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Influence on platelet function by heparin in men with unstable coronary artery disease
1Department of Internal Medicine, University Hospital, Linköping, Sweden.
Insights
Heparin treatment in men with unstable coronary artery disease (CAD) increases platelet sensitivity to ADP and reduces prostacyclin
Area of Science:
- Cardiology
- Hematology
- Pharmacology
Background:
- Unstable coronary artery disease (CAD) involves complex platelet activation.
- Heparin is a common anticoagulant used in managing unstable CAD.
- Understanding heparin's effects on platelet function is crucial for optimizing treatment.
Purpose of the Study:
- To investigate the impact of intravenous heparin on platelet aggregation and prostacyclin inhibition in patients with unstable CAD.
- To assess changes in platelet function after 5 days of heparin treatment compared to placebo.
Main Methods:
- A double-blind, placebo-controlled study involving 97 men with unstable CAD.
- Ex vivo platelet aggregation assays were performed using collagen and ADP.
- Platelet inhibitory effects of prostacyclin were measured before and after 5 days of treatment with heparin or placebo.
Main Results:
- Heparin significantly increased platelet aggregation induced by ADP (1 microM).
- Heparin significantly reduced the inhibitory effect of prostacyclin (1.0 ng/ml) on platelet aggregation.
- No significant changes in platelet function were observed in the placebo group.
Conclusions:
- Intravenous heparin therapy in unstable CAD enhances platelet sensitivity to ADP.
- Heparin treatment diminishes the antiplatelet efficacy of prostacyclin in these patients.
- Concomitant acetylsalicylic acid may counteract heparin's effect on ADP-induced aggregation but not its interaction with prostacyclin.
Abstract:
Ninety-seven men with unstable coronary artery disease (CAD), i.e. unstable angina or a non Q-wave myocardial infarction, entered a double-blind placebo-controlled study with heparin intravenously 30,000-40,000 U daily. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP and as the platelet inhibitory effect of prostacyclin, before and after 5 days of treatment. Heparin increased aggregation induced by ADP 1 microM from 39.6 +/- 3.1% to 52.1 +/- 4.1% (p = 0.014) and reduced the inhibition of aggregation by prostacyclin 1.0 ng/ml from 59.6 +/- 3.7% to 39.3 +/- 5.6% (p less than 0.001). No changes occurred in the placebo group. Thus, treatment with heparin enhances the platelet sensitivity to ADP and decreases the platelet inhibitory effect of prostacyclin in men with unstable CAD. Concomitant treatment with acetylsalicylic acid abolishes the increased response to ADP, but does not seem to influence the interaction between heparin and prostacyclin.