Role of PLA2 polymorphism on clinical events after percutaneous coronary intervention

George Syros1, Roxana Mehran, Giora Weisz

  • 1Columbia University Medical Center-Cardiology, New York 10032, USA.

Acute Cardiac Care
|June 16, 2009
PubMed
Abstract

Insights

The platelet GPIIIa PlA2 polymorphism, common in patients undergoing percutaneous coronary intervention (PCI), did not impact major adverse cardiac events (MACE) or cardiac enzyme elevation within one year. This genetic variant showed no influence on clinical outcomes post-PCI.

Area of Science:

  • Cardiovascular Genetics
  • Interventional Cardiology
  • Thrombosis Research

Background:

  • Platelet glycoprotein IIIa (GPIIIa) PlA2 polymorphism is linked to thrombosis and myocardial infarction.
  • The impact of PlA2 polymorphism on major adverse cardiac events (MACE) following percutaneous coronary intervention (PCI) remains undetermined.

Purpose of the Study:

  • To investigate the association between the GPIIIa PlA2 polymorphism and MACE in patients undergoing PCI.
  • To determine if the PlA2 genetic variant influences peri-procedural or long-term clinical outcomes after PCI.

Main Methods:

  • A cohort of 200 patients with symptomatic coronary artery disease undergoing non-urgent PCI were genotyped for the PlA2 polymorphism.
  • Patients were followed for one year while on dual antiplatelet therapy (aspirin and clopidogrel), with MACE adjudicated by an independent committee.
  • Baseline characteristics, platelet aggregation, and activated clotting time were assessed.

Main Results:

  • The PlA2 polymorphism variants (A1A1, A1A2, A2A2) were present in 72%, 27.5%, and 0.5% of patients, respectively.
  • No significant difference in 1-year MACE rates was observed between patients with and without the PlA2 polymorphism (7.1% vs. 6.5%, P=NS).
  • Peri-procedural creatine kinase-MB (CKMB) elevation rates were similar between groups (39% vs. 38%, P=NS).

Conclusions:

  • The GPIIIa PlA2 polymorphism is common in patients undergoing PCI, although the homozygous variant is rare.
  • The presence of the PlA2 polymorphism did not affect peri-procedural cardiac enzyme elevation or one-year MACE after PCI.
  • This genetic marker does not appear to be a significant predictor of clinical outcomes in this patient population.

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...
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...
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 V: Interprofessional Care01:27

Coronary Artery Disease V: Interprofessional Care

Interprofessional care for coronary artery disease includes pharmacological therapy and revascularization procedures.Pharmacological therapy for Coronary Artery Disease (CAD) aims to manage symptoms, prevent complications, and improve patient outcomes through various classes of medications:Antiplatelet Agents:Aspirin and Clopidogrel: These medications inhibit platelet aggregation, preventing blood clots, which is crucial for avoiding heart attacks and strokes. Doctors often prescribe these...
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...
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...