Abstract

Background: Up to 35% of patients with SLE have abnormalities on myocardial perfusion imaging (MPI).It is postulated that endothelial dysfunction (EdF) is a precursor to atherosclerosis and may contribute to abnormalities on MPI. Aim: To determine the relationship between EdF measured using brachial artery Doppler ultrasound and MPI in patients with SLE. Method: This was a prospective study of 76 women with SLE, without clinical CAD. Assessment of EdF using brachial artery Doppler ultrasound was performed in all patients. Endothelium-dependent ( ed) and independent ( eid) flow mediated dilatation (FMD) was measured in response to post-ischemic reactive hyperemia and sublingual GTN respectively. All patients also underwent rest-stress MPI using SPECT 99mTc sestamibi using dipyridamole stress. MPI was interpreted using a 20 segment model. Summed stress score (SSS) were computed. Results: 40(52.6%) patients had both normal FMD and MPI. 7(9.2%) patients had both abnormal FMD and MPI. 8(10.5%) patients had abnormal FMD alone while 21(27.6%) patients had abnormal MPI alone. 36(47.4%) had an abnormality in either or both investigations. There was no agreement between FMD and MPI (Kappa=9.2%, correlation coefficient = −0.01, NS). However in an analysis of continuous variables, there was a statistically significant but weak negative correlation between eid and MPI (correlation coefficient = −0.35, p=0.002). Conclusion: In this study there was no agreement between FMD and MPI. Abnormal FMD with normal MPI is in keeping with the hypothesis that endothelial dysfunction is a precursor to myocardial ischemia, whereas normal FMD with abnormal MPI may reflect external influences such as treatment with statins at the time of study. Our findings indicate that brachial FMD and myocardial scintigraphy are complementary investigations in assessing the cardiovascular health of patients with SLE and should not be used interchangeably. When used in combination, brachial FMD and myocardial scanning identify around 47.4% of patients with SLE who may be at risk of developing clinical coronary artery disease.

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