Magnetic Resonance Imaging of a Posttraumatic Myocardial Infarction and Ventricular Septal Defect With a Closure Device in Place
A 16-year-old boy sustained blunt trauma as a passenger in a high-speed motor vehicle accident 2 years earlier. Before the accident, he was healthy with no known cardiac disease or murmur. On admission after the accident, he was noted to have a loud IV/VI holosystolic murmur along the left sternal border. One month after admission, an echocardiogram revealed a 1.5-cm muscular ventricular septal defect with a left-to-right shunt, enlargement of the right atrium and ventricle, elevated pulmonary arterial pressure, and moderate tricuspid regurgitation (Figure 1 and Movie I).
Two years after the incident, the patient underwent percutaneous closure of the ventricular septal defect with a 14-mm Amplatzer septal occluder. The Qp:Qs ratio before device deployment was 2.8:1, and after closure, the Qp:Qs ratio was 1.1:1. Cardiac magnetic resonance imaging was performed to evaluate the extent of the ventricular septal defect and any residual postprocedural left-to-right shunting.
In the region of the muscular ventricular septal defect, cardiac magnetic resonance imaging demonstrates delayed enhancement of the septum, which is consistent with readily identifiable myocardial infarction despite the adjacent metallic closure device. Additional cine images demonstrate a small residual left-to-right shunt across the ventricular septal defect and akinetic-to-dyskinetic motion of the septal segment of the left ventricle (Figures 2 and 3⇓ and Movies II). Right ventricular enlargement and tricuspid regurgitation are also identified (Figure 4 and Movie II).
The current case shows that delayed-contrast cardiac magnetic resonance imaging could demonstrate the chronic infarct (fibrotic scar) despite the adjacent metallic closure device; indeed, the enhanced segment is located between the 2 limbs of the device. This case also illustrates that the extent of the scar is substantially larger than the defect. Cardiac injuries from blunt chest trauma include acute myocardial infarction, valvular disruption, pericardial trauma, myocardial contusion, or rupture. Ventricular septal defects attributable to blunt trauma are rare and may be caused by extremely elevated intrathoracic pressures or by compression of the heart between the sternum and the spine, resulting in septal contusion or rupture. An additional hypothesis implicates tearing of a coronary artery with thrombosis or spasm leading to an acute myocardial infarction and postinfarction rupture.1,2 Traumatic ventricular septal defects tend to occur in the muscular septum. Large and hemodynamically significant or symptomatic traumatic ventricular septal defects can be treated with surgical repair or percutaneously with a closure device.3,4
The online-only Data Supplement, which contains 4 movies, can be found at http://circ.ahajournals.org/cgi/content/full/115/2/e13/DC1.