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 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.