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 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.