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Change of plasma leukotriene C4 during myocardial ischemia in humans
B Takase1, A Kurita, T Maruyama
1Department of Internal Medicine-1, National Defense Medical College, Saitama, Japan.
Insights
Leukotriene C4 levels increase in acute myocardial infarction but not transient ischemia. Leukocyte function may be key in heart attack pathogenesis.
Area of Science:
- Biochemistry
- Cardiology
- Immunology
Background:
- Leukotriene C4 (LTC4) is a mediator implicated in inflammatory processes.
- Myocardial ischemia, particularly acute myocardial infarction (AMI), involves complex inflammatory responses.
- The role of LTC4 in different severities of myocardial ischemia requires further elucidation.
Purpose of the Study:
- To investigate changes in plasma leukotriene C4 levels during transient and prolonged myocardial ischemia in humans.
- To compare LTC4 levels in patients with chronic stable angina versus those with acute myocardial infarction.
- To explore the potential involvement of leukocyte function in AMI pathogenesis.
Main Methods:
- Radioimmunoassay was used to measure plasma leukotriene C4 levels.
- Patients with chronic stable angina underwent exercise or angioplasty-induced ischemia.
- Temporal changes in LTC4 were monitored in patients with acute myocardial infarction over one month.
Main Results:
- Transient myocardial ischemia (exercise or angioplasty) did not significantly alter LTC4 levels in stable angina patients.
- Patients with acute myocardial infarction exhibited significantly elevated plasma LTC4 levels in the acute phase compared to controls.
- Elevated LTC4 levels in AMI persisted in arterial and pulmonary artery blood, suggesting a role in prolonged ischemia.
Conclusions:
- Leukotriene C4 is significantly involved in prolonged myocardial ischemia, particularly in acute myocardial infarction.
- The findings suggest that leukocyte function plays a crucial role in the pathogenesis of acute myocardial infarction.
- LTC4 may serve as a biomarker or therapeutic target in managing acute myocardial infarction.
Abstract:
Changes in leukotriene C4 levels during different degrees of myocardial ischemia in humans were examined by comparing radioimmunoassay measures of leukotriene C4 plasma levels obtained during transient and prolonged myocardial ischemia. Leukotriene C4 levels in systemic arterial and coronary sinus blood were determined in patients with chronic stable angina before and after myocardial ischemia induced either by exercise (supine bicycle ergometer exercise stress testing; n = 14; age, 52 +/- 8 years) or by coronary occlusion during angioplasty (n = 14; age 53 +/- 7 years). Temporal changes of leukotriene C4 were also followed in arterial and pulmonary artery blood within 24 h after the onset of chest pain (acute phase), and 1 day, 1 week, and 1 month later in 22 patients with acute myocardial infarction (AMI) (12 patients with thrombolytic therapy, age 61 +/- 10 years; 10 patients without thrombolytic therapy, age 60 +/- 11 years). Clinical characteristics, including coronary risk factors and the severity of coronary artery disease, were not significantly different among the groups. Exercise-induced myocardial ischemia and coronary occlusion did not induce any significant leukotriene C4 changes in the chronic stable angina patients, whereas AMI patients had significantly higher plasma leukotriene C4 levels in both arterial and pulmonary artery blood in the acute phase compared with those of chronic stable angina patients (arterial blood, 471 +/- 164 pg/ml and 477 +/- 235 pg/ml vs. 275 +/- 254 pg/ml or 240 +/- 66 pg/ml, p < 0.05; pulmonary artery blood in AMI, 543 +/- 162 pg/ml vs. 234 +/- 125 pg/ml or 225 +/- 64 pg/ml, coronary sinus blood in chronic stable angina, p < 0.05). These results suggest that leukotriene C4 is involved more in prolonged myocardial ischemia than in transient myocardial ischemia, and that leukocyte function might play a significant role in the pathogenesis of patients with AMI.