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Title: T lymphocytes alterations are associated with oxidized LDL, troponin T, white blood cells and C-reactive protein during acute myocardial infarction
Author: Napoleão, Patrícia
Selas, Mafalda
Freixo, Cláudia
Carmo, Miguel Mota
Viegas-Crespo, Ana Maria
Ferreira, Rui Cruz
Pinheiro, Teresa
Keywords: Acute coronary syndromes
C-reactive protein
Cardiac troponin T
Longitudinal study
Oxidized LDL
T lymphocytes
Issue Date: 2014
Publisher: IOS Press
Abstract: BACKGROUND: Auto-immune responses are associated with oxidized LDL (ox-LDL) release, a key factor in plaque destabilization. Data on the relationship between ox-LDL and T lymphocytes in human populations remains scarce. T cells also react with other molecules from the lesion and/or damage the myocardium. OBJECTIVE: The objective of the present study was to examine the relationship between circulating T lymphocytes, ox-LDL, markers of myocardial necrosis (cTnT), myocardial dysfunction (N-terminal pro-brain natriuretic peptide – NT-proBNP) and inflammation (C-reactive protein – CRP) in the setting of acute myocardial infarction. METHODS: A longitudinal study of 55 patients with ST-elevation myocardial infarction (STEMI) were evaluated at three time points: admission, 2 and 40 days following admission, together with 30 patients with stable angina (SA) and 56 subjects without coronary artery disease serving as controls (CTR). RESULTS: STEMI patients had maximal ox-LDL values and minimal levels of CD3+ T lymphocytes at admission, which was normalized during the recovery period. The increasing trend of CD3+ T cells was positively associated with an ox-LDL decline over time. CRP and cTnT longitudinal variations were negatively associated with the CD3+ T-cell increasing trend. These associations were not found in SA patients or controls. CONCLUSIONS: The associations found between CD3+ T lymphocytes, ox-LDL and cTnT suggest a specificity of the immune response in AMI towards arterial and myocardial inflammation and remodelling.
Peer review: yes
DOI: 10.3233/CH-121644
ISSN: 1386-0291
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