Role of 9p21 and 2q36 variants and arterial stiffness in the prediction of coronary artery disease. (August 2014)

• Record Type: Journal Article
• Authors: Vakalis, Konstantinos; Bechlioulis, Aris; Naka, Katerina K.; Chatzikyriakidou, Anthoula; Gartzonika, Konstantina; Vezyraki, Patra; Kolios, Georgios; Pappas, Konstantinos; Katsouras, Christos S.; Georgiou, Ioannis; Michalis, Lampros K.
• Is Part Of: European journal of clinical investigation. Volume 44:Number 8(2014:Aug.)
• Page Start: 784
• Page End: 794
• Publication Date: 2014-08
• Subjects: Pathology -- Periodicals; Medical research -- Periodicals; 616.075
• DOI: 10.1111/eci.12295
• Languages: English
• ISSNs: 0014-2972

Abstract

<abstract abstract-type="main" id="eci12295-abs-0001"> <title>Abstract</title> <sec id="eci12295-sec-0001" sec-type="section"> <title>Background</title> <p>Genetic polymorphisms and arterial stiffness indices have been associated with cardiovascular prognosis and the presence and extent of angiographic coronary artery disease (CAD). We aimed to investigate whether arterial stiffness indices and 9p21 and 2q36 variants may improve prediction of CAD presence and extent when added to classical cardiovascular risk factors in patients at high risk for CAD.</p> </sec> <sec id="eci12295-sec-0002" sec-type="section"> <title>Materials and methods</title> <p>In this cross‐sectional study, we enrolled 183 consecutive patients with suspected stable CAD (age 61 ± 9 years, 134 males) referred for diagnostic coronary angiography. Framingham risk score (FRS) was calculated. Arterial stiffness was assessed by carotid–femoral pulse wave velocity (PWV) and central augmentation index (AIx) using applanation tonometry. Genetic polymorphisms of 9p21 (<italic>rs1333049</italic>) and 2q36 (<italic>rs2943634</italic>) loci were also analysed.</p> </sec> <sec id="eci12295-sec-0003" sec-type="section"> <title>Results</title> <p>Higher FRS and PWV and the presence of <italic>rs2943634</italic> risk allele were independent predictors of CAD (Nagelkerke R<sup>2</sup> 0·252, <italic>P</italic> < 0·001), while higher FRS and the presence of <italic>rs1333049</italic> risk allele were independent predictors of multivessel CAD (Nagelkerke R<sup>2</sup> 0·190, <italic>P</italic> < 0·001). Genetic polymorphisms and vascular indices did not improve the predictive accuracy of FRS‐based models (<italic>P</italic> > 0·1 for all) for CAD presence or extent.</p> </sec> <sec id="eci12295-sec-0004" sec-type="section"> <title>Conclusions</title> <p>In these high‐risk patients, 9p21 and 2q36 variants and PWV were independently associated with CAD presence and extent, but the addition of both genetic data and arterial stiffness indices to FRS did not improve the prediction of CAD compared with FRS alone. Further studies are needed to clarify the prognostic role of genetic and vascular indices in the prediction of angiographic CAD.</p> </sec> </abstract>