Cardiac injury is a common complication of BCT [2,3,4,5]. The common injuries include cardiac contusion, valvular damage, and aortic insufficiency [2, 3]. Myocardial contusion is the most frequent cardiac injury following BCT and occurs in 16–76% of patients in motor vehicle accidents; however, traumatic VSR is a rare complication of BCT [1, 4, 6]. VSR may be delayed for several hours to several days after trauma, and its clinical presentation varies from immediate death to complete spontaneous closure [7]. The most common localization of traumatic VSR is in the muscular portion of the interventricular septum near the cardiac apex [3, 5, 7]. In the present case, the patient had no history of congenital heart disease.

The first postulated mechanism of VSR is acute compression of the heart between the sternum and the vertebral column, with a resultant sudden rise in intracardiac pressure at the end of diastole or isovolumetric systole. The second postulated mechanism is microvascular disruption caused by myocardial injury, leading to infarction and liquefaction of the septum [1, 2, 4]. The contused myocardium can become necrotic and, subsequently, perforate. Therefore, VSR may occur several hours or months after BCT [7]. The former postulation was considered to be the underlying mechanism in this case, because the rupture occurred in the acute phase and there was no myocardial infarction around the defect. The high pressure of compressed and filled left ventricle caused the VSR in this case; however it is the pressure toward the free wall of left ventricle that caused the fatal cardiac rupture. Right ventricle is more vulnerable site rather than left ventricle. However, in this situation, myocardial damage should have occurred in the left side of the heart not to right side because the pressure of right ventricle is quite low. A conservative approach has been recommended for patients with stable hemodynamics and small defects when the ratio of pulmonary-to-systemic flow is less than 2:1 because spontaneous closure may occur [3, 7]. Echocardiography is a useful method for the diagnosis of VSR, however in the presented case, examination of the heart at the admission detected no VSR. If it is a large automobile accident, computed tomography and echocardiography should be examined in detail, keeping in mind the possibility of cardiac injury even if the hemodynamics are stable for the first time. The only way to treat a large defect and a patient with unstable hemodynamics is prompt diagnosis and emergent operation.

We approached the VSR through the right ventricle, not the left ventricle, to prevent left ventricular function. In the case of VSR after myocardial infarction, we used a large patch to close the infarcted myocardium, the so-called infarct exclusion technique [8], which is placed from inside of the ventricular cavity to the free wall with viable myocardium just to the coronary artery to avoid cutting and residual shunting. In this case, a double patch was used to close the defect. Interrupted, pledgetted horizontal mattress sutures were placed on the healthy ventricular septal wall and not on the left ventricular anterior wall [9]. We think the right ventricular approach and the double-patch method is a suitable and standard technique for this situation.

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