Related Experiment Video

Updated: May 23, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Platelet glycoprotein IIIA PIA2 polymorphism is associated with ST elevation acute myocardial infarction in young

David Santiago-Germán1, Alfredo Leaños-Miranda, Ethel García-Latorre

  • 1Unidad de Investigación Médica en Trombosis, Hemostasia y Aterogénesis, H.G.R. No 1. Dr. Carlos Mac Gregor Sánchez Navarro Instituto Mexicano del Seguro Social, Mexico, DF, Mexico.

Journal of Thrombosis and Thrombolysis
|April 3, 2012
PubMed

Insights

Genetic variations in platelet glycoprotein GPIIIa (PLA/A2) and plasminogen activator inhibitor (4G/5G) are linked to ST-elevation myocardial infarction (STEMI) in young Mexicans. A synergistic effect between PIA2 and 4G alleles increases STEMI risk.

Area of Science:

  • Cardiovascular Genetics
  • Thrombosis and Hemostasis
  • Molecular Biology

Background:

  • Platelet glycoprotein IIb/IIIa is crucial for platelet adhesion and aggregation.
  • Gene polymorphisms in platelet activation and fibrinolysis pathways are controversially linked to myocardial infarction (MI).
  • The interaction between platelet and fibrinolytic gene polymorphisms in young individuals with ST-elevation acute myocardial infarction (STEMI) remains understudied.

Purpose of the Study:

  • To investigate the frequency distribution of platelet glycoprotein GPIIIa PLA/A2 and plasminogen activator inhibitor (PAI) 4G/5G polymorphisms.
  • To determine the association of these polymorphisms with STEMI in young Mexican patients.
  • To explore the potential synergistic interaction between PIA2 and 4G alleles in STEMI risk.

Main Methods:

  • Case-control study involving 254 young STEMI patients (≤45 years) and 254 age- and gender-matched healthy controls.
  • Genotyping of PIA1/A2 and 4G/5G polymorphisms using Polymerase Chain Reaction (PCR) with restriction endonuclease digestion.
  • Statistical analysis to compare allele frequencies and assess risk association.

Main Results:

  • Significant differences in PIA2 allele distribution between STEMI patients and controls (P=0.001).
  • Increased prevalence of the 4G allele in STEMI patients compared to controls (P=0.001).
  • Carriage of both PIA2 and 4G alleles conferred a significantly increased risk for STEMI (OR=4.3, 95% CI 1.7-6.5).

Conclusions:

  • This study is the first to examine gene polymorphisms in both thrombotic and fibrinolytic pathways in young Mexican STEMI patients.
  • The PIA2 allele and 4G allele are independently associated with increased STEMI risk in this population.
  • A synergistic effect between the PIA2 and 4G alleles may contribute to the risk of STEMI in young Mexican individuals.

More Related Videos

A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene07:00

A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene

Published on: April 1, 2019

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...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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...
Myocarditis II: Clinical Features and Diagnostic Tests01:27

Myocarditis II: Clinical Features and Diagnostic Tests

Myocarditis is an inflammation of the heart muscle. The symptoms vary widely, encompassing asymptomatic presentations to severe, acute manifestations.Clinical PresentationAsymptomatic cases: In some instances, myocarditis may be asymptomatic, with the infection resolving without intervention. These cases often go undetected unless discovered incidentally through diagnostic imaging or tests conducted for other reasons.General Early Symptoms: Early symptoms of myocarditis are non-specific and can...