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 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.