The total population of this study consisted of 235 Egyptian individuals divided into two groups: 116 unrelated individuals consisting of 90 males and 26 females (mean age 42.4 ± 7.3 years) with documented CAD (PCAD group), age at the time of CAD diagnosis 45 years or less in men and 55 years or less in women, and 119 unrelated control subjects with mean age of 41.9 ± 6.4 years (63 males and 56 females). Therefore, the aim of our study was to investigate the association between CRP gene polymorphism and metabolic syndrome with PCAD in the Egyptian population in Zagazig.
Therefore, its correlation with the pathogenesis of CAD remains unknown. Another study showed that the CRP + 1059 G>C polymorphism was neither associated with future myocardial infarction (MI) and stroke, nor with post-angioplasty restenosis (Zee et al., 2004). This relationship was present in subjects with and without prevalent coronary disease in the Caucasian population (Suk et al., 2005). Prior studies showed that CRP + 1059 G>C polymorphism was associated with plasma concentrations of CRP (Zee and Ridker, 2002). Because the prevalence of MetS is increasing among young adults due to adverse physical activity and dietary patterns (de Ferranti et al., 2004), it is important to quantify its relation with premature CAD. In 2001, the National Cholesterol Educational Program Adult Treatment Panel III (NCEP-ATP-III, 2001) defined the metabolic syndrome as a clustering of 3 or more vascular risk factors, including abdominal obesity, high triglycerides, decrease in high-density lipoprotein cholesterol (HDLc) level, high blood pressure, and high fasting glucose. The presence of metabolic syndrome (MetS) imparts a high risk of development of early-onset premature CAD (PCAD) (Iribarren et al., 2006). Elevated hs-CRP levels may be predictive of the development of the metabolic syndrome (Abdel-Aziz and Mohamed, 2013, Grassi et al., 2009, Haffner, 2006). The interplay between genetic and environmental factors is important in the phenotype development of complex traits as CAD. Several single nucleotide polymorphisms (SNPs) in the CRP gene were reported to be associated with circulating CRP concentrations and/or risk of vascular disease (Carlson et al., 2005). The human CRP gene is located on chromosome 1q21 to 1q23, spanning approximately 1.9 kb and containing two exons. The realization that certain CRP genetic polymorphisms influence blood CRP levels could be of great clinical importance, because genetic predisposition to high baseline CRP might increase the risk of CAD in a significant proportion of people (Montecucco and Mach, 2008, Hingorani et al., 2006, Zebrack et al., 2002). A strong association between high-sensitivity C-reactive protein (hs-CRP) and cardiovascular disease was established in previous studies in healthy subjects and in patients with coronary artery disease (CAD) (Ikonomova, 2004).
Inflammation plays an important role in the initiation and progression of atherosclerosis (Speidl et al., 2002).