Subclinical Carotid Atherosclerosis in a Patient with Systemic Lupus Erythematosus

Deborah Alpert; Adrienne Davis; Doruk Erkan; Mary J Roman; Jane E Salmon


Nat Clin Pract Rheumatol. 2007;3(8):473-478. 

In This Article

Discussion of Diagnosis

Following the patient's diagnosis of SLE and her initial treatment, her early disease course was uneventful; however, she later suffered recurrent SLE flares in the setting of poor medical compliance, and developed new carotid atherosclerotic plaque.

Over the last half century, the prognosis of patients with SLE has dramatically improved as a result of early diagnosis, aggressive immunomodulatory therapy and improved infection control.[1] In this setting, atherosclerosis has increasingly contributed to the morbidity and mortality of these patients. Observational studies of patients with SLE have demonstrated a prevalence of 6-20% for symptomatic coronary artery disease (CAD), and 2-15% for stroke.[2] These findings highlight the importance of identifying markers of subclinical atherosclerosis in patients with SLE, which could potentially allow for prevention of future ischemic events.

The prevalence of subclinical atherosclerosis in patients with SLE over a broad age range is estimated to be 30-40%.[1] Carotid plaque is a manifestation of systemic atherosclerosis; although it is an indication of cerebrovascular disease, carotid plaque is actually a stronger predictor of myocardial infarction than stroke.[3] Notably, the observational study that the patient was enrolled in found a significantly increased prevalence of carotid plaque in patients with SLE compared with controls (37.1% versus 15.2%, P <0.001), and also demonstrated that patients with plaque were more likely to have pre-existing CAD.[4]

Noninvasive imaging techniques that assess definite or presumptive subclinical atherosclerosis in patients with SLE are described in Table 2 ;[1,2] however, the use of such techniques to screen for subclinical atherosclerosis in individual patients is currently experimental, and not yet recommended for clinical practice. It is unclear which patients with SLE should be screened, or which tests are most useful for predicting the risk of cardiovascular events. At present, treating physicians should be vigilant for symptoms of CAD, and have a low threshold for initiating standard diagnostic evaluations. In patients with SLE without overt CAD symptoms, such as the case patient, appropriate detection and management of atherosclerotic risk factors are warranted.


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