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 1-month-old boy weighing 3.1 kg was admitted to repair a VSD and atrial septal defect (ASD). The patient was born at 34 weeks, weighing 1.7 kg, and was admitted to the neonatal intensive care unit (ICU). There were no congenital anomalies found except large VSD and ASD in the routine neonatal check. Clinicians decided to perform correction surgery after the patient gained weight. Preoperative medication included diuretics, and there was no abnormal finding in laboratory data, chest radiography, and brain sonography.\nBefore surgery, transthoracic echocardiography revealed a huge (8 mm) perimembranous VSD with trabecular and outlet extensions, and a 2.5-mm secundum ASD. A bidirectional shunt was found through the VSD with interventricular septal flattening and right ventricular enlargement, attesting to severe pulmonary hypertension.\nSurgical correction was performed with cardiopulmonary bypass (CPB) at moderate hypothermia (30’C) after 100U/kg of heparin was administered. Activated clotting time was maintained above 450 s throughout the CPB. The VSD was closed with glutaraldehyde-fixed auto-pericardium and 7-0 Prolene sutures through a transatrial approach. The total CPB time and aorta cross-clamp time were 118 and 68 min, respectively, and the patient was successfully weaned from cardiopulmonary bypass under inotropic support, including dopamine and milrinone. Post-CPB TEE revealed no VSD leakage and good ventricular function with mild interventricular septal flattening.\nHowever, approximately 40 min later, two anechoic masses were found within the interventricular septum (Fig. , Additional file : Video S1). Low-velocity flow color Doppler echocardiography showed no communication between the ventricles and anechoic masses (Fig. , Additional file : Video S2). The larger mass was 1.51 1.48 cm, and interventricular septal hematomas were suspected (Fig. ). The attending surgeon and pediatric cardiologist were immediately notified of these echocardiography findings. The swollen interventricular septum compressed both the right and left ventricles. However, there were no significant mitral stenosis, tricuspid stenosis, and both right and left ventricular outflow tract obstruction. As there was no hemodynamic instability such as arrhythmia or hypotension, and the sternum was already closed, the surgeon decided to observe the patient. The size of hematomas and vital signs did not show any change during 30 min of observation. Therefore, expecting spontaneous resolution of the hematomas, a decision was made not to perform surgical exploration and incisional drainage. The patient was transferred to the ICU, and no specific treatment for hematoma was provided.\nOn postoperative day (POD) 4, follow-up transthoracic echocardiography revealed that thrombi were filling the hematomas (Fig. , Additional file : Video S3). Both ventricular functions were good, with an ejection fraction of 61%, and the interventricular septum thickness was reduced by 5.5 mm. There was no significant hemodynamic instability during the ICU stay. Follow-up echocardiography on POD 14 revealed cystic lesions in the apical ventricular septum, and on POD 40 (Fig. , Additional file : Video S4), there was no lesion in the interventricular septum, indicating complete resolution of the hematomas.