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The effect of enteric-coated aspirin on the morning increase in platelet activity
N T McCall1, G H Tofler, A I Schafer
1Department of Medicine, New England Deaconess Hospital, Boston, MA 02215.
Insights
Morning increases in platelet activity and myocardial infarction are reduced by aspirin. This study shows aspirin eliminates the morning surge in platelet aggregation and thromboxane A2 production, suggesting a link to reduced heart attacks.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pharmacology
Background:
- Platelet aggregability and myocardial infarction (MI) frequency exhibit a diurnal variation, peaking in the morning.
- Understanding the mechanisms behind this morning surge is crucial for MI prevention.
Purpose of the Study:
- To investigate if other platelet activity measures show morning increases.
- To determine if aspirin can mitigate these morning increases in platelet activity.
Main Methods:
- A single-blind, randomized, cross-over study involving 15 healthy males.
- Administration of 325 mg enteric-coated aspirin (ECA) or placebo.
- Measurement of platelet aggregability, thromboxane A2 production, and tissue plasminogen activator.
Main Results:
- During placebo, platelet thromboxane A2 production and aggregability to ADP, epinephrine, and collagen increased significantly post-awakening.
- ECA markedly reduced baseline thromboxane A2 production and abolished the morning increase.
- ECA also eliminated morning increases in aggregability to ADP and epinephrine, and lengthened collagen lag time.
Conclusions:
- The morning increase in platelet activity contributes to the higher incidence of myocardial infarction in the morning.
- Aspirin's antiplatelet effects, particularly its ability to blunt morning platelet activation, likely underlie its cardioprotective benefits.
- These findings support the role of aspirin in reducing morning cardiovascular events.
Abstract:
In vitro platelet aggregability to adenosine diphosphate (ADP) and epinephrine increases in the morning, as does the frequency of myocardial infarction. A single-blind, randomized, cross-over study of 15 healthy males was conducted to determine: (1) if other measures of platelet activity show a morning increases and (2) if aspirin eliminates any increases in platelet activity detected. Subjects received 325 mg of enteric-coated aspirin (ECA) or placebo. During placebo therapy,platelet thromboxane A2 production (following collagen stimulation) increased significantly after the subjects got up, as did platelet aggregability to ADP, epinephrine, and collagen. ECA markedly reduced baseline platelet thromboxane A2 production and eliminated the increase after the subjects got up. It also abolished biphasic aggregation in response to epinephrine and ADP (thereby eliminating the morning increase in aggregability to these agents), lengthened collagen lag time, reduced synergistic aggregation to combined agonists, was effective on day 2, and did not alter increases of tissue plasminogen activator that occurred following the subjects' arising. If aspirin prevents myocardial infarction by its antiplatelet action, as seems likely, the preferential reduction of morning infarction observed in the Physicians' Health Study, and the demonstration that aspirin eliminates the morning increase in platelet activity, suggest that the morning increase in myocardial infarction is due in part to a concurrent relatively modest increase in platelet activity.