Analysis of the variation in the hsp70-1 and hsp90alpha mRNA expression in human myocardial tissue that has undergone surgical stress.

In the present work we reported a semiquantitative detection of messenger ribonucleic acids (mRNAs) encoding the human heat shock proteins Hsp70-1, the stress inducible member of the HSP70 family, and hsp90alpha, the inducible member of the HSP90 family. We investigated the change in the expression of these mRNAs in tissue samples taken from the right atrium of 48 pediatric patients, soon after the ischemic period during surgery to correct congenital heart diseases, in which a crystalloid cold cardioplegic solution was used. No significant variations were found for either hsp70-1 or hsp90alpha expressions. Moreover, we searched for an association between the hsp70-1 promoter region polymorphism and the expression of the hsp70-1 in a smaller group of these patients (n = 27). The -110AA genotype was on average significantly associated with a decrease in the hsp70-1 mRNA level (P < 0.05), whereas the other genotypes -110AC or -110CC did not seem to be associated with the hsp70-1 expression level. The lack of any observed increase in the hsp70-1 expression level may be due to the high basal level of the Hsp70 protein in the tissues examined.

Repair of complete atrioventricular septal defects in patients weighing less than 5 kg.

BACKGROUND: The aim of this study was to evaluate the impact of weight less than 5 kg at operation on mortality and morbidity in patients with atrioventricular septal defect (AVSDc) undergoing total correction. METHODS: Between January 1990 and December 2002, 190 consecutive patients with AVSDc underwent total biventricular correction. They were divided into two groups: group I (n = 64 patients weighing < 5 kg) and group II (n = 126 patients weighing > 5 kg). Associated major cardiac malformations were found in 49 (25.8%) patients. Associated left atrioventricular valve (LAVV) malformations were found in 35 (18.4%) patients. The mean follow-up time was 4.1 +/- 2.9 years (range 2 months-10.7 years). RESULTS: The in-hospital mortality in group I was 7.8% (5 patients) versus 8.7% (11 patients) in group II (p = 0.95). Major associated cardiac malformations (p < 0.001) and pulmonary hypertension (p = 0.006) were found to be strong predictors for poor postoperative survival. At discharge the mean LAVVR grade in group I was 1.45 +/- 1.2 versus 1.2 +/- 1 in group II (p = 0.13). The actuarial overall survival rates at 1, 3, 5, and 7 years were 96.5%, 92.5%, 91.5%, and 89% respectively and the actuarial overall reoperation free survival rates at 1, 3, 5, and 7 years were 95%, 87%, 84%, and 73%. Twenty-three patients underwent reoperation due to severe left atrioventricular valve regurgitation (LAVVR). Strong predictors for overall reoperation free survival were the operation year before 1995 (p < 0.001), postoperative LAVVR greater than or equal to 2 (p = 0.006), major associated cardiac malformations (p = 0.00034), associated LAVV malformations (p = 0.0044), and non or partial LAVV cleft closure (p = 0.012). The actuarial survival rates between patients weighing less than 5 kg versus patients weighing more than 5 kg were similar (p = 0.51); instead the overall reoperation free survival was significantly lower in patients weighing less than 5 kg (p = 0.022) according to the log-rank test. Weight less than 5 kg (p = 0.023, beta = -0.6) was one of the predictors for reoperation due to severe LAVVR in this series. CONCLUSIONS: We may conclude that in the current era repair of AVSDc can be carried out successfully in patients less than 5 kg, however, weight less than 5 kg at initial complete repair seems to be a predictor for late reoperation due to LAVVR. Suture separation at the cleft site or between the leaflets of the newly created mitral valve and the patch remain the main causes of postoperative LAVVR in patients weighing less than 5 kg.

Total correction of complete atrioventricular septal defect with tetralogy of Fallot.

BACKGROUND AND AIM OF THE STUDY: The authors' experience in surgical management of tetralogy of Fallot in association with complete atrioventricular septal defect (CAVSD-TOF) is reported. METHODS: Between January 1990 and September 2001, 146 children with CAVSD underwent complete correction. ASD closure was performed using a one-patch technique, with autologous pericardial patch. Seventeen patients presented with CAVSD-TOF, of whom nine (53%) had undergone previous palliation. Mean age at repair was 2.9 +/- 1.9 years. The mean gradient across the right ventricular outflow tract (RVOT) was 63 +/- 16 mmHg. Six patients (35%) required a transannular patch. RESULTS: Overall in-hospital mortality was 10%. Among patients with CAVSD-TOF, three died in hospital (18%); causes of death were progressive heart failure (n = 2) and multiple organ failure (n = 1). Two patients required mediastinal exploration due to significant bleeding, and two late reoperation for severe left atrioventricular valve regurgitation after intracardiac repair. Mean follow up was 36 +/- 34 months. All patients survived and are currently in NYHA class I or II. At follow up, mean gradient across the RVOT was 17 +/- 6 mmHg, significantly less than the preoperative value (p < 0.001). CONCLUSION: Complete repair in patients with CAVSD-TOF offers acceptable early and mid-term outcome in terms of mortality, morbidity and reoperation rate. Palliation prior to repair may be preferred in cases with small pulmonary arteries, or in severely cyanotic neonates. The RVOT should be managed as for isolated TOF, but a transatrial-transpulmonary approach is the surgery of choice.

Heat shock protein 70-1 gene expression in pediatric heart surgery using blood cardioplegia.

BACKGROUND: In response to many stress stimuli, cardiomyocytes produce a common set of heat shock proteins (HSP). Up-regulation of HSP70-1 (the inducible isoform) is known to reduce the risk of myocardial cell damage during open-heart surgery and seems to be protective against ischemia. We assessed hsp70-1 gene expression during blood cardioplegic arrest in children undergoing surgical correction of congenital heart defects. METHODS: In tissue samples taken from the right atrium of 59 pediatric patients, we examined hsp70-1 gene expression using a real-time quantitative reverse transcription PCR, with 18S rRNA as internal standard. RESULTS: On average, hsp70-1 gene expression was higher than the baseline level by a factor of 1.44+/- 0.17 (mean+/-SEM). A significant relationship between hsp70-1 mRNA levels and aortic cross-clamp time was observed (R(2)=0.069, p=0.044). Conversely, no significant correlation was observed between hsp70-1 mRNA levels and temperature. CONCLUSIONS: These data suggest that blood cardioplegia can induce an increment in the expression of hsp70-1, confirming its protective role in ischemia/reperfusion injury.

Anomalous origin of the left pulmonary artery from the aorta. Our experience and literature review.

Three patients with anomalous origin of the left pulmonary artery (AOLPA) from the aorta underwent surgical correction. Two patients presented with an isolated malformation and one with an associated ventricular septal defect. One of the patients with an isolated malformation presented with an AOLPA from the descending thoracic aorta. Implantation of the AOLPA to the main PA trunk was performed by direct anastomosis in two patients and by interposition of a synthetic graft in the other patient with AOLPA from the descending aorta. All patients survived the operation. Low cardiac output was identified in one patient. The mean residual gradient through the anastomotic site was 21 mmHg at follow-up. We found almost 72 cases with AOLPA reported in the literature with a high mortality rate in patients not undergoing surgery. The most frequently found associated malformation is tetralogy of Fallot and ventricular septal defect. AOLPA from the aorta is a rare but important entity, necessitating a scrupulous preoperative and intraoperative evaluation. Patients with AOLPA can undergo surgical repair with excellent results.