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Platelet release and thromboxane synthesis in symptomatic coronary artery disease
Insights
Platelet activation markers, thromboxane B2 (TXB2) and beta thromboglobulin (beta TG), are elevated in myocardial ischemia and infarction. However, these markers have limited clinical value for diagnosing or differentiating these conditions.
Area of Science:
- Cardiology
- Hematology
- Biochemistry
Background:
- Platelet activation is implicated in myocardial ischemia.
- Biomarkers of platelet activation may aid in diagnosis.
Purpose of the Study:
- To evaluate the incidence and significance of platelet activation in patients with chest pain.
- To assess the clinical utility of plasma thromboxane B2 (TXB2) and beta thromboglobulin (beta TG) in myocardial ischemia and infarction.
Main Methods:
- Serial measurements of plasma and urine TXB2 and beta TG in 98 patients.
- Patients were categorized into noncardiac chest pain, myocardial infarction, and angina groups.
Main Results:
- Elevated plasma TXB2 and beta TG in myocardial infarction and angina groups, but not in noncardiac chest pain.
- Urine beta TG levels were not significantly elevated.
- Beta TG remained normal in 61% of patients with ischemia.
- Higher TXB2 levels correlated with recurrent angina.
Conclusions:
- Platelet activation is frequent in myocardial ischemia and infarction.
- TXB2 and beta TG measurements have limited value in detecting or differentiating myocardial ischemia from infarction.
- These markers lack significant clinical utility in managing ischemic heart disease.
Abstract:
The incidence and significance of platelet activation in myocardial ischemia was evaluated by serial measurement of plasma thromboxane B2 (TXB2) and beta thromboglobulin (beta TG) in plasma and urine in 98 patients admitted to a coronary care unit with chest pain. All measurements were normal in the 26 patients with noncardiac chest pain. Mean plasma TXB2 and beta TG concentration, but not urine beta TG, were elevated in the 25 patients with myocardial infarction and the 47 patients with angina. The beta TG levels remained normal in 61% of the patients with angina or infarction. The TXB2 levels were significantly higher in patients with recurrent episodes of angina at rest than in those without ischemic episodes after admission. There was a weak correlation between plasma TXB2 and plasma beta TG (r = 0.20, p less than 0.01) and between plasma and urine beta TG (r = 0.31, p less than 0.01). Results indicate that platelets are frequently activated with myocardial ischemia or infarction. However, the measurement of beta TG and TXB2 is of limited value in detecting or differentiating myocardial ischemia from infarction and therefore lacks clinical value in the management of patients with ischemic heart disease.