Blood adipocytokine concentration in patients with peripheral artery disease.
Journal
International angiology : a journal of the International Union of Angiology
ISSN: 1827-1839
Titre abrégé: Int Angiol
Pays: Italy
ID NLM: 8402693
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
pubmed:
23
10
2020
medline:
18
9
2021
entrez:
22
10
2020
Statut:
ppublish
Résumé
Inflammatory responses mediated by adipocytokines may affect both atherosclerosis development and progression, as well as the risk of in-stent restenosis. The aim of this study was to determine the relationships between blood leptin, adiponectin and tumor necrosis factor-α (TNF-α) concentrations and the 1-year outcome of superficial femoral artery (SFA) stenting. Blood concentrations of leptin, adiponectin and TNF-α were determined in 70 patients undergoing SFA stenting due to intermittent claudication and in 40 patients undergoing carotid artery stenting (CAS). All subjects were followed up for at least 1 year in relation to the occurrence of clinically driven target lesion revascularization (TLR) or a major adverse cardiovascular event (MACE). Patients undergoing SFA stenting and CAS had similar blood adipocytokine concentrations. Patients with diabetes mellitus presented a higher leptin concentration, lower adiponectin-to-leptin ratio, and lower blood adiponectin concentration indexed to fat mass (FM) and to visceral adiposity score (VAS). In Kaplan-Meier analysis, blood concentration of TNF-α indexed to FM and to VAS was higher in patients who underwent TLR and MACE. However, in multifactorial analysis, the severity of atherosclerosis lesions in the femoropopliteal vascular region, estimated in relation to TASC-II classification, was the only predictor of TLR. Circulating adipocytokines did not distinguish patients with different clinical manifestations of atherosclerosis. Higher ratios of TNF-α -to-FM and to VAS before SFA stenting were related to TLR and MACE occurrence. Dysregulation in adipocytokine secretion may be a potential mediator of a proatherogenic action of diabetes mellitus in patients with peripheral artery disease.
Sections du résumé
BACKGROUND
BACKGROUND
Inflammatory responses mediated by adipocytokines may affect both atherosclerosis development and progression, as well as the risk of in-stent restenosis. The aim of this study was to determine the relationships between blood leptin, adiponectin and tumor necrosis factor-α (TNF-α) concentrations and the 1-year outcome of superficial femoral artery (SFA) stenting.
METHODS
METHODS
Blood concentrations of leptin, adiponectin and TNF-α were determined in 70 patients undergoing SFA stenting due to intermittent claudication and in 40 patients undergoing carotid artery stenting (CAS). All subjects were followed up for at least 1 year in relation to the occurrence of clinically driven target lesion revascularization (TLR) or a major adverse cardiovascular event (MACE).
RESULTS
RESULTS
Patients undergoing SFA stenting and CAS had similar blood adipocytokine concentrations. Patients with diabetes mellitus presented a higher leptin concentration, lower adiponectin-to-leptin ratio, and lower blood adiponectin concentration indexed to fat mass (FM) and to visceral adiposity score (VAS). In Kaplan-Meier analysis, blood concentration of TNF-α indexed to FM and to VAS was higher in patients who underwent TLR and MACE. However, in multifactorial analysis, the severity of atherosclerosis lesions in the femoropopliteal vascular region, estimated in relation to TASC-II classification, was the only predictor of TLR.
CONCLUSIONS
CONCLUSIONS
Circulating adipocytokines did not distinguish patients with different clinical manifestations of atherosclerosis. Higher ratios of TNF-α -to-FM and to VAS before SFA stenting were related to TLR and MACE occurrence. Dysregulation in adipocytokine secretion may be a potential mediator of a proatherogenic action of diabetes mellitus in patients with peripheral artery disease.
Identifiants
pubmed: 33086778
pii: S0392-9590.20.04479-X
doi: 10.23736/S0392-9590.20.04479-X
doi:
Substances chimiques
Adipokines
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM