Platelet function during ticlopidine and eicosapentaenoic Acid administration in patients with coronary heart disease

G Davi1, M Belvedere, I Catalano

  • 1Ematologia, Università di Chieti, Via Marchese Ugo, 52, 90141, Palermo.

Platelets
|November 4, 2010
PubMed

Insights

Combining ticlopidine and eicosapentaenoic acid (EPA) in coronary heart disease (CHD) patients significantly inhibits platelet activation. This dual therapy targets both ADP-dependent and thromboxane A(2)-mediated pathways, offering enhanced antiplatelet effects.

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Unstable angina and coronary heart disease (CHD) involve platelet activation.
  • Antiplatelet drugs are crucial in managing these conditions.
  • Understanding combined therapeutic effects on platelet function is vital.

Purpose of the Study:

  • To investigate the combined effects of ticlopidine and eicosapentaenoic acid (EPA) on platelet function in CHD patients.
  • To determine if simultaneous administration offers synergistic antiplatelet activity.
  • To explore the impact on different platelet activation pathways.

Main Methods:

  • Patients with coronary heart disease received ticlopidine and eicosapentaenoic acid (EPA) (fish oil).
  • Platelet aggregation induced by ADP, collagen, and arachidonate was measured.
  • Thromboxane A(2) formation and urinary 11-dehydrothromboxane B(2) excretion were assessed.

Main Results:

  • Ticlopidine significantly reduced ADP- and collagen-induced platelet aggregation.
  • EPA intake reduced but did not completely inhibit thromboxane A(2) formation.
  • Combined therapy showed a more pronounced inhibition of platelet aggregation and reduced thromboxane metabolite excretion.

Conclusions:

  • Combined ticlopidine and EPA therapy in CHD patients enhances antiplatelet effects.
  • This combination inhibits both ADP-dependent and thromboxane A(2)-dependent platelet activation mechanisms.
  • Ticlopidine plus fish oil may be a beneficial therapeutic strategy for managing platelet activation in CHD.

Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Peripheral Artery Disease III: Interprofessional Care01:27

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease (PAD) is characterized by narrowed arteries that diminish blood flow to the extremities. Effective management of PAD requires an interprofessional approach involving various healthcare professionals. The critical aspects of interprofessional care for PAD patients focus on risk factor modification, drug therapy, exercise therapy, nutrition therapy, critical limb ischemia care, and interventional radiology and surgical procedures.The primary treatment goal for PAD...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...