Myocardial ischemia in the absence of obstructive coronary artery disease in systemic lupus erythematosus

Objectives: the purpose of this study was to evaluate the presence of myocardial ischemia measured by adenosine stress cardiac magnetic resonance (CMR) using visual myocardial perfusion and a quantitative myocardial perfusion reserve index (MPRI) in the absence of obstructive coronary artery disease (CAD) in women with systemic lupus erythematosus (SLE) with anginal chest pain (CP).

Background: ischemic heart disease is a leading cause of morbidity and mortality in SLE. Previous studies demonstrated the presence of perfusion defects using adenosine stress CMR in patients with CP and no obstructive CAD, consistent with microvascular coronary dysfunction in patients without SLE.

Method: Twenty female SLE patients with typical and atypical anginal CP were prospectively enrolled. Patients with established cardiovascular disease were excluded. CMR was performed with 0.05 mmol/kg gadolinium adenosine stress first-pass perfusion in SLE patients and in 10 asymptomatic reference control women. SLE patients also underwent 64-slice coronary computed tomography angiography. CMR was scored visually and quantitatively (MPRI).

Results: among 18 patients with complete data, no patient had obstructive CAD; however, 8 of 18 (44%) displayed visual perfusion defects on stress CMR compared with 0 in 10 control subjects (p = 0.014). The mean MPRI in patients versus controls was 2.0 ± 0.4 versus 2.4 ± 0.4 (p = 0.031) in the subepicardium and 1.8 ± 0.3 versus 2.1 ± 0.4 (p = 0.24) in the subendocardium. Multivariate linear regression revealed that SLE was the only predictor of subepicardial (p < 0.0025; β = -1.059) and subendocardial (p < 0.05; β = -0.529) MPRIs.

Conclusions: we observed a 44% prevalence of abnormal stress myocardial perfusion by CMR in the absence of obstructive CAD in SLE patients with anginal CP. Compared with controls, reduced MPRI was observed in SLE patients, and SLE presence was a significant predictor of an abnormal MPRI. These findings are consistent with the hypothesis that anginal CP in SLE patients without obstructive CAD is due to myocardial ischemia potentially caused by microvascular coronary dysfunction. Further research in a larger SLE population is warranted.