Abnormal PFA-100 closure time is associated with increased platelet aggregation in patients presenting with chest

Andrew D Atiemo1, Ladina S Ng'Alla, Dhananjay Vaidya

  • 1Department of Medicine, Johns Hopkins Medical Institute, Baltimore, MD, USA.

Insights

Aspirin non-responsiveness in chest pain patients, identified by PFA-100, indicates increased platelet activation. However, this aspirin resistance did not lead to more clinical events during hospitalization.

Area of Science:

  • Cardiology
  • Hematology
  • Clinical Medicine

Background:

  • Antiplatelet therapy, including aspirin, is crucial for preventing cardiovascular events like myocardial infarction and stroke.
  • A significant number of patients exhibit reduced responsiveness to aspirin, which is linked to an increased risk of ischemic events.
  • Assessing platelet function is vital for understanding treatment efficacy and patient outcomes.

Purpose of the Study:

  • To evaluate platelet function in patients presenting with chest pain using the PFA-100 point-of-care assay.
  • To correlate PFA-100 results with traditional platelet aggregometry.
  • To determine if aspirin non-responsiveness is associated with increased clinical sequelae in these patients.

Main Methods:

  • Platelet function was assessed in 94 chest pain patients using PFA-100, flow cytometry, and optical aggregometry.
  • All participants were receiving daily aspirin (81-325 mg).
  • Clinical events during the index hospitalization were recorded.

Main Results:

  • Half of the patients (50%) were classified as aspirin non-responders based on PFA-100 results (closure time ≤ 193).
  • Aspirin non-responders showed significantly higher platelet aggregation to ADP and epinephrine, and increased PAC-1 expression compared to responders.
  • No significant difference in clinical events was observed between aspirin non-responders and responders during the index hospitalization.

Conclusions:

  • Abnormal PFA-100 closure times in chest pain patients reflect heightened platelet aggregation and activation.
  • Aspirin non-responsiveness, as indicated by PFA-100, did not correlate with an increased incidence of clinical events during the index hospitalization.
Abstract

Related Concept Videos

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...
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...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...