A 77-year-old male patient presented to a secondary care hospital with persistent left-sided chest pain during exercise for one week with mild dyspnoea. His past medical history included coronary artery disease with previous coronary artery bypass surgery in 2009, chronic obstructive pulmonary disease on inhaler steroid therapy, dyslipidaemia, and arterial hypertension. The clinical examination showed no abnormality on respiratory examination, normal heart sounds, and normal abdominal findings. The initial electrocardiogram (ECG) showed sinus rhythm, a heart rate of 79 b.p.m. with a right bundle branch block as well as isolated ventricular extrasystoles (). The initial echocardiography showed a mildly reduced LV systolic function with moderate tricuspid valve insufficiency. Coronary angiography was organized because of typical chest pain and elevated cardiac biomarkers on Day 1, including troponin I at a level of 22 114 pg/mL (normal < 57 pg/mL), CK at a level of 707 U/L (normal < 190 U/L) and CK-MB at a level of 44 ng/mL (normal < 3.6 ng/mL). The patient was diagnosed with a NSTEMI. Coronary intervention with drug-eluting stent implantation (Coroflex® ISAR NEO) into the proximal and mid-right coronary artery (RCA) was performed. An ostial stenosis of the left anterior descending artery (LAD) and a 50% stenosis of the proximal left circumflex artery was left untreated. The venous bypass on the RCA showed a stenosis of the proximal anastomosis, the arterial bypass (left internal mammary artery on LAD) was patent and functional. The patient was loaded on dual anti-platelets with 500 mg aspirin and 600 mg clopidogrel following coronary angioplasty. The post-procedural echocardiogram demonstrated normal findings.\nThe following day transthoracic echocardiography (TTE) showed an unidentified right ventricular (RV) mass occluding the RV cavity. Main differential diagnoses were an intraventricular thrombus or an overlooked myocardial tumour mass like sarcoma or metastasis. Computed tomography confirmed the finding () and demonstrated a widening of the ventricular septum to 40 mm. Intramyocardial haematoma was suspected and confirmed by magnetic resonance imaging ().\nDue to the large, interventricular haematoma, the patient was transferred to our cardiac surgery department because a substantial risk of developing a ventricular septal defect.\nUpon admission to our cardiac surgery intermediate care unit, the patient was clinically stable and asymptomatic. His blood pressure was 90/60 mmHg with a heart rate of 77 beats per minute and oxygen saturation of 91% on room air without added breath sounds on auscultation. In a repeat TTE as performed 2 days later, the intramyocardial haematoma was unchanged (). CK and troponin I levels peaked on Day 1 and then gradually declined with final CK at a level of 93 U/L and final troponin I below 57 pg/mL on Day 7.\nPatient developed atrial fibrillation with a ventricular rate of 110–120 b.p.m. without haemodynamic instability during cardiac monitoring, which lasted for more than 24 h. This was electrically converted to sinus rhythm after a guideline-based exclusion of an intra-atrial thrombus by transoesophageal echocardiography. The decision to perform an electrical cardioversion followed an institutional policy. On Day 11 after the initial diagnosis, a slight decrease of the haematoma and the septal thickness (37 mm) was noted in the four-chamber view of the TTE (). The patient was discharged.\nTransthoracic echocardiography done after 3-month follow-up revealed an almost complete regression of the haematoma (). The patient had remained symptom-free.
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.