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Effect of high dose aspirin on coronary hemodynamics during pacing-induced myocardial ischemia
Insights
Aspirin did not alter coronary blood flow or myocardial function during stress in patients with coronary disease. These findings suggest thromboxane A2 does not significantly contribute to ischemia pathogenesis.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Thromboxane A2 (TXA2) is implicated in platelet activation and vasoconstriction.
- The role of TXA2 in stress-induced myocardial ischemia requires further investigation.
Purpose of the Study:
- To evaluate the effects of aspirin on coronary hemodynamics and transcardiac TXA2 concentrations during myocardial ischemia.
- To determine if TXA2 plays a significant role in the pathogenesis of stress-induced ischemia.
Main Methods:
- 11 patients with coronary disease underwent pacing-induced myocardial ischemia.
- Measurements included coronary hemodynamics, arterial and coronary sinus TXA2 levels, and myocardial lactate extraction.
- TXA2 production was assessed before and after aspirin administration.
Main Results:
- Aspirin significantly inhibited thromboxane B2 (TXB2) production.
- Coronary blood flow, myocardial lactate extraction, and anginal threshold remained unchanged by aspirin at rest and during ischemia.
- No adverse coronary hemodynamic effects were observed with aspirin treatment.
Conclusions:
- Aspirin does not possess vasoconstrictive properties in the context of coronary artery disease.
- TXA2 production does not appear to be a major factor in the development of stress-induced myocardial ischemia.
- Patients with evidence of intracoronary TXA2 production may benefit from aspirin therapy for potential antiplatelet effects.
Abstract:
The effects of aspirin on coronary hemodynamics and transcardiac concentrations of thromboxane B2 (the stable metabolite of thromboxane A2) were determined at rest and during pacing-induced myocardial ischemia in 11 patients with coronary disease. Control coronary sinus pacing increased both arterial thromboxane B2 (331 +/- 70 to 623 +/- 132 pg/ml, p less than 0.02) and coronary sinus thromboxane B2 (184 +/- 3 to 403 +/- 156 pg/ml, p less than 0.05), but positive transmyocardial gradients developed in only three patients. After 650 mg of oral aspirin, more than 90% inhibition of in vitro thromboxane B2 production was demonstrated and circulating thromboxane B2 was undetectable at rest and during pacing in all patients. Despite these changes in thromboxane B2 concentrations, coronary blood flow was unchanged by aspirin at rest (107 +/- 14 versus 112 +/- 13 ml/min, p = NS) and during pacing (189 +/- 29 versus 181 +/- 25 ml/min, p = NS). Myocardial lactate extraction was also unchanged at rest (24 +/- 7 versus 19 +/- 5%, p = NS) and during pacing (5 +/- 6 versus 9 +/- 5%, p = NS). No change occurred in the anginal threshold. Thus, aspirin does not have the vasoconstrictive properties that have been reported with another cyclo-oxygenase inhibitor, indomethacin. These findings also suggest that thromboxane A2 production does not play a major role in the pathogenesis of stress-induced ischemia. Nonetheless, intracoronary thromboxane A2 production in some patients may potentiate platelet activation and coronary thrombosis. Such patients may benefit from long-term aspirin therapy and can be treated with aspirin without risk of adverse coronary hemodynamic effects.