Key result
Metabolic syndrome correlates with a heightened inflammatory response and greater TNF-alpha after elective PCI.
Why the study?
Does metabolic syndrome correlate with a heightened inflammatory response following elective PCI?
Observational (n=40)
Does metabolic syndrome correlate with a heightened inflammatory response following elective PCI?
Metabolic syndrome is associated with a heightened inflammatory response following elective percutaneous coronary intervention.
Metabolic syndrome was associated with higher post-PCI TNF-alpha; hypothesis-generating for targeted anti-inflammatory strategies in elective PCI.
There are few data concerning the relationship between diabetes mellitus, the metabolic syndrome and inflammation following elective percutaneous coronary intervention (PCI). The purpose of this study was to assess basal and peak levels of candidate cytokines in 40 patients undergoing elective PCI. Patients were categorised as having diabetes mellitus, the metabolic syndrome, or neither. Patients with the metabolic syndrome exhibited significantly greater levels of tumour necrosis factor-alpha over the study period, although this was unrelated to PCI. There was a trend for increased levels of interleukin-6 following PCI, primarily among patients with metabolic syndrome. Basal levels of monocyte chemoattractant protein-1 (MCP-1) were not different among study groups; however, the metabolic syndrome cohort had a trend towards increased circulating levels of MCP-1 after PCI. In this patient population, the metabolic syndrome correlates with a heightened inflammatory response following elective PCI.
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Marso et al. (2005) conducted an observational in Elective percutaneous coronary intervention (n=40). Metabolic syndrome vs. Patients with neither diabetes mellitus nor metabolic syndrome was evaluated on Basal and peak levels of candidate cytokines (TNF-alpha, IL-6, MCP-1). Metabolic syndrome correlates with a heightened inflammatory response following elective PCI, including significantly greater levels of tumour necrosis factor-alpha.
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