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Systemic inflammatory responses in acute coronary syndrome: increased activity observed in polymorphonuclear
S Takeshita1, T Isshiki, M Ochiai
1Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan. satoshi-t@in.aix.or.jp
Insights
Systemic inflammation in acute coronary syndrome involves increased polymorphonuclear leukocyte (PMN) activity and decreased T-lymphocyte activity. This contrasts with local inflammation, suggesting dual inflammatory processes in acute coronary syndrome pathogenesis.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Inflammation Research
Background:
- Local inflammation in coronary arteries contributes to acute coronary syndrome (ACS) pathogenesis.
- The role of systemic inflammation in ACS is not well understood.
- This study investigates systemic inflammatory responses in ACS patients.
Purpose of the Study:
- To characterize systemic inflammatory responses in patients with acute coronary syndrome.
- To compare systemic inflammation markers between ACS patients and those with stable angina.
- To explore the relationship between systemic inflammation and ACS.
Main Methods:
- Studied 83 patients with ischemic heart disease (15 stable angina, 68 ACS).
- Measured polymorphonuclear leukocyte (PMN) activation using luminol-dependent chemiluminescence (CL).
- Assessed T-lymphocyte activation via soluble interleukin-2 receptor (sIL-2R) levels.
Main Results:
- ACS patients showed significantly higher PMN activation (CL counts) than stable angina patients.
- No significant differences in CL counts were found between unstable angina and acute myocardial infarction.
- ACS patients exhibited significantly lower T-lymphocyte activity (sIL-2R levels) compared to stable angina patients.
Conclusions:
- Acute coronary syndrome is associated with systemic increases in PMN activity.
- A decrease in T-lymphocyte activity is observed in patients with acute coronary syndrome.
- These systemic changes suggest independent local and systemic inflammatory processes in ACS pathogenesis.
Background:
Local inflammation within the coronary arteries is involved in the pathogenesis of acute coronary syndrome. However, the contribution of a systemic inflammatory response to the pathogenesis of this syndrome has not been well characterized. Accordingly, we investigated systemic inflammatory responses in patients with acute coronary syndrome.
Methods:
A total of 83 patients with ischemic heart disease (15 with stable exertional angina and 68 with acute coronary syndrome) were studied. The luminol-dependent chemiluminescence (CL) response of polymorphonuclear leukocytes (PMNs), which reflects their ability to generate oxygen species, was used as a marker for PMN activation. Soluble interleukin-2 receptor (sIL-2R) levels were measured to assess T-lymphocyte activation.
Results:
CL counts of whole blood from patients with acute coronary syndrome were twice those of patients with stable angina (2.38 +/- 0.22 vs 1.10 +/- 0.17 x 10(6) counts, P < 0.05). A comparison of CL counts between patients with unstable angina and those with acute myocardial infarction revealed no significant differences. T-lymphocyte activity, measured by serum sIL-2R, was significantly lower in patients with acute coronary syndrome than those with stable angina (214.3 +/- 11.5 vs. 358.3 +/- 115.7 U/ml, P < 0.05).
Conclusions:
This investigation shows that there is a systemic increase in PMN activity and a decrease in T-lymphocyte activity in patients with acute coronary syndrome. This contrasts with the pattern of cellular activation seen at sites of local inflammation within atherosclerotic plaques, suggesting that two independent inflammatory processes (local and systemic) may be involved in the pathogenesis of this syndrome.