Increased morning ADP-dependent platelet aggregation persists despite dual antiplatelet therapy in patients with

Marek Koziński1, Liliana Bielis, Joanna Wiśniewska-Szmyt

  • 1Department of Cardiology and Internal Medicine, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz, Poland. marekkozinski@wp.pl

Cardiology Journal
|November 29, 2008
PubMed

Insights

Morning platelet aggregation remains elevated in ST-elevation myocardial infarction (STEMI) patients despite dual antiplatelet therapy. This persistent morning surge in adenosine diphosphate (ADP)-dependent aggregation warrants further investigation into its clinical significance.

Area of Science:

  • Cardiology
  • Hematology
  • Circadian Biology

Background:

  • Numerous studies link morning hours to increased risk of myocardial infarction, stroke, and sudden cardiac death.
  • Enhanced morning platelet aggregation is observed in healthy individuals and those with coronary artery disease, particularly without adequate antiplatelet treatment.

Purpose of the Study:

  • To assess circadian variation in platelet aggregation among patients experiencing their first ST-elevation myocardial infarction (STEMI).
  • To evaluate platelet aggregation patterns in STEMI patients receiving primary percutaneous coronary interventions (pPCI) and dual antiplatelet therapy.

Main Methods:

  • Prospective recruitment of fifteen STEMI patients (12 men, 3 women).
  • Blood sample collection at 6 a.m., 10 a.m., 2 p.m., and 7 p.m. on the third day of hospitalization.
  • Assessment of whole blood aggregation response to arachidonic acid and adenosine diphosphate (ADP) using an impedance aggregometer.

Main Results:

  • A significant 75% morning increase in ADP-dependent platelet aggregation was observed (p < 0.04).
  • No significant diurnal variation was found in arachidonic acid-mediated platelet aggregation.
  • The magnitude of the morning surge in ADP-dependent aggregation did not correlate with baseline levels.

Conclusions:

  • Elevated morning ADP-dependent platelet aggregation persists even with dual antiplatelet therapy in STEMI patients treated with pPCI.
  • The clinical implications of this persistent morning aggregation surge require further research and demonstration.
Abstract

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...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade 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...
Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
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...