Impact of PlA2 Polymorphism on Cardiovascular Disease and Outcome after Percutaneous Coronary Intervention: A Review of Current Evidence and Future Perspectives

REVIEW, February 2011, VOL I ISSUE III, ISSN 2042-4884
10.5083/ejcm.20424884.28 , Cite or Link Using DOI
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Roberta De Rosa, MD, Gennaro Galasso, MD, PhD, Guido Iaccarino, MD, PhD, Salvatore Cassese, MD, Raffaele Piccolo, MD, Teresa Strisciuglio, MD & Federico Piscione, MD, PhD

INTRODUCTION

Coronary artery disease (CAD) is a multifactorial disease with the environment and multiple genes implicated in its pathogenesis. Thus, during the last decade several genes involved in the atherosclerotic process and their polymorphisms have been suspected to increase the thrombotic predisposition and to influence the risk for acute coronary syndromes (ACS). It is well-known that platelets play a significant role in the pathogenesis and development of CAD and its clinical manifestations. Therefore, platelet polymorphisms have been extensively studied in order to clarify their contribution to atherothrombotic process and their role in CAD.

Glycoprotein IIb/IIIa receptor and PlA2 polymorphism

The GPIIb/IIIa receptor represents the final common pathway for platelet activation and several studies pointed out the role of this gene polymorphism on the pathogenesis and development of CAD. GPIIb/IIIa receptor is present on platelet membrane as a non-covalent heterodimeric complex, composed of an alpha subunit (GPIIb, also named αIIb) and a beta unit (GPIIIa, also named β3).