Association of monocyte tumor necrosis factor α expression and serum inflammatory biomarkers with walking impairment in peripheral artery disease

Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular and skeletal muscle function. We explored the association of inflammation to maximal walking time (MWT) in patients with claudication. Circul...

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Published inJournal of vascular surgery Vol. 61; no. 1; pp. 155 - 161
Main Authors Pande, Reena L., Brown, Jonathan, Buck, Stewart, Redline, Whitney, Doyle, Jeanne, Plutzky, Jorge, Creager, Mark A.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.01.2015
Subjects
Adult
Aged
Aged, 80 and over
Biomarkers - blood
Case-Control Studies
Cross-Sectional Studies
Exercise Test
Exercise Tolerance
Female
Humans
Inflammation Mediators - blood
Intermittent Claudication - blood
Intermittent Claudication - diagnosis
Intermittent Claudication - genetics
Intermittent Claudication - immunology
Intermittent Claudication - physiopathology
Male
Middle Aged
Monocytes - metabolism
Peripheral Arterial Disease - blood
Peripheral Arterial Disease - diagnosis
Peripheral Arterial Disease - genetics
Peripheral Arterial Disease - immunology
Peripheral Arterial Disease - physiopathology
Predictive Value of Tests
Real-Time Polymerase Chain Reaction
RNA, Messenger - blood
Severity of Illness Index
Surgery
Time Factors
Tumor Necrosis Factor-alpha - blood
Tumor Necrosis Factor-alpha - genetics
Walking
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Abstract Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular and skeletal muscle function. We explored the association of inflammation to maximal walking time (MWT) in patients with claudication. Circulating inflammatory biomarkers, including tumor necrosis factor α (TNF-α), C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule 1 (sICAM), were measured in 75 subjects with intermittent claudication as well as in 43 healthy subjects. Real-time polymerase chain reaction was used to quantify mRNA expression of TNF-α, IL-6, interferon-γ, and CD36 from peripheral blood monocytes. Treadmill testing was performed in PAD subjects to assess MWT. Compared with healthy subjects, PAD subjects had higher levels of circulating TNF-α (P < .0001), CRP (P = .003), sICAM (P < .0001), and IL-6 (P < .0001). Expression of both IL-6 (P = .024) and CD36 (P = .018) was greater in PAD subjects than in healthy subjects. Among subjects with PAD, higher gene expression of TNF-α was associated inversely with MWT (P = .01). MWT was also associated inversely with greater levels of circulating TNF-α (P = .028), CRP (P = .024), IL-6 (P = .03), and sICAM (P = .018). Systemic inflammation, as indicated by TNF-α inflammatory gene expression in peripheral blood monocytes and by circulating biomarker levels, is associated with impairment in walking time in patients with PAD and intermittent claudication.
AbstractList Objective Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular and skeletal muscle function. We explored the association of inflammation to maximal walking time (MWT) in patients with claudication. Methods Circulating inflammatory biomarkers, including tumor necrosis factor α (TNF-α), C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule 1 (sICAM), were measured in 75 subjects with intermittent claudication as well as in 43 healthy subjects. Real-time polymerase chain reaction was used to quantify mRNA expression of TNF-α, IL-6, interferon-γ, and CD36 from peripheral blood monocytes. Treadmill testing was performed in PAD subjects to assess MWT. Results Compared with healthy subjects, PAD subjects had higher levels of circulating TNF-α ( P  < .0001), CRP ( P  = .003), sICAM ( P  < .0001), and IL-6 ( P  < .0001). Expression of both IL-6 ( P  = .024) and CD36 ( P  = .018) was greater in PAD subjects than in healthy subjects. Among subjects with PAD, higher gene expression of TNF-α was associated inversely with MWT ( P  = .01). MWT was also associated inversely with greater levels of circulating TNF-α ( P  = .028), CRP ( P  = .024), IL-6 ( P  = .03), and sICAM ( P  = .018). Conclusions Systemic inflammation, as indicated by TNF-α inflammatory gene expression in peripheral blood monocytes and by circulating biomarker levels, is associated with impairment in walking time in patients with PAD and intermittent claudication.
Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular and skeletal muscle function. We explored the association of inflammation to maximal walking time (MWT) in patients with claudication.OBJECTIVEInflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular and skeletal muscle function. We explored the association of inflammation to maximal walking time (MWT) in patients with claudication.Circulating inflammatory biomarkers, including tumor necrosis factor α (TNF-α), C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule 1 (sICAM), were measured in 75 subjects with intermittent claudication as well as in 43 healthy subjects. Real-time polymerase chain reaction was used to quantify mRNA expression of TNF-α, IL-6, interferon-γ, and CD36 from peripheral blood monocytes. Treadmill testing was performed in PAD subjects to assess MWT.METHODSCirculating inflammatory biomarkers, including tumor necrosis factor α (TNF-α), C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule 1 (sICAM), were measured in 75 subjects with intermittent claudication as well as in 43 healthy subjects. Real-time polymerase chain reaction was used to quantify mRNA expression of TNF-α, IL-6, interferon-γ, and CD36 from peripheral blood monocytes. Treadmill testing was performed in PAD subjects to assess MWT.Compared with healthy subjects, PAD subjects had higher levels of circulating TNF-α (P < .0001), CRP (P = .003), sICAM (P < .0001), and IL-6 (P < .0001). Expression of both IL-6 (P = .024) and CD36 (P = .018) was greater in PAD subjects than in healthy subjects. Among subjects with PAD, higher gene expression of TNF-α was associated inversely with MWT (P = .01). MWT was also associated inversely with greater levels of circulating TNF-α (P = .028), CRP (P = .024), IL-6 (P = .03), and sICAM (P = .018).RESULTSCompared with healthy subjects, PAD subjects had higher levels of circulating TNF-α (P < .0001), CRP (P = .003), sICAM (P < .0001), and IL-6 (P < .0001). Expression of both IL-6 (P = .024) and CD36 (P = .018) was greater in PAD subjects than in healthy subjects. Among subjects with PAD, higher gene expression of TNF-α was associated inversely with MWT (P = .01). MWT was also associated inversely with greater levels of circulating TNF-α (P = .028), CRP (P = .024), IL-6 (P = .03), and sICAM (P = .018).Systemic inflammation, as indicated by TNF-α inflammatory gene expression in peripheral blood monocytes and by circulating biomarker levels, is associated with impairment in walking time in patients with PAD and intermittent claudication.CONCLUSIONSSystemic inflammation, as indicated by TNF-α inflammatory gene expression in peripheral blood monocytes and by circulating biomarker levels, is associated with impairment in walking time in patients with PAD and intermittent claudication.
Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular and skeletal muscle function. We explored the association of inflammation to maximal walking time (MWT) in patients with claudication. Circulating inflammatory biomarkers, including tumor necrosis factor α (TNF-α), C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule 1 (sICAM), were measured in 75 subjects with intermittent claudication as well as in 43 healthy subjects. Real-time polymerase chain reaction was used to quantify mRNA expression of TNF-α, IL-6, interferon-γ, and CD36 from peripheral blood monocytes. Treadmill testing was performed in PAD subjects to assess MWT. Compared with healthy subjects, PAD subjects had higher levels of circulating TNF-α (P < .0001), CRP (P = .003), sICAM (P < .0001), and IL-6 (P < .0001). Expression of both IL-6 (P = .024) and CD36 (P = .018) was greater in PAD subjects than in healthy subjects. Among subjects with PAD, higher gene expression of TNF-α was associated inversely with MWT (P = .01). MWT was also associated inversely with greater levels of circulating TNF-α (P = .028), CRP (P = .024), IL-6 (P = .03), and sICAM (P = .018). Systemic inflammation, as indicated by TNF-α inflammatory gene expression in peripheral blood monocytes and by circulating biomarker levels, is associated with impairment in walking time in patients with PAD and intermittent claudication.
Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular and skeletal muscle function. We explored the association of inflammation to maximal walking time (MWT) in patients with claudication. Circulating inflammatory biomarkers, including tumor necrosis factor α (TNF-α), C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule 1 (sICAM), were measured in 75 subjects with intermittent claudication as well as in 43 healthy subjects. Real-time polymerase chain reaction was used to quantify mRNA expression of TNF-α, IL-6, interferon-γ, and CD36 from peripheral blood monocytes. Treadmill testing was performed in PAD subjects to assess MWT. Compared with healthy subjects, PAD subjects had higher levels of circulating TNF-α (P < .0001), CRP (P = .003), sICAM (P < .0001), and IL-6 (P < .0001). Expression of both IL-6 (P = .024) and CD36 (P = .018) was greater in PAD subjects than in healthy subjects. Among subjects with PAD, higher gene expression of TNF-α was associated inversely with MWT (P = .01). MWT was also associated inversely with greater levels of circulating TNF-α (P = .028), CRP (P = .024), IL-6 (P = .03), and sICAM (P = .018). Systemic inflammation, as indicated by TNF-α inflammatory gene expression in peripheral blood monocytes and by circulating biomarker levels, is associated with impairment in walking time in patients with PAD and intermittent claudication.
Author Pande, Reena L.
Buck, Stewart
Brown, Jonathan
Creager, Mark A.
Redline, Whitney
Doyle, Jeanne
Plutzky, Jorge
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Snippet Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting vascular...
Objective Inflammation contributes to the development of peripheral artery disease (PAD) and may contribute to intermittent claudication by adversely affecting...
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StartPage 155
SubjectTerms Adult
Aged
Aged, 80 and over
Biomarkers - blood
Case-Control Studies
Cross-Sectional Studies
Exercise Test
Exercise Tolerance
Female
Humans
Inflammation Mediators - blood
Intermittent Claudication - blood
Intermittent Claudication - diagnosis
Intermittent Claudication - genetics
Intermittent Claudication - immunology
Intermittent Claudication - physiopathology
Male
Middle Aged
Monocytes - metabolism
Peripheral Arterial Disease - blood
Peripheral Arterial Disease - diagnosis
Peripheral Arterial Disease - genetics
Peripheral Arterial Disease - immunology
Peripheral Arterial Disease - physiopathology
Predictive Value of Tests
Real-Time Polymerase Chain Reaction
RNA, Messenger - blood
Severity of Illness Index
Surgery
Time Factors
Tumor Necrosis Factor-alpha - blood
Tumor Necrosis Factor-alpha - genetics
Walking
Title Association of monocyte tumor necrosis factor α expression and serum inflammatory biomarkers with walking impairment in peripheral artery disease
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https://www.clinicalkey.es/playcontent/1-s2.0-S0741521414012853
https://dx.doi.org/10.1016/j.jvs.2014.06.116
https://www.ncbi.nlm.nih.gov/pubmed/25095746
https://www.proquest.com/docview/1640328448
Volume 61
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