Vascular responsiveness in the microcirculation of patients with systemic lupus erythematosus is not impaired

Leeuw, de Karina; Blaauw, Judith; Smit, Andries J.; Kallenberg, Cornelis; Bijl, Marc

doi:10.1177/0961203308091968

Cited by 11 publications

(9 citation statements)

References 39 publications

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“…The main finding in the present study was that the skin microcirculation in the SLE patients did not differ in responses to ACh and sodium nitroprusside compared with controls; this finding was also confirmed in a recent publication [20]. However, in larger vessels, a reduction in the flow-mediated dilatation in SLE patients has been shown [16][17][18], why regional variation in the vascular tree might exist.…”

Section: Discussionsupporting

confidence: 87%

“…Laser Doppler flowmetry (LDf) is another non-invasive method that can be used to investigate endothelium-dependent and -independent vasoreactivity in the cutaneous microcirculation. Performing this method, the endotheliumdependent vasodilatation in SLE patients was not altered compared to controls [20]. Patients with congestive heart failure with the same method have been reported to have impaired endothelium-dependent and -independent vasoreactivity [21].…”

mentioning

confidence: 97%

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Effect of Medication on Microvascular Vasodilatation in Patients with Systemic Lupus Erythematosus

Bengtsson¹,

Andersson²,

Edvinsson³

et al. 2010

Basic Clin Pharma Tox

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The aim of this study was to investigate the microvascular responses in the skin, to local heat, iontophoretically administered acetylcholine and to sodium nitroprusside in relation to cardiovascular damage in patients with systemic lupus erythematosus (SLE) and matched controls. We also wanted to examine if the ongoing medication in SLE patients influenced this vascular response. We investigated 30 women with SLE and compared them with 20 age and sex-matched controls. The cutaneous blood flow response to local heat (+44°C), iontophoretically administered endothelium-dependent (acetylcholine), as well as independent (sodium nitroprusside) vasodilatation, was measured by laser Doppler flowmetry. Clinical data and medication were retrieved from the clinical database and patient records. The cutaneous microvascular reactivity did not differ between SLE patients and a group of matched controls nor did it correlate with cardiovascular damage [assessed by Systemic Lupus International Collaborating Clinics ⁄ American College of Rheumatology Damage Index (SLICC ⁄ ACR-DI)]. However, patients on antimalarial drugs (hydroxychloroquine n = 8 and chloroquine diphosphate n = 3) responded more strongly to sodium nitroprusside (endothelium-independent vasodilatation) compared with those without antimalarial drugs (p < 0.01). The response to acetylcholine was higher among patients on warfarin compared with those without (p < 0.05), whereas glucocorticoid use ( ‡5 mg daily) was associated with reduced response to acetylcholine (p < 0.05). Smokers in general tended to have a lower response to acetylcholine (p = 0.064). Smoking SLE patients versus non-smoking SLE patients had a significantly lower response to acetylcholine (p = 0.01). Medication with antimalarial drugs-enhanced endothelium-independent vasodilatation, while glucocorticoid use was associated with reduction and warfarin-treatment with enhancement of endothelium-dependent vasodilatation. Therefore, despite there is no difference in microvascular endothelium-dependent vasodilatation, other factors such as medication and smoking may affect vasodilatation in SLE patients.As Urowitz described the 'bimodal pattern of systemic lupus erythematosus (SLE)' some 30 years ago [1], later studies have confirmed that cardiovascular disease is greatly overrepresented in SLE patients compared with controls [2,3]. Traditional risk factors as well as SLE-specific risk factors have been thoroughly studied and both are of importance for the development of cardiovascular disease in SLE [4][5][6]. It has been suggested that antimalarial (hydroxychloroquine and chloroquine diphosphate) treatment might improve the blood lipid profile in SLE and reduce the risk of diabetes mellitus [7][8][9][10][11].There is a clinical need for non-invasive techniques to ensure the presence of and predict the development of cardiovascular disease in SLE. Non-invasive methods have been used to investigate vessel wall changes, and revealed increased vessel wall stiffness and increased pulse wave veloci...

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Section: Discussionsupporting

confidence: 87%

mentioning

confidence: 97%

Effect of Medication on Microvascular Vasodilatation in Patients with Systemic Lupus Erythematosus

Bengtsson¹,

Andersson²,

Edvinsson³

et al. 2010

Basic Clin Pharma Tox

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“…vWF has been considered a specific plasma marker of endothelial cell activation and the best indicator of vascular integrity. Its raised levels are believed to predict cardiovascular events [50], and numerous researchers reported increases in plasma vWF of SLE patients [8,40,42,44,51].…”

Section: Discussionmentioning

confidence: 99%

Pentraxin 3 as a biomarker of local inflammatory response to vascular injury in systemic lupus erythematosus

