The Inconclusive Results of the Studies on Glycoprotein IIIa Platelet Receptor Gene Polymorphism and Coronary Artery Disease

We thank Dr Koza for his interest in our article entitled ‘‘Relationship between glycoprotein IIIa platelet receptor gene polymorphism and coronary artery disease,’’ addressing the relationship between platelet glycoprotein (GP) IIb/IIIa polymorphism and the prevalence and extent of coronary artery disease (CAD). Considerable attention has been focused on the identification of new risk factors for CAD, including platelet function and genetics, and in particular on the specific mutation of platelet GP IIIa. Several studies have suggested an increased platelet reactivity in patients carrying such a polymorphism and higher cardiovascular risk. However, few studies have investigated the relationship between this polymorphism and CAD by angiography; that was the aim of our study. We disagree with some considerations of Koza and Senocak. First, our population represents a consecutive cohort of patients, and Dr Koza will certainly agree that in public hospitals around the world, acute coronary syndrome (ACS) represents the most common indication for coronary angiography. We understand his point of view concerning the potential mechanisms of ACS; however, he will agree that nowadays the vast majority of patients with ACS undergo angioplasty or surgery, due to the presence of significant coronary stenosis. A similar proportion is observed in elective patients. Therefore, we do not believe that the results would have changed by selecting only elective patients. Our findings of a lack of relationship between platelet IIb/IIIa polymorphism and CAD were then in line with more recent literature. Indeed, different considerations can be performed for the occurrence of myocardial infarction or ACS, where, indeed, pharmacological interaction and platelet hyper-reactivity could have played a more relevant role. However, the risk of cardiovascular events was not an aim of our study, which was not prospectively designed. Moreover, we previously reported that the carriers of the mutated allele did not display an increased platelet baseline reactivity or a different response to direct GP IIb/IIIa antagonists, among 80 patients undergoing percutaneous coronary intervention (PCI). Finally, contrasting with the statement by Koza and Senocak, we do not think that the treatment of a coronary lesion, either by percutaneous coronary intervention or surgery, can be equalized with a normal coronary artery. In fact, those patients already developed significant coronary atherosclerosis and therefore cannot be considered healthy patients.