SAGE-Hindawi Access to Research Cardiology Research and Practice Volume 2011, Article ID 578390, 6 pages doi:10.4061/2011/578390 Case Report Aggressive Cardiac Involvement in Systemic Lupus Erythematosus: A Case Report and a Comprehensive Literature Review Reza Ashraﬁ,1 Pankaj Garg,1 Ewan McKay,1 John Gosney,2 Som Chuah,1 and Gershan Davis1 1 Aintree Cardiac Centre, University Hospital Aintree, Lower Lane, Liverpool L9 7AL, UK 2 Department of Pathology, The Royal Liverpool University Hospital, Prescot Street, Liverpool L7 8XP, UK Correspondence should be addressed to Reza Ashraﬁ, reza.ashraﬁ@aintree.nhs.uk Received 12 November 2010; Revised 24 December 2010; Accepted 7 January 2011 Academic Editor: Jalal K. Ghali Copyright © 2011 Reza Ashraﬁ et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. We present the case of a 35-year-old gentleman who presented with an aggressive cardiomyopathy with normal coronary arteries. He was later diagnosed with systemic lupus-related cardiomyopathy. Methods. We undertook an extensive review of the literature regarding cardiac manifestations of lupus and used over 100 journals to identify the key points in pathology, diagnosis, and treatment. Results. We have shown that cardiac lupus can be rapidly progressive and, unless treated early, can have severe consequences. The predominant pathologies are immune complex and accelerated atherosclerosis drive. Treatment comprised of high-level immunosuppression. 1. Initial Referral A 35-year-old UK born man was referred to the cardiology department at University Hospital Aintree in October 2009 with a few troublesome palpitations a day, which had increased in frequency over the preceding 4 months, and occasional dizziness. His background was as a law student who was a non- smoker and consumed no alcohol. His family history re- vealed a ﬁt and well mother, father, and sister but, interest- ingly, two paternal uncles who had died suddenly of an unknown cause. His examination was unremarkable, and his ECG was normal apart from a few isolated unifocal ventricular ec- topics and a normal echocardiogram apart from some mild distal inferior septal hypokinesis with an ejection fraction of 57.3% using the Simpson’s biplane method. Plans were made for him to have an outpatient 24-hour tape and to be reviewed again in clinic. 2. First Admission Unfortunately, he was admitted via the emergency depart- ment three days later with constant palpitations, dizziness, and increasing shortness of breath. Clinically, there were no signs of heart failure or thyroid disease. He was found to have a Troponin T of 1.02 µg/L (1.39 at twelve hours), and his ECG showed sinus rhythm with septal Q waves, poor septal R wave progression, and ventricular couplets. While on telemetry, he was noted to have short runs of ventricular tachycardia (VT) with a high background burden of ventricular ectopics. He was started on treatment for his heart failure and arrhythmia comprising of bisoprolol 2.5 mg, aspirin 75 mg, and ramipril 1.25 mg (the dosages were maximised as far as his blood pressure would allow). He had a repeat echocardiogram, which revealed a worsening of his inferoseptal hypokinesis from mild to severe and some anterior/apicoanterior hypokinesis. He was also noted to have multiple strands/trabeculae in the LV apex. To further investigate, a 3D echocardiogram was organ- ised which revealed a false tendon but also hypertrabecula- tion in the apex and a 3-way connection between the inferior, septal, and anterior walls. A diagnosis of LV compaction was mooted, and his angiogram was scheduled for the next day. A picture of the 3D echocardiogram, Figure 1 is showing spontaneous echo contrast and trabeculations in the apex