Be vigilant for asymptomatic coronary artery calcifications in men with SLE

By Liz Meszaros, MDLinx
Published April 19, 2018

Key Takeaways

The risk of asymptomatic coronary artery calcifications (CACs) is higher in men with systemic lupus erythematosus (SLE) compared with men without SLE, and this increased risk is associated with older age, increased chronic damage, and cumulative dose of corticosteroids, as per results from a recent study published in the Journal of Rheumatology.

According to estimates from the Lupus Foundation of America, 1.5 million Americans have some form of SLE. Although SLE primarily affects young women, approximately 10% of those affected are men.

Circulatory diseases are a leading cause of mortality in these patients.1 Studies have shown that premature atherosclerosis occurs more often in individuals with SLE than in the general population. The incidence of myocardial infarction and subclinical atherosclerosis is higher, and is caused by traditional cardiovascular risk factors as well as the underlying inflammatory nature of SLE and its treatment.2

“Because of the scarcity of data about premature atherosclerosis in men with SLE, we aimed to determine whether the prevalence and extent of asymptomatic coronary artery atherosclerosis are increased in men with SLE compared with age- and sex-matched controls, and to define the associated risk factors,” wrote these researchers, led by Juanita Romero-Diaz, MD, MS, Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico.

Researchers included 95 patients (mean age: 34.7 years) with SLE and 100 age- and sex-matched controls who had no history of coronary artery disease. Patients were Hispanic, and had been followed regularly from 2007 to 2013. Patients or controls with a history of cardio-cerebrovascular disease were excluded.

Cardiovascular risk factors were assessed in all subjects, and included arterial hypertension, diabetes, family history of MI, smoking status, dyslipidemia, body mass index, waist circumference, and metabolic syndrome. Researchers also determined the Framingham 10-year risk factor profile for each.

Using multidetector computed tomography (CT), researchers screened subjects for CAC, and measured the result using the Agatston score. They acquired images of the coronary artery via a 256-slice Multidetector CT system.

They found that more SLE patients were hypertensive compared with controls (39% vs 4%, respectively; P < 0.001), had higher homocysteine levels (14.3 vs 9.6; P < 0.001), and were less likely to have normal glomerular filtration rates (84% vs 100%; P < 0.001). Other risk factors, however, were evenly distributed.

Coronary artery calcifications occurred in 12% of all subjects but were more frequent in SLE patients compared with controls (18% vs 7%, respectively; OR: 2.89; 95% CI: 1.07-8.65; P=0.02).

Among patients with calcifications, the median calcium did not differ significantly between SLE patients and controls. Upon multivariate analysis, researchers found that the following factors were independently associated with the presence of calcifications: age, diagnosis of SLE, diabetes, Framingham risk score, and glomerular filtration rate.

Patients with SLE exhibited CACs beginning at age 32 and within 2.3 years of a diagnosis of SLE. Independent risk factors for CAC included increasing age, Systemic Lupus International Collaborating Clinics score, and cumulative dose of prednisone.

“Our study shows that in men, as it has been reported in women, SLE is an independent risk factor for developing premature atherosclerosis. In another study conducted in our center among 128 Hispanic females with SLE of recent onset at start of follow-up, mean age was 31.7 years, and mean disease duration 4.9 years at screening, while the prevalence of coronary artery calcifications was 6%. Therefore, in comparison to the 18% prevalence observed in men with SLE, the burden of coronary artery calcifications is higher in men than women (OR 3.27, 95% CI 1.35–7.94),3” concluded Dr. Romero-Diaz and colleagues.


  1. Bernatsky S, Boivin JF, Joseph L, et al. Mortality in systemic lupus erythematosus. Arthritis Rheum. 2006;54:2550-2557.
  2. Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. Arthritis Rheum. 2001;44:2331-2337.
  3. Romero-Diaz J, Vargas-Vorackova F, Kimura-Hayama E, et al. Systemic lupus erythematosus risk factors for coronary artery calcifications. Rheumatology. 2012;51:110-119.
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