Cardiology Research and Practice 3 Figure 3 He improved in a short period of time with the same medications and was discharged with followup arranged for the results of his biopsy. 4. Third Admission This patient was readmitted two weeks into the year 2010 with chest tightness and orthopnoea, his exercise tolerance dropping to 50 yards. His oxygen saturations on air were 89%, and apart from a displaced apex beat there were no signs of heart failure. During this time, he was noted to have lost a considerable amount of weight and to have developed a widespread myopathy. He had an autoimmune screen, which was positive for anti-RO and LA antibodies with an ANA titre of 1 : 640 with a membrane speckling pattern and a CK of 10,000. His lupus coagulant and anticardiolipin antibodies were negative. His forced vital capacity was normal at 5.8l. CT pulmonary angiography was negative. The histology of his cardiac biopsy revealed extensive myocardiolysis and interstitial ﬁbrosis with no abnormal staining for amyloid or iron, a result suggestive of ischaemia consistent with a possible diagnosis of SLE. He went on to have a muscle biopsy, which showed widespread skeletal muscle necrosis. His genetic tests for the various types of muscular dystrophy were negative. Histology of his cardiac biopsy, showing ﬁbrosis in between the few surviving myocardial ﬁbres, is shown in Figure 3. He had his echocardiogram repeated, and all his cham- bers had become dilated with severely impaired LV and RV function with spontaneous echo contrast and an ejection fraction of 16%. His pulmonary artery pressure was 9.4 plus right atrial pressure. This reduction had occurred over a period of 3 months. As a result of severe cardiac impairment and the presence of spontaneous echo contrast, he had his aspirin replaced with warfarin to cover for the high thromboembolic risk. He continued on the ramipril 1.25 mg, bisoprolol 2.5 mg with furosemide 40 mg bd, and spironolactone 25 mg with warfarin added. Unfortunately, despite the maximum anti- heart failure treatment his blood pressure would tolerate, he did not make any signiﬁcant improvement 5. Most Recent Admission He was readmitted two weeks after his most recent discharge again with worsening shortness of breath and fatigue. After a multidisciplinary discussion with neurology and rheumatology, a diagnosis of systemic lupus erythematosus (SLE) was made, and he was put on high-dose steroids and given a short course of immunoglobulins. He improved clinically with a larger appetite, better mobility, and a reduction in his CK to only 3000. He was given 6 cycles of outpatient cyclophosphamide before being put on maintenance Azathioprine 100 m/day in addition to his existing treatment. Aggressive immunosup- pressives helped clinically, and there was a small improve- ment in his end diastolic diameters and an improvement in his ejection fraction by 2%. As the antiheart-failure treat- ment remained the same, it was felt that the improvement in his echo parameters was due to his immunosuppression. 6. Current Condition Mr. A has begun to deteriorate once again and is currently being seen by both the transplant and rheumatology teams to see what the beneﬁts and risks of cardiac transplant would be. 7. Review Methodology Three reviewers undertook literature searches using PubMed and MEDLINE with search terms including SLE myocarditis, SLE cardiomyopathy, SLE with cardiac involvement, treat- ment of SLE cardiomyopathy, and cardiac/heart transplant in SLE. Lupus replaced SLE in all the above searches in a second round to ensure maximum data collection. We excluded animal studies work on patients under 18, and studies which did not focus on the cardiac manifestations of SLE. There were no date restrictions, and only articles in English were used for the review. Over 100 articles were identiﬁed and were then systemat- ically reviewed to extrapolate important applicable points for future use in four key areas: pathology, imaging, treatment, and transplant. 8. Discussion We present below a review of the literature as SLE cardiomy- opathy carries a signiﬁcant mortality risk over SLE without cardiac involvement [1], but it is important to remember that all cardiomyopathy has a poor prognosis with studies looking at cardiomyopathy not related to coronary artery disease having a 5-year mortality of 20% [2]. We will now look systematically at the incidence, diag- nosis, treatment, and outcomes in SLE with cardiac involve- ment.