Abstract 14713: The Impact of AMPD1 Gene Polymorphism on Endothelial Function and Arterial Stiffness in Patients With Coronary Artery Disease
Background: Reduced activity of adenosine monophosphate deaminase (AMPD) may increase production of cardioprotective adenosine. A common point variant of the AMPD1 gene (C34T) results in enzymatic inactivity of AMPD and has been associated with prolonged survival in coronary artery disease (CAD) patients. Measurement of endothelial function and arterial stiffness are well validated in large population studies as strong predictors of adverse cardiovascular outcomes. We examined the impact of C34T AMPD1 polymorphism on endothelial function and arterial stiffness in CAD patients.
Methods: The study included 186 patients with stable CAD, one month after percutaneous coronary intervention. AMPD1 genotyping was performed by real-time polymerase chain reaction. CAD patients were divided in two groups. Group A consisted of patients homozygous for the wild type and group B consisted of patients carrying at least one AMPD1 loss-of-function allele. Endothelial function was evaluated by flow-mediated dilatation (FMD). Augmentation index (AIx) was measured as an index of arterial stiffness. Serum levels of intracellular adhesion molecule-1 (ICAM-1) were measured by ELISA.
Results: Group A included 143 patients (77%) and group B 43 patients (23%). There was no significant difference between group A and B in age (61±11 vs. 61±10 years, p=0.88), the presence of dyslipidemia (72% vs. 69%, p=0.72), diabetes mellitus (25% vs. 32%, p=0.30), arterial hypertension (87% vs. 86%, p=0.92) and smoking habits (smokers: 21% vs. 19%, p=0.32). Interestingly, there was no difference between group A and B in FMD (5.00±2.01% vs. 5.14±2.74%, p=0.72) and AIx (23.98±9.04% vs. 22.23±8.16%, p=0.26). Nevertheless, group B patients had significantly lower levels of ICAM-1 (233.94±77.44ng/ml vs. 286.74±107.44ng/ml, p=0.01).
Conclusions: C34T polymorphism of AMPD1 is not associated with endothelial function and arterial stiffness in CAD patients. Further research is needed to elucidate the impact of this polymorphism in the prognosis of CAD.
- © 2013 by American Heart Association, Inc.