Key result
The frequency of the GPIbα Kozak polymorphism did not differ significantly between patients with early-onset acute coronary syndrome and healthy controls (23% vs 22.5%, p=0.812).
Why the study?
Is the Glycoprotein Ibα Kozak sequence polymorphism associated with an increased risk of early-onset acute coronary syndrome?
Case-Control (n=400)
No
Is the Glycoprotein Ibα Kozak sequence polymorphism associated with an increased risk of early-onset acute coronary syndrome?
The Glycoprotein Ibα Kozak sequence polymorphism is not significantly associated with early-onset ACS overall, but may be more frequent in patients presenting with NSTEMI compared to STEMI.
No association with early-onset ACS overall; hypothesis-generating for borderline NSTEMI link in observational data.
Introduction: Glycoprotein Ib (GPIb) receptor is the chief molecule responsible for initial platelet adhesion to the subendothelium. A thymidine to cytosine single nucleotide substitution at position -5 from the ATG start codon characterizes the Kozak sequence polymorphism. The Kozak sequence polymorphism may increase the surface expression of GPIb and contribute to thrombogenesis. We evaluated the allele frequencies of GPIb Kozak sequence polymorphism in the Turkish population and examined the relationship between GPIb Kozak sequence polymorphism and early-onset acute coronary syndrome (ACS). Material and methods: This study enrolled 200 patients (122 male, 78 female, mean age: 39 5 years) and 200 healthy control subjects (110 male, 90 female, 41 4 years). The patient group was composed of patients admitted to our coronary care unit with early-onset ACS and patients who attended to our cardiology outpatient clinic after hospital discharge with a diagnosis of early-onset ACS. Results: Kozak polymorphism frequencies in patients and control subjects did not differ significantly (23% versus 22.5%, p = 0.812, respectively). In patients who presented with non-ST elevation myocardial infarction (NSTEMI), the frequency of GPIb Kozak polymorphism was borderline significantly higher when compared with patients who presented with ST elevation myocardial infarction (STEMI) (35% vs. 20%, p = 0.05, respectively). Allele frequencies of T and C were calculated to be 0.873 and 0.128. Conclusions: Although the frequency of GPIb Kozak polymorphism did not differ significantly in early-onset ACS patients versus control subjects, Kozak polymorphism frequency was borderline significantly higher in patients who presented with NSTEMI when compared to patients with STEMI.
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Gölcük et al. (2016) conducted a case-control in Early-onset acute coronary syndrome (n=400). GPIbα Kozak sequence polymorphism vs. Healthy controls was evaluated on Frequency of GPIbα Kozak polymorphism (p=0.812). The frequency of the GPIbα Kozak polymorphism did not differ significantly between patients with early-onset acute coronary syndrome and healthy controls (23% vs 22.5%, p=0.812).
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