Endothelial Dysfunction in Systemic Lupus Erythematosus: Evaluation with ¹³N-Ammonia PET

Abstract

Systemic lupus erythematosus (SLE) affects multiple organs and systems, severely involving the cardiovascular system. The aim of this study was to evaluate the presence of endothelial dysfunction with 13 N-ammonia PET in asymptomatic SLE patients. Methods: We enrolled 16 women with SLE and 16 healthy women. Myocardial blood flow (MBF) was quantified in a 64-slice PET/CT scanner at rest, during a cold pressor test (CPT), and during stress. Endothelium-dependent vasodilation index, %DMBF, and myocardial flow reserve (MFR) were calculated. Results: There were 16 women in the SLE group (mean age 6 SD, 31.4 6 8.3 y) and 16 women in the healthy control group (31.5 6 11.1 y). Mean endothelium-dependent vasodilatation index and %DMBF were significantly lower in SLE patients (1.18 6 0.55 vs. 1.63 6 0.65, P 5 0.04, and 18 6 55 vs. 63 6 65, P 5 0.04, respectively). MFR was also lower in the SLE group (2.41 6 0.59 vs. 2.73 6 0.77, P 5 0.20). Conclusion: SLE patients who are free of active disease present abnormal coronary flow and endothelial dysfunction. It is necessary to develop and intensify treatment strategies directed to CAD in SLE patients.

Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus

“…Hemodynamic changes are not uncommon to SLE, with reports showing that brachial artery blood flow is impaired in patients with SLE (16,22,36,47). Impaired hemodynamic responses have also been recently extended to the coronary circulation in patients with SLE (2). Consistent with data from human studies, we previously demonstrated peripheral vascular changes in NZBWF1 mice, including impaired endothelial dependent relaxation and enhanced smooth muscle cell contraction (40).…”

Chronic Hydroxychloroquine Improves Endothelial Dysfunction and Protects Kidney in a Mouse Model of Systemic Lupus Erythematosus

“…Endothelial cell dysfunction represents the earliest indication of the development of cardiovascular disease and is also a principal element of SLE. 46 In large vessels, flow-mediated dilatation is impaired in patients with SLE. [47][48][49] However, the cutaneous microvascular reactivity to local heat or iontophoretically administered acetylcholine did not differ between patients with SLE and matched controls.…”

Lack of nitric oxide synthases increases lipoprotein immune complex deposition in the aorta and elevates plasma sphingolipid levels in lupus

“…Macrophage activation and intima-infiltration, and in turn atherogenesis, are often preceded by endothelial damage or dysfunction. Endothelial cell dysfunction represents the earliest indication of the development of CVD and is also a principal element of SLE [7]. Nitric Oxide (NO) secretion is required for normal endothelium-dependent vasodilation in SLE [8].…”