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Modification of platelet function by isosorbide dinitrate in patients with coronary artery disease
H Sinzinger1, I Virgolini, J O'Grady
1Wilhelm Auerswald-Atherosclerosis Research Group (ASF) Vienna, Austria.
Insights
Isosorbide dinitrate (ISDN) treatment for four weeks significantly reduced platelet activation in patients with coronary artery disease. This antiplatelet effect may enhance the drug
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hematology
Background:
- Platelet activation plays a crucial role in the pathophysiology of coronary artery disease (CAD).
- Understanding the effects of common cardiovascular medications on platelet function is essential for optimizing patient outcomes.
Purpose of the Study:
- To evaluate the impact of oral isosorbide dinitrate (ISDN) on platelet function in patients with established coronary artery disease.
Main Methods:
- A four-week oral treatment with 100 mg isosorbide dinitrate (ISDN) daily was administered to 40 patients (aged 40-65 years) with diagnosed CAD.
- Platelet reactivity to adenosine diphosphate (ADP) and prostacyclin (PGI2), thromboxane B2 (TXB2) production, and circulating platelet aggregates (Wu-test) were assessed.
- Plasma concentrations of beta-thromboglobulin and platelet factor 4 were also measured.
Main Results:
- Isosorbide dinitrate significantly decreased platelet reactivity to ADP and reduced TXB2 production from both endogenous and exogenous substrates.
- A marked reduction in circulating platelet aggregates was observed, alongside increased platelet sensitivity to PGI2.
- Plasma levels of beta-thromboglobulin and platelet factor 4 showed minimal changes.
Conclusions:
- Four weeks of isosorbide dinitrate treatment effectively reduces platelet activation in patients with coronary artery disease.
- The observed antiplatelet effects of ISDN may contribute to its therapeutic benefits in managing CAD.
Abstract:
The effect of a four weeks oral treatment with 100 mg isosorbide dinitrate (ISDN) daily on platelet function was evaluated in 40 patients (aged 40-65 years) with proven coronary artery disease. Isosorbide dinitrate decreased platelet reactivity to ADP (p less than 0.001), increased platelet sensitivity to PGI2 (p less than 0.01) while the production of TXB2 from exogenous arachidonic acid substrate and from endogenous substrate were both significantly reduced. Circulating platelet aggregates as measured by the Wu-test were markedly reduced (p less than 0.001) but there was little change in the plasma concentration of the platelet proteins beta-thromboglobulin and platelet factor 4. Overall, platelet activation correlated with smoking, hypertension and a family history of coronary artery disease. The reduced platelet activation seen during treatment with isosorbide dinitrate may contribute to the therapeutic benefit seen with this drug in patients with coronary artery disease.