Timing of Repair in Tetralogy of Fallot: Effects on Outcomes and Myocardial Health.

07:00 EST 2nd January 2020 | BioPortfolio

Summary of "Timing of Repair in Tetralogy of Fallot: Effects on Outcomes and Myocardial Health."

Early complete repair of Tetralogy of Fallot (ToF) prior to 1 year of age has been demonstrated to be safe and has survival benefits over late repair. The age at repair of ToF affects long-term outcomes. This may largely be related to preserved, or comparatively better, myocardial health. Most studies advocate for an age of repair between 3-6 months and certainly below the age of 1 year. Patients with severe right ventricular outflow tract obstruction represent an exception to this rule and may require neonatal repair or surgical and catheter-based palliation before surgery. Older age at repair beyond the first birthday leads to unfavorable right ventricular remodeling with increased right ventricular stiffness and hypertrophy, and is associated with increased long-term ventricular tachycardia and all-cause mortality. In this article, we review the short and long-term benefits of early repair, with a focus on long-term morbidity. In conclusion, we emphasize the importance of myocardial health and the relationship to early repair, and advocate for the use of magnetic resonance imaging in adult patients with repaired ToF in order to detect myocardial fibrosis.


Journal Details

This article was published in the following journal.

Name: Cardiology in review
ISSN: 1538-4683


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Medical and Biotech [MESH] Definitions

A homeobox-containing transcription factor that functions in heart development. Mutations in the NKX2-5 gene are associated with ATRIAL SEPTAL DEFECTS and TETRALOGY OF FALLOT.

A combination of congenital heart defects consisting of four key features including VENTRICULAR SEPTAL DEFECTS; PULMONARY STENOSIS; RIGHT VENTRICULAR HYPERTROPHY; and a dextro-positioned AORTA. In this condition, blood from both ventricles (oxygen-rich and oxygen-poor) is pumped into the body often causing CYANOSIS.

The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.

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