ABSTRACT
Cardiovascular diseases (CVDs) continue to be the major cause of morbidity and mortality in developed countries [1-3], and so our future understanding of their homeostasis and pathogenesis is an important factor when considering therapy and prevention targets. In this regard, it is well known that CVDs are a paradigm of multifactorial disorders related to genetic and modiable risk factors (Figure 5.1). The inuence of modiable risk factors, such as smoking status, physical activity, and dietary intake, has been clearly established and nowadays, nobody questions the negative effect of tobacco, a sedentary lifestyle, or high-saturated fat diets. However, in clinical practice, it is not uncommon to nd patients with premature CVD without any of these conventional risk factors. These situations are probably because of the inuence of genetic factors, which could lead toward a susceptibility to atherosclerosis. Indeed, it is well known that genetic variations lead to phenotypic variations and that these variations on the key players involved in the process of atherosclerosis lead to changes in cellular response that accelerate, or predispose someone to, the development of CVD. Nowadays, the subject of genetic markers is one of the areas in which our understanding of the development and progression of CVD has been studied in greater depth over the past 10 years [4-6]. However, it is important to note that in our current knowledge about CVD, the role of genetic factors needs to be claried and strengthened, so that they acquire the status they deserve inside of the cardiovascular risk factors.
