The effects of CYP2C9 and VKORC1 gene polymorphisms on warfarin maintenance dose in Turkish cardiac patients.

Aim: Our aim was to examine the effect of CYP2C9 and VKORC1 polymorphisms on warfarin dose requirements in Turkish patients. Materials & methods: 24 warfarin prescribed patients were included and analyzed for eight VKORC1 and 6 CYP2C9 polymorphisms in the study. Results: Patients with CYP2C9 *1/*1 and VKORC1 -1639 GG and GA genotypes required higher warfarin doses in comparison to wild type VKORC1 genotype. Patients with CYP2C9 *1/*3 and VKORC1 -1639 GG genotypes simultaneously, required the lowest dose of warfarin (4.64 mg/day). Patients with CYP2C9 *1/*1 and VKORC1 9041 AA genotype were found to require higher warfarin doses. Conclusion: Our results provide additional evidence to support the hypothesis that CYP2C9 *2, *3, VKORC1 9041 G > A polymorphisms explain considerable proportion of inter-individual variability in warfarin dose requirement.

Postoperative Myocardial Injury Does Not Predict Early and 1-Year Mortality After Living Donor Liver Transplantation.

BACKGROUND: Preoperative cardiac troponin-I (cTnI) elevation has been shown to be a predictor of mortality after liver transplantation. Myocardial injury after non-cardiac surgery (MINS) has been defined as elevation of serum cardiac troponin levels in the perioperative period that does not fulfill the criteria for myocardial infarction. MINS has been shown to be a prognostic factor for in-hospital and long-term mortality, but there is limited data in patients undergoing living-donor liver transplantation (LDLT). In this study, we aimed to evaluate the relationship between MINS and postoperative mortality. MATERIAL AND METHODS: Patients who had undergone adult LDLT at Florence Nightingale Hospital Liver Transplantation Unit between December 2012 and December 2015 were retrospectively analyzed for 30-day in-hospital and 1-year mortality. Myocardial injury was defined as cTnI level above 0.04 ng/mL. Patients (N = 214) were divided into 2 groups according to postoperative cTnI levels. The following were the exclusion criteria: 1. patients under 18 years old, 2. patients undergoing deceased-donor liver transplantation or dual liver-kidney transplantation, 3. cTnI elevation due to other causes (sepsis, renal failure, pulmonary embolism, myocardial infarction), and 4. patients without postoperative troponin levels. RESULTS: MINS occurred in 123 (57.4%) patients after LDLT. There was no difference between the groups according to age, sex, creatinine levels, presence of ischemic heart disease, hypertension, diabetes mellitus, and tobacco use. The presence of MINS did not predict 30-day and 1-year mortality in the study population. CONCLUSION: Myocardial injury detected by serum cTnI elevation was frequent after LDLT; however, it was not associated with 30-day in-hospital and 1-year mortality.

Glycoprotein Ibα Kozak polymorphism in patients presenting with early-onset acute coronary syndrome.

INTRODUCTION: Glycoprotein Ibα (GPIbα) 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 GPIbα and contribute to thrombogenesis. We evaluated the allele frequencies of GPIbα Kozak sequence polymorphism in the Turkish population and examined the relationship between GPIbα 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 GPIbα 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 GPIbα 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.