This study has been performed so that the Children with complex congenital heart disease involving right-sided obstructive lesions such as tetralogy of Fallot, pulmonary atresia/intact ventricular septum, and hypoplastic left heart syndrome or pulmonary hypertension are at risk for right ventricular (RV) failure and decreased survival.1–3 However, the incidence and timing of RV failure varies,2,4 and current noninvasive and invasive diagnostic modalities can neither predict which patients will progress to RV failure nor detect the preceding subclinical changes occurring on the molecular and cellular level. In addition, standard heart failure therapies such as angiotensin-converting enzyme inhibitors and β blockers are ineffective in the treatment of RV failure.5

We focused on the critical role of oxidative stress on mitochondrial bioenergetics during RV hypertrophy and the progression to RV failure in congenital heart disease involving right-sided obstructive lesions. The human heart is a highly oxidative organ cycling a daily amount of ATP (adenosine triphosphate) up to 15 to 20 times its own weight,6 and is thus particularly vulnerable to oxidative damage. Oxidation of membrane phospholipids, known as lipid peroxidation, is the most prominent manifestation of oxidative stress in the heart in aging and in ischemia/reperfusion injury, and is uniformly detrimental to cardiac function.


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