ABSTRACT
Ventricular septal defects (VSDs) represent the most common congenital heart disease and account for approximately 20-30% of all congenital cardiac malformations.1 Perimembranous VSDs (PmVSDs) involve the membranous portion of the ventricular septum and represent approximately 70-80% of all VSDs. On the other hand, Muscular VSDs (mVSDs) are located entirely in the muscular septum and account for approximately 10-15% of all VSDs. These latter defects can be further classified in order of frequency into apical, mid septal, anterior, and posterior defects. In addition, they can be either solitary or multiple (‘Swiss cheese’ VSDs). Patients with VSDs who show evidence of left atrial and ventricular volume overload require closure of these defects in order to prevent the development of pulmonary hypertension, ventricular dilatation, aortic regurgitation, doublechambered right ventricle, and endocarditis.2 Surgical closure of these defects is currently widely acceptable but is still associated with significant morbidity, especially in the case of the muscular type. This includes the potential risk for complete heart block, chylothorax, phrenic nerve injury, wound infection, neurologic sequelae of cardiopulmonary bypass, and a thoracotomy scar.3-7 Patients with mVSDs, in particular, also present a significant challenge to the surgeon. Various surgical approaches have been attempted to close these defects: right ventriculotomy tends to provide suboptimal exposure due to the heavy right ventricle (RV) trabeculations, while left ventriculotomy has been associated with significant ventricular dysfunction.8
In addition, the rate of residual defects remains significant after surgical repair. Hence, with the availability of new effective occluders, device closure of both mVSDs and PmVSDs is a promising alternative to surgery.
