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Revista Mexicana de Cardiología

ISSN 0188-2198 (Print)
En 2019, la Revista Mexicana de Cardiología cambió a Cardiovascular and Metabolic Science

Ver Cardiovascular and Metabolic Science


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2002, Number 2

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Rev Mex Cardiol 2002; 13 (2)

Late complications after surgical correction of tetralogy of Fallot. Case report

Parra-Bracamonte F, González-Godínez H, Alvarado-Montes OM, Rangel A, Solorio S, Albarrán H
Full text How to cite this article

Language: Spanish
References: 0
Page: 62-66
PDF size: 98.61 Kb.


Key words:

Tetralogy of Fallot, aortic valve regurgitation, ventricular septal defect, residual subvalvular aortic septal defect, pulmonary arterial hypertension, surgical correction of tetralogy of Fallot.

ABSTRACT

Background: Tetralogy of Fallot is a common cyanotic congenital heart disease in the childhood, whose surgical correction presents a high rate of success at short and long terms. Complications of surgical correction may and should be corrected promptly. Objective: The objective of this article is to present and discuss, based on the documental investigation, the clinical case of an adult woman operated in the childhood of Tetralogy of Fallot. Belatedly, the patient developed severe pulmonary arterial hypertension due to aortic valve regurgitation and residual subvalvular aortic septal defect secondary to postoperatory complications. Case presentation: A 27 year-old woman with Tetralogy of Fallot corrected when she was 5 years old. At the moment, with atrial fibrillation, in stage III New York Heart Association classification, with severe aortic valve regurgitation, residual ventricular septal defect, dysfunctional pulmonary valve bioprosthesis, severe tricuspid regurgitation, and severe pulmonary arterial hypertension (88/8-40 mmHg). Discussion: Total surgical correction of Tetralogy of Fallot has shown excellent results. There is a certain number of cases with residual defects which must be appropriately corrected, to avoid that postoperatory complications: severe pulmonary valve regurgitation, pulmonary arterial hypertension. Although, before the surgical correction, our patient presented cyanosis, polyglobulia and right ventricular overload, the pulmonary valve stenosis “protected” the pulmonary circulation of the hypertension. In the course of the time, the residual defects such as the ventricular septal defect and the aortic valve regurgitation have provoked the transmission of the right ventricular hypertension to the pulmonary circulation in absence of pulmonary valve stenosis. Conclusion: The bad surgical results and residual defects should diagnosed properly to avoid long term complications that give place to doubts in the indication of surgical reintervention because of severe developed pulmonary hypertension, such as in the case of our patient.





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C?MO CITAR (Vancouver)

Rev Mex Cardiol. 2002;13