ArticleInflammation2011
Inflammatory cytokines imbalance in the very early phase of acute coronary syndrome: correlations with angiographic findings and in-hospital events.
Article in Inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Risks of acute coronary syndrome in patients with osteoarthritis: a nationwide population-based cohort study.Clinical rheumatology · 2016Article
- 'Hot stuff': inflammatory lymphocyte populations in acute coronary syndrome.Cellular & molecular immunology · 2015Review
- The evaluation of plasma and leukocytic IL-37 expression in early inflammation in patients with acute ST-segment elevation myocardial infarction after PCI.Mediators of inflammation · 2015Article
- Pleural tissue repair with cord blood platelet gel.Blood transfusion = Trasfusione del sangue · 2014Article
- Plasma granzyme B in ST elevation myocardial infarction versus non-ST elevation acute coronary syndrome: comparisons with IL-18 and fractalkine.Mediators of inflammation · 2013Article
- Neural acupuncture unit: a new concept for interpreting effects and mechanisms of acupuncture.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- The interplay of inflammation and cardiovascular disease in systemic lupus erythematosus.Arthritis research & therapy · 2011Review
- Relationship between site of myocardial infarction, left ventricular function and cytokine levels in patients undergoing coronary artery surgery.Cardiovascular journal of AfricaArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study is to investigate the release of some inflammatory cytokines (Cks) during the very early phase (first 24 h) of acute coronary syndrome (ACS). Twenty-six consecutive subjects admitted to coronary care unit with ACS underwent serial blood sampling in order to evaluate concentrations of interleukin (IL)-2, IL-10, IL-18, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ. Blood samples were taken within 6 h after onset of chest pain (T₀), at 12 h (T₁), and at 24 h (T₂). Patients were thus divided into four groups comparing pro-inflammatory Ck release (IL-2, TNF-α, and IFN-γ) and anti-inflammatory activity (IL-10). Clinical features, risk factors, incidence of adverse events, and coronary angiography findings were compared with Ck activation. Ck levels were significantly increased if compared with baseline. Subjects with marked inflammatory response showed a higher incidence of left anterior descending coronary disease (IL-2, p < 0.001; TNF-α and IFN-γ, p < 0.05) and more often incurred early complications (IL-2, p < 0.05; IFN-γ, p < 0.001). A correlation was detectable between IL-18 levels and myocardial enzyme release (creatine kinase, r = 0.47; lactate dehydrogenase, r = 0.54; troponin I, r = 0.58; p < 0.05). TNF-α levels were associated with a worse prognosis at follow-up (Log rank, p < 0.05). A Ck activation characterizes the early phase of ACS. Early inflammatory reaction seems to correlate with coronary disease and adverse events.
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