] had to be operated upon on an emergency basis. For supracardiac and infracardiac connections, a posterior approach was used for anastomosis. In cardiac type, coronary sinus was unroofed and the resultant defect along with atrial septal defect was closed with a single patch. All the patients were operated upon using moderately hypothermic cardiopulmonary bypass. There were 2 [7.1%] in-hospital deaths. Two patient died of pulmonary arterial hypertensive crisis. One of them had preoperative pulmonary venous obstruction. Follow-up ranged from 7 to 97 months [mean 57 months]. There were no late deaths, but 2 patients developed venous obstruction and required balloon dilatation. Mortality continues to be relatively high in infants with total anomalous pulmonary venous connection. Severe pulmonary arterial hypertension appears to be the most important predictor of operative mortality. Severe malnutrition, delayed diagnosis and late referrals possibly contribute to the high mortality

Follow-up of small muscular ventricular septal defects after surgical closure of large ventricular septal defect

Background: closure of ventricular septal defects [VSDs] in infancy due to pulmonary hypertension has greatly replaced pulrnonary artery banding. This approach has been extended to infants with multiple VSDs, closing large VSD and in many cases leaving small muscular VSDs behind. The hemodynamic relevance and rate of closure of these VSDs are unknown. The purpose of this study was to assess the outcome of infants with multiple VSDs after surgical closure of a large VSD leaving another small muscular VSD [s] behind

Patients and Methods: this prospective study was done between January 2004 and December 2005, in the department of Cardio-thoracic Surgery, Abu El-Rish Children Hospital Aff./ Kasr El-Ainy Hospital, Faculty of Medicine, Cairo University. The study sample consisted of 20 infants who were operated for closure of multiple VSDs, closing only the large haemodynamically significant VSD and leaving other small muscular VSD[s]. Tran thoracic echocardiography [TTE], preoperative and postoperative, in the intensive care unit, at hospital discharge, and during follow-up, were performed for all patients. Intra-operative transesophageal echocardiography [TEE] was performed for last 9 patients. Mean follow-up time was 1.5 years [range 0.25- 3.0 years]. Residual defects were graded as absent, < 2 m or between 2 and 4 mm

Results:- due to a pulmonary hypertensive crisis, one patient [5%], died in the 1.C.U comprising our single early postoperative hospital mortality. Morbidity occurred in only one patient [5%] in the form of conduction disturbances which needs implanting a permanent DDD-pacemaker. Follow-up was complete in 17 patients [85%] as only 3 patients [15%] were lots of follow-up. During follow-up no reoperations were necessary for closing a residual VSD. After discharge, all residual defects less than 2 mm closed. Of residual defects greater than 2 mm. only one closed after a man follow-up of 2.4 years. All patients with residual shunts, were hemodynamically stable, requiring no or minimal medication and in none of them endocarditis was noted

Conclusion: our results showed that in infants, postsurgical residual muscular VSDs less than 2mm closed spontaneously in the majority within 1.5 years. Defects greater than 2mm are less likely to close spontaneously. At early follow-up. Residual shunts remained hemodynamically and clinically irrelevant