In postnatal life progression of heart disease has been clearly documented. Natural history studies have been performed and as a consequence, guidelines for interventions (drugs, interventional or surgical procedures) have been developed. Early detection of fetal heart disease, even in the first trimester, is feasible and these fetuses can be followed in-utero for months. Progression of fetal congenital heart disease has been widely documented in case reports and small case series. Any cardiac valve can become more stenotic, even atretic or more incompetent during the course of pregancy, potentially leading to secondary damage to the heart and lungs. Consecutive impaired growth of ventricles and/or vessels may result in a univentricular circulation postnatally. Valve regurgitations have the potential to lead to hypertrophy, congestive heart failure and hydrops. Theoretically, as in postnatal life, timely fetal intracardiac intervention should lead to normalization or improvement of flows, pressures and hemodynamics, thus preventing secondary damage to the fetal heart and organs, congestive heart failure or fetal death. Cardiac lesions, that might profit from timely interventions could be subgroups of: critical valvar aortic stenosis, critical valvar pulmonary stenosis, pulmonary atresia with intact septum or a closed or severely restrictive foramen ovale in cases of left heart obstructive lesions like e.g. hypoplastic left heart syndrome. Successful in-utero dilatation of aortic and pulmonary valve, perforation of valvar pulmonary atresia and atrio-septostomy with ballon dilation of the created ASD have already been reported. As these procedures carry a high risk of technical problems, morbidity and mortality, careful patient selection is crucial.