Case Presentation: A 34-year-old female with a history of hypertension, hyperlipidemia, and SLE presented with acute substernal tightness associated with nausea and vomiting. She denied fever, chills, diaphoresis, or palpitations. Her EKG showed sinus rhythm with new T wave inversions in anterior leads. Troponin elevation was noted with a peak of 4.48. Echocardiogram showed normal ejection fraction without regional wall motion abnormalities. Her TIMI score was 2, corresponding to 8% risk of all-cause mortality at 14 days. She was treated symptomatically for possible myopericarditis however continued to have repetitive episodes of chest discomfort and nausea.Subsequent nuclear stress test showed large, fixed myocardial perfusion defect of the mid-inferior, inferolateral, and inferoseptal wall with regional wall motion abnormalities. Cardiac catheterization revealed diffuse 70% stenosis in proximal and middle LAD, 90% stenosis in LCX artery, 99% stenosis in middle RCA. Cardiothoracic surgery did not consider the patient a candidate for bypass surgery. The patient had revascularization with drug-eluting stents in RCA and LAD. She was treated with dual antiplatelet therapy and high-intensity statins. Her SLE directed therapy was escalated by rheumatologist.

Discussion: Premature atherosclerosis is a major cause of death in patients with SLE, especially in young women, for whom the background rate of coronary heart disease (CHD) outcomes is very low. The odds ratio of CHD and myocardial infarction in women with SLE in their 20s and 30s is 7 and 2 respectively compared to their peers. The pathogenesis of this phenomenon has been under the scope of studies for the past decade. Young patients with SLE have a higher prevalence of classic Framingham risk factors compared to their healthy peers. However, traditional risk factors do not fully account for accelerated CHD in these patients. Thus, hyperlipidemia and hypertension are the strongest predictors of CHD, when diabetes mellitus appears to be a very poor predictor. At the same time, specific lupus-associated risk factors have been discussed in the literature. Hypercoagulable state, antiphospholipid syndrome, and lupus nephritis are most consistently associated with CHD in young patients with SLE. Not without significance, the treatment used for SLE, such as corticosteroids use, was shown to contribute to endothelial damage.As speculated above, traditional risk stratification models TIMI score, HEART score may inadequately assess the likelihood of acute coronary syndrome in young patients with SLE. Further studies are needed to explore this problem and improve clinical practice. In the meanwhile, we should consider SLE as an additional risk factor for CHD, when we see young patients presenting with acute chest pain as a proactive approach may be beneficial in these patients.

Conclusions: 1. SLE should be considered as an additional risk factor for CHD in a young patient presenting with acute chest pain.2. A tight control of classic risk factors is beneficial for patients with SLE.