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The aim of this systematic review was to identify the minimum investigations to optimally monitor CHD risk in SLE.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods.<\/jats:title><jats:p>English-restricted literature review was performed using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines through Ovid Medline, Embase, and Cochrane Central databases, from inception until May 2014 (Medline until October 2014). Specific search terms included, among others, \u201cSLE,\u201d \u201catherosclerosis,\u201d \u201cCHD,\u201d \u201cmyocardial ischemia,\u201d \u201cacute coronary syndrome,\u201d \u201cmyocardial infarction,\u201d and \u201cangina pectoris.\u201d We identified 101 eligible articles, 23 with cardiovascular events (CVE) as endpoints and 78 with measures of subclinical atherosclerosis. The Newcastle-Ottawa scale was used for quality assessment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results.<\/jats:title><jats:p>Certain traditional and disease-specific factors were identified as independent predictors for CHD. Among the former were age (particularly postmenopausal state), male sex, arterial hypertension, dyslipidemia, and smoking. Disease activity and duration, cumulative damage, antiphospholipid antibodies, high sensitivity C-reactive protein, and renal disease were the most consistent disease-related factors. Corticosteroids were linked to increased CHD risk whereas antimalarials were protective. Concerning imaging techniques, carotid ultrasonography (intima-media thickness and plaque) was shown to independently predict CVE.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion.<\/jats:title><jats:p>Premature CHD in SLE is multifactorial; modifiable variables should be monitored at frequent intervals to ensure prompt management. Disease-specific factors also affect the atherogenic process and should be evaluated regularly. 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