A 59-year-old gentleman with a background history of hypertension, diabetes mellitus, and dyslipidaemia presented to our hospital on 23 October 2018, having been referred to our centre for further management of a late presenting anterior MI. He had chest pain for the preceding week but delayed seeking medical attention due to its mild nature. On presentation he reported central chest discomfort, and on examination, was evidently breathless. His blood pressure was 88/70 mmHg, with a heart rate 110 b.p.m., a respiratory rate of 30 breaths per minute, and oxygen saturations of 89% on room air. Fine crackles were audible up to the middle zone of both lungs, the jugular venous pressure was raised and he exhibited pedal oedema in both lower limbs. Auscultated heart sounds were normal. The electrocardiogram showed extensive Q-waves throughout the anterior to the lateral leads (Figure ). Hence a diagnosis of Late Presentation Extensive Myocardial Infarction complicated by Cardiogenic Shock was made.\nHis care level was escalated rapidly to the coronary care unit and an urgent TTE revealed generalized hypokinesia, a depressed ejection fraction (EF) of 20% and the presence of a large echogenic mass abutting the apical to mid-segment of the anterolateral wall of the LV. The first operator had made a provisional diagnosis of an LV clot. Prior to starting anticoagulation, a repeat TTE was ordered, clearly demonstrating a dissection in the basal anterolateral LV wall, extending into the aforementioned mass. Thus a diagnosis of LV IMH was made. The myocardium seen covering the intramyocardial haematoma was akinetic. He did not have pericardial effusion, and the interventricular septum was intact. There were no valvular abnormalities. Notable biochemical abnormalities at presentation included raised Troponin T at a level of 772 ng/L (normal < 14 ng/L), in keeping with the extensive degree of myocardial damage. His renal and hepatic function were also impaired, indicating organ damage from the cardiogenic shock.\nA joint decision for conservative management was made by the cardiologist and cardiothoracic surgeon, because of the markedly reduced cardiac function and multiorgan impairment. In view of these factors, he was deemed to be of prohibitively high risk of surgery, and he did not consent to it.\nThe treating team embarked on an uphill task of treating his acute heart failure with medical management. Inotropic support together with judicious infusions of Furosemide were the cornerstone of our treatment. He was given single antiplatelet therapy with oral Clopidogrel, and anticoagulated with subcutaneous Enoxaparin. His haemodynamics were closely monitored with real-time measurement of arterial blood pressure, calculated cardiac output, cardiac index, and peripheral vascular resistance by means of the Edwards EV1000 clinical platform.\nEarly initiatives were taken to address the various organs which were impaired due to the acute heart failure. He received continuous veno-venous haemodialysis for worsening renal function, was electively intubated for progressive respiratory failure, and received judiciously selected antibiotics when he exhibited clinical signs of infection and raised inflammatory markers.\nDespite exhaustive medical and supportive management, his condition progressively deteriorated. Death as a consequence of LV failure occurred 13 days after admission.
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.