ETIOLOGY OF TRICUSPID INCOMPETENCE 

(REGURGITATION)

 

Physiological Tricuspid Regurgitation

3-5% of pregnancies between 18-24 weeks.

Usually resolves during pregnancy

Congenital Heart Disease

·      Tricuspid valve dysplasia:

o     Ebstein's anomaly.

o     Tricuspid valve dysplasia.

·      RV outflow tract obstruction:
* Pulmonary atresia.
* Pulmonary stenosis.

·      Premature ductal constriction.

·      “Facultative” TR:
* AV canal defect.
* Hypoplastic left heart syndrome.

     * Coarctation of the aorta.

         * Double outlet RV.

Volume overload

·      Arrhythmias.

·      Cardiomegaly.

·      Ascites.

·      IUGR.

·      Reversed flow in MCA.

·      Fetal anemia.

·      Peripheral AV malformation (vein of Galen AVM,

         sacrococcygeal teratoma,  hemangioendothelioma    

         of the liver, chorioangioma).

Impaired Myocardial Contractility

·      Myocarditis:

o     Infection.

o     Autoimmune disease (SLE especially).

·      Cardiomyopathy:

o     Arrhythmia.

o     Volume overload.

o     Dilated cardiomyopathy.

·      Endocardial fibroelastosis.