**3. Genetic polymorphisms**

Despite being complex disorders CVDs are preventable. Coronary heart disease, hypertonia, and thrombophilia are some examples of these disorders, that have been shown to develop from a combination of genetic mutations and environmental factors [58, 59]. Fiatal *et al*., [59] reported that the current advances in the genomics of CVDs have created opportunities for the use of predisposition genetic polymorphisms for prevention, diagnosis and treatment in the future. Multiple polymorphisms (**Table 2**) have been identified as contributing factors to CVR, namely: C174G (IL-6 association) [62], methylenetetrahydrofolate reductase (MTHFR) C667T/A1298C (hyperhomocysteinaemia) [131], VII R353Q (coagulation factor VII association) [113], rs247616/rs1968905/rs1270922 (cholesteryl ester transfer protein







**Table 2.**

*Genes controlling the CVR factors.*

(CEPT) - cholesterol metabolism) [132, 133], Angiotensinogen (AGT) M235T (hypertension) [134], G308A (pro-inflammatory) [135], A522T (dyslipidaemia) [136] and rs9939609 (obesity predisposition) [137]. Most of the studies investigating genetic polymorphisms associated with CVD in the past 10 years have been conducted in populations of different ancestry and ethnicity [58, 59]. Identifying populations that are at risk of developing CVDs may assist in developing prevention programs which may reduce disease progression. However, there is a paucity of information about CVR and genetic polymorphisms [59]. The aim of this chapter was thus to review the literature investigating the prevalence of the various CVR factors in relation to their genetic polymorphisms.