Cieślik

Hrycek

2014

Autoimmunity

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Systemic lupus erythematosus (SLE) is an autoimmune disorder with organ injury related to vasculitis. Inflammation of blood vessels results from auto-immunological activation of endothelial cells. The pentraxin 3 (PTX3), might act as an indicator of vasculitides in many diseases. The aim of this study was to determine whether PTX3 might be useful as a marker of vascular injury in SLE. This study was carried out in a group of 56 SLE women, and in the 28 female volunteers control group. All participants' plasma and serum samples were collected to estimate concentrations (ELISA) of PTX3, soluble thrombomodulin, soluble E-selectin (sE-selectin), soluble P-selectin (sP-selectin), soluble form of vascular cell adhesion molecule 1 (sVCAM-1), soluble inter-cellular adhesion molecule-1 (sICAM-1), soluble platelet endothelial cell adhesion molecule 1, monocyte chemotactic protein-1 (MCP-1) and von Willebrand factor (vWF) activity. Anthropometric, demographic and lifestyle characteristics of SLE patients were also performed. The SLE patients had higher PTX3, vWF, MCP-1, sE-selectin and sVCAM-1 levels than the controls (1.82 ± 1.56 ng/mL, 237 ± 101%, 70.05 ± 18.31 ng/mL, 111.16 ± 49.15 ng/mL and 978.78 ± 462.35 ng/mL vs. 0.86 ± 0.40 ng/mL, 138 ± 43%, 58.56 ± 13.91 ng/mL, 66.04 ± 27.18 ng/mL and 499.07 ± 125.67 ng/mL, respectively). The independent factors affecting PTX3 expression included Systemic Lupus Erythematosus Disease Activity Index, prednisone dose and anemia severity. Moreover, the PTX3 areas under the curve-receiver operating characteristics curves 0.717 ± 0.056 with cut-off level of 1.96 ng/mL was comparable to vWF, MCP-1, sE-selectin, sP-selectin and sICAM-1. PTX3 and sVCAM-1 were the only factors related to SLE activity. Other vascular injury indicators associated with PTX3 were vWF and sVCAM-1. In conclusion, PTX3 concentrations in SLE patients might serve as a indicator of the activation/dysfunction of vascular endothelium.

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“…Using laser Doppler fluxmetry, vascular responsiveness in the cutaneous microcirculation of patients with SLE was not significantly different than controls unless the patients also had Raynaud's phenomenon. Therefore, initial studies do not support the use of laser Doppler fluxmetry in distinguishing patients with SLE at an increased risk of CVD and patients with SLE not at increased risk of CVD [55]. …”

Section: Imaging Modalitiesmentioning

confidence: 99%

Management of cardiovascular complications in systemic lupus erythematosus

Skamra¹,

Ramsey‐Goldman

2010

International Journal of Clinical Rheumatology

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Cardiovascular disease (CVD) is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Patients with SLE have an excess risk compared with the general population; this is particularly pronounced in younger women with SLE who have an excess risk of over 50-fold compared with population controls. There is a higher prevalence of subclinical atherosclerosis in patients with SLE compared with controls, as demonstrated by a variety of imaging modalities discussed in this review. The causality of the excess risk of CVD and subclinical atherosclerosis is multifactorial in patients with SLE. While traditional risk factors play a role, after controlling for the traditional Framingham risk factors, the excess risk is still 7.5-fold greater than the general population. This review will also cover novel cardiovascular risk factors and some SLEspecific variables that contribute to CVD risk. This review discusses the risk factor modification and the evidence available for treatment of these risk factors in SLE. There have not yet been any published randomized, controlled trials in patients with SLE with respect to CVD risk factor modifications. Thus, the treatment and management recommendations are based largely on published guidelines for other populations at high risk for CVD. Keywordscardiac imaging; cardiovascular disease; cardiovascular risk factors; subclinical atherosclerosis; systemic lupus erythematosusIn the last few decades, the prognosis of patients with systemic lupus erythematosus (SLE) has improved immensely. In the 1950s, the 5-year survival rate for SLE was approximately 50% according to a study performed in Toronto, Canada. Subsequent studies have found 5-year survival rates of 90% in patients with SLE [1]. A bimodal mortality pattern was first described in 1976 by Urowitz et al. in the Toronto Lupus cohort. Septicemia in the setting of high-dose prednisone was identified as an early cause of death in patients with more active SLE. Later in the disease course, death was associated with inactive SLE, long duration of prednisone therapy and myocardial infarction (MI) due to atherosclerotic heart disease [2]. More recent data from a large international cohort revealed a 60% decrease in the standardized all-cause mortality rates (SMR) from 1970-1979 (SMR: 4.9) to 1990. However, the SMR trend for cardiovascular disease (including heart disease, arterial disease and stroke) did not decline from 1970 to 2001 [3]. A Swedish cohort followed from 1964 to 1994 demonstrated similar findings of improved overall survival for patients with SLE over the last two decades, but the risk of cardiovascular death remained (by 1985-1994 NIH Public Access Author ManuscriptInt J Clin Rheumtol. Author manuscript; available in PMC 2010 December 1. Published in final edited form as:Int J Clin Rheumtol. This review will discuss the increased risk of CVD observed in patients with SLE, the role of traditional cardiovascular risk factors, the role of novel risk factors (some of which are lu...

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Vascular responsiveness in the microcirculation of patients with systemic lupus erythematosus is not impaired

Cited by 11 publications

References 39 publications

Effect of Medication on Microvascular Vasodilatation in Patients with Systemic Lupus Erythematosus

Effect of Medication on Microvascular Vasodilatation in Patients with Systemic Lupus Erythematosus

Pentraxin 3 as a biomarker of local inflammatory response to vascular injury in systemic lupus erythematosus

Management of cardiovascular complications in systemic lupus erythematosus

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