We describe 60-year-old man with acute left ventricular free wall rupture due to AMI. He was admitted in emergency department with severe retrosternal chest pain, dyspnea, and sweating. A presumed diagnosis of anterior wall AMI with ST segment elevation was made. Treatment with streptokinase was started. Retrosternal chest pain was relieved, but the ST segment elevations did not resolve. The patient was transferred to a cardiac care unit.\nThe coronary angiography demonstrated a three-vessel disease with proximal significant stenosis of the left anterior descending (LAD) and right coronary (RCA) arteries and totally occluded left circumflex artery (LCX) filling via collaterals ().\nThe patient was discharged after 7 days and candidate for elective coronary artery bypass graft (CABG). Six hours after discharge, he was brought back to emergency department in a state of hemodynamic collapse. His blood pressure was 60/45 mmHg; his heart rate was 130 beats/minute; and an electrocardiogram showed sinus tachycardia. Signs of systemic hypoperfusion and cardiogenic shock were noted, and intra-aortic balloon pump (IABP) support was started immediately. Further electrocardiography revealed sinus tachycardia, low-voltage QRS complexes with diffuse ST segment elevation, and no electrical changes. Echocardiography revealed a moderate pericardial effusion and manifestations of early cardiac tamponade [right atrium (RA) and right ventricle (RV) diastolic collapse] but no signs of myocardial tear, mitral regurgitation, or ventricular septal defect.\nThe patient was transported to the operating room, and midsternotomy was done. Later, 300 ml of blood and clot was drained from the pericardium, and cardiopulmonary bypass (CPB) was established. Rupture of anterolateral wall of LV was repaired via Gore-Tex and Dacron patch, and CABG was done (-).\nThe patient recovered quickly and after 12 days, he was discharged from the hospital.\nAt the 18-month follow-up, the patient was taking statins, diuretics, β-blockers, angiotensin-converting enzyme (ACE) inhibitors, and warfarin. Follow-up echocardiography revealed a left ventricular ejection fraction of 35% to 40%, mild enlargement of the left ventricle, and mild mitral valve regurgitation.
A 7-week-old male infant was noted to be hypoxemic prior to repair of an inguinal hernia. A postoperative echocardiogram demonstrated a large membranous VSD and a long segment coarctation of the aorta. Three months after repair of the coarctation the infant was in congestive heart failure and was brought to the operating room for VSD repair. Preoperative transesophageal echocardiography (TEE) demonstrated a large membranous VSD that extended into the inlet septum and a widely patent left ventricular outflow tract ().\nVSD repair was performed using aortobicaval cannulation with mild hypothermia and antegrade cardioplegeic arrest. The echocardiographic findings were confirmed at surgery, and the VSD was closed in the standard manner using a Dacron patch and 5–0 Prolene pledgeted suture. The initial suture line was carried clockwise avoiding the crest of the ventricular septum. Near the septal leaflet of the tricuspid valve, sutures were placed superficially to avoid the conduction system. The VSD was then closed in a counterclockwise fashion staying away from the crest of the ventricular septum, across the ventricular infundibular fold avoiding the aortic annulus, and eventually transitioning to the septal leaflet of the tricuspid valve. The remainder of the VSD underneath the septal leaflet of the tricuspid valve was closed by weaving in and out of the valve leaflet and the VSD patch. The suture was then tied over an autologous pericardial patch.\nPostoperative TEE (), performed immediately after coming off of cardiopulmonary bypass, demonstrated an echo lucent region beneath the VSD patch that was surrounded by a thin membrane protruding into the LVOT, findings consistent with a DVSH. During systole the anterior mitral leaflet/chordal apparatus came in contact with the DVSH resulting in severe LVOT obstruction with a peak instantaneous Doppler gradient between 70–80 mmHg which was confirmed by direct pressure measurement. The patient was placed back on cardiopulmonary bypass and an oblique aortotomy was made allowing retraction of the aortic valve leaflets to inspect the ventricular septum. The hematoma was identified and the thin membrane overlying the hematoma was incised and evacuated. The remainder of the hematoma was unroofed and LVOT patency was confirmed with a 9 mm dilator. Postevacuation TEE confirmed a widely patent LVOT with no residual gradient (). The LVOT remained widely patent on transthoracic echocardiography performed five days later.