A 79-year-old, hypertensive, diabetic, male patient with a thoracic aortic aneurysm and aortic valve stenosis was scheduled for total aortic arch replacement and simultaneous aortic valve replacement. Following sternal entry, CPB was established by right axillary and femoral arterial cannulation with bicaval cannulation. After aortic cross-clamping, myocardial protection was achieved with antegrade, retrograde, and selective cold blood cardioplegia without any technical problem. The aortic valve was replaced with a 21-mm bioprosthesis (Inspiris Resilia, Edwards Life Sciences, Irvine, CA). Subsequent total aortic arch replacement was performed under antegrade selective cerebral perfusion with moderate hypothermic circulatory arrest. After aortic declamping, a small point of oozing hemorrhage was identified on the epicardial surface of the right ventricular outflow tract. The oozing was controlled by hemostatic agent application, followed by the reconstruction of the arch vessels. The surgical maneuver was completed without any technical difficulty; however, we noticed the progressively expanding hematoma at the right ventricular surface to the size of a Japanese rice ball measuring 50 × 50 mm (Fig. ). The hematoma was hard, and the epicardial surface was dark red and notably swollen with multiple oozing ruptures. There was no evidence of ST-T changes on electrocardiogram. No cardiac wall motion abnormalities were observed on transesophageal echocardiography. Because of the rapid growth of the hematoma, we decided that early discontinuation of CPB and protamine administration should be mandatory. After termination of CPB, followed by the administration of protamine and fresh frozen plasma/platelet transfusion, manual compression with hemostatic agents such as Surgicel (Ethicon, Somerville, NJ, USA) and Tachosil (CSL Behring, Tokyo, Japan) were applied for 15 min. Thereafter, hemostasis was achieved on the epicardial surface, and the hematoma did not expand further without hemodynamic deterioration. The patient showed uneventful postoperative course. Postoperative computed tomography showed hematoma absorption, and transthoracic echocardiography revealed normal ventricular function of both the right and left ventricles. He is doing well 1 year after surgery.
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.