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Increased concentrations of inflammatory mediators in unstable angina: correlation with serum troponin T
A Mazzone1, S De Servi, I Mazzucchelli
1Istituto di Terapia Medica e Nefrologia, Policlinico S Matteo, Pavia, Italy.
Insights
Inflammatory markers interferon gamma and monocyte chemotactic protein-1 (MCP-1) are elevated in unstable angina patients, especially those with elevated cardiac troponin T. These cytokines may indicate myocardial damage or plaque instability.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Unstable angina is a critical manifestation of coronary artery disease.
- Inflammatory processes play a significant role in the pathophysiology of acute coronary syndromes.
- Biomarkers reflecting inflammation and myocardial injury are crucial for risk stratification.
Purpose of the Study:
- To quantify plasma levels of interferon gamma, monocyte chemotactic protein-1 (MCP-1), and interleukin 6 in patients with unstable angina.
- To investigate the correlation between these inflammatory markers and cardiac troponin T levels.
- To elucidate the role of specific cytokines in the context of myocardial damage in unstable angina.
Main Methods:
- Blood samples were collected from 76 patients undergoing coronary arteriography.
- Patients were categorized into three groups: unstable angina, stable angina, and a control group with normal coronary arteries.
- Plasma concentrations of interleukin 6, interferon gamma, MCP-1, and troponin T were measured.
Main Results:
- Interferon gamma and MCP-1 levels were significantly higher in patients with unstable angina compared to stable angina and control groups.
- Patients with unstable angina and elevated troponin T showed increased concentrations of interferon gamma and MCP-1.
- No significant difference in plasma interleukin 6 was observed between unstable angina patients with and without elevated troponin T.
Conclusions:
- Elevated plasma levels of interferon gamma and MCP-1 are associated with unstable angina.
- The increased concentrations of these cytokines, particularly in the presence of elevated troponin T, suggest a link to myocardial cell damage or plaque instability.
- These findings highlight the potential role of specific inflammatory cytokines as indicators of acute myocardial injury in unstable angina.
Objective:
To measure plasma interferon gamma, monocyte chemotactic protein-1 (MCP-1), and interleukin 6 and to assess their correlation with cardiac troponin T in unstable angina.
Design:
Blood sampling in patients undergoing coronary arteriography for known or suspected ischaemic heart disease.
Patients:
76 patients divided in three groups: 29 with unstable angina (group 1), 28 with stable angina (group 2), and 19 without ischaemic heart disease and with angiographically normal coronary arteries (group 3).
Main Outcome Measures:
Plasma interleukin 6, interferon gamma, MCP-1, and troponin T in the three groups of patients.
Results:
Interleukin 6 was increased in group 1 (median 2.19 (range 0.53-50.84) pg/ml) compared with the control group (1.62 (0.79-3.98) pg/ml) (p < 0.005), whereas interferon gamma was higher in group 1 (range 0-5.51 pg/ml) than in the other two groups (range 0-0.74 pg/ml and 0-0.37 pg/ml; p < 0.005 and p < 0.001, respectively). Patients with unstable angina (group 1) and positive troponin T had higher concentrations of interferon gamma than those with negative troponin T (0-5.51 pg/ml v 0-0.60 pg/ml, p < 0.001). Plasma MCP-1 was also higher in group 1 (median 267 (range 6-8670) pg/ml) than in the other two groups (134 (19-890) pg/ml and 84.5 (5-325) pg/ml; p < 0.005 and p < 0.001, respectively), and among group 1 patients with a positive troponin T assay than in those with normal troponin T (531 (14.5-8670) pg/ml v 69 (6-3333) pg/ml; p < 0.01). There was no difference in plasma interleukin 6 in group 1 patients between those with and without raised troponin T.
Conclusions:
The inflammatory cytokines interferon gamma and MCP-1 are increased in patients with unstable angina, particularly in those with raised concentrations of troponin T, suggesting that they are probably related to myocardial cell damage or to plaque rupture and thrombus formation.
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