Superior vena cava and innominate vein dimensions in growing children : an aid for interventional devices and transvenous leads.

Transvenous (TV) pacing and defibrillation leads are frequently implanted in children as part of treatment for various congenital and acquired rhythm abnormalities. However, the lead-vascular endothelial interaction is not a benign process and is associated with a risk of progressive venous obstruction. Often, this obstruction requires surgical or interventional relief. The risk of obstruction is related to venous diameters at implant and lead size. Since venous diameters are largely unknown at different ages, the purpose of this study was to correlate innominate vein (INN) and superior vena cava (SVC) diameters with body dimensions in growing children.

DNA damage is an early event in doxorubicin-induced cardiac myocyte death.

Anthracyclines are antitumor agents the main clinical limitation of which is cardiac toxicity. The mechanism of this cardiotoxicity is thought to be related to generation of oxidative stress, causing lethal injury to cardiac myocytes. Although protein and lipid oxidation have been documented in anthracycline-treated cardiac myocytes, DNA damage has not been directly demonstrated. This study was undertaken to determine whether anthracyclines induce cardiac myocyte DNA damage and whether this damage is linked to a signaling pathway culminating in cell death. H9c2 cardiac myocytes were treated with the anthracycline doxorubicin at clinically relevant concentrations, and DNA damage was assessed using the alkaline comet assay. Doxorubicin induced DNA damage, as shown by a significant increase in the mean tail moment above control, an effect ameliorated by inclusion of a free radical scavenger. Repair of DNA damage was incomplete after doxorubicin treatment in contrast to the complete repair observed in H2O2-treated myocytes after removal of the agent. Immunoblot analysis revealed that p53 activation occurred subsequent in time to DNA damage. By a fluorescent assay, doxorubicin induced loss of mitochondrial membrane potential after p53 activation. Chemical inhibition of p53 prevented doxorubicin-induced cell death and loss of mitochondrial membrane potential without preventing DNA damage, indicating that DNA damage was proximal in the events leading from doxorubicin treatment to cardiac myocyte death. Specific doxorubicin-induced DNA lesions included oxidized pyrimidines and 8-hydroxyguanine. DNA damage therefore appears to play an important early role in anthracycline-induced lethal cardiac myocyte injury through a pathway involving p53 and the mitochondria.

Is it safe to perform cardiac catheterizations on adults with congenital heart disease in a pediatric catheterization laboratory?

OBJECTIVE: To determine the complication rate during the catheterization in adults with congenital heart disease (CHD) in a pediatric catheterization laboratory (PCL). BACKGROUND: An increasing number of patients with CHD are surviving into adulthood, with diagnostic and interventional cardiac catheterization being essential for the management of their disease. The complication rate during the catheterization of adults with CHD has not been reported. METHODS: A retrospective chart review was performed on all adult patients (>18 years) with CHD who underwent diagnostic or interventional catheterization in our PCL within the past 8.5 years. RESULTS: A total of 576 procedures were performed on 436 adult patients (median age 26 years). Complex heart disease was present in 387/576 (67%) procedures. An isolated atrial septal defect or patent foramen ovale was present in 115/576 (20%) procedures, and 51/576 (9%) procedures were performed on patients with structurally normal hearts with arrhythmias. Interventional catheterization was performed in 378/576 (66%) procedures. There were complications during 61/576 (10.6%) procedures; 19 were considered major and 42 minor. Major complications were death (1), ventricular fibrillation (1), hypotension requiring inotropes (7), atrial flutter (3), retroperitoneal hematoma, pneumothorax, hemothorax, aortic dissection, renal failure, myocardial ischemia and stent malposition (1 each). The most common minor complications were vascular entry site hematomas and hypotension not requiring inotropes. Procedures performed on patients > or = 45 years of age had a 19% occurrence of complications overall compared with 9% occurrence rate in patients of age < 45 years (P < 0.01). CONCLUSIONS: The complication rate during the catheterization of adults with CHD in a PCL is similar to the complication rate of children with CHD undergoing cardiac catheterization. The older subset of patients are more likely to encounter complications overall. The encountered complications could be handled effectively in the PCL. With screening in place, it is safe to perform cardiac catheterization on most adults with CHD in a PCL.

Role of plasma B-type natriuretic peptide in screening for hemodynamically significant patent ductus arteriosus in preterm neonates.

BACKGROUND: B-type natriuretic peptide (BNP) is a hormone secreted by the ventricles under hemodynamic stress and congestive failure. OBJECTIVE: The objective of the present study was to evaluate whether BNP can be used as a valid screening test for the presence of a hemodynamically significant patent ductus arteriosus (hsPDA) in the preterm neonate. MATERIALS AND METHODS: This was a prospective blinded study involving preterm neonates with birth weights