Congenital tricuspid insufficiency due to rupture of chordae tendinea secondary to intrauterine obliteration of ductus arteriosus

Abstract

Congenital rupture of tricuspid chordae tendinea leading to severe tricuspid insufficiency is an extremely rare pathology associated with signs and symptoms of congestive heart failure presenting at birth. If the diagnosis and treatment of this pathology are not made early in life fetal demise may become inevitable. We herein present a neonate with central cyanosis and congestive heart failure due to rupture of an anterior leaflet chordae resulting in severe insufficiency of the tricuspid valve who was treated with appropriate surgery.

Diagnosis and intervention of severe tricuspid regurgitation secondary to rupture of the chordae tendineae: A case report and literature review

“…Premature closure or constriction of ductus arteriosus in fetuses can cause overload volume, high pressure of the right ventricle, and pulmonary hypertension ( 11 ). Four articles reported patients with ruptured papillary muscles related to premature constriction of ductus arteriosus, which might be associated with maternal intake of nonsteroidal anti-inflammatory drugs (NSAIDs), structural cardiac lesions such as tetralogy of Fallot, or spontaneous occurrence ( 11 – 14 ). In patients with systemic lupus erythematosus (SLE), the immune reaction within the myocardium extended to the subvalvular apparatus, caused fetal discomfort and hypoxic insult, and finally led to excessive fiber tension, papillary muscle rupture, and critical valve regurgitation ( 1 ).…”

Case Report: unexpected cause of cyanosis in an infant after acute exposure to high altitude—severe tricuspid regurgitation secondary to tricuspid valve prolapse

“…However, it is noteworthy that pressure overload of the RV can also cause rupture of the chordae or papillary muscles. This phenomenon has been described in cases with premature closure of the ductus arteriosus in utero, persistent fetal circulation, PH, and congenital heart defects such as dextro-or levo-transposition of the great arteries, and tetralogy of Fallot (13,22,(32)(33)(34), which account for high pressure in the systolic phase and pronounced mechanical stress on both the valvular and subvalvular apparatus.…”