The prognostic importance of large artery structure and function in relation to cardiovascular morbidity and
mortality, together with the identification of new genetic risk factors have been two major areas of investigation in recent
years. Carotid intima-media thickness (CIMT), as measured by B-mode ultrasound, is a surrogate marker for
atherosclerosis and can be used to detect an accelerated disease process as well as subclinical disease. However, the
genetic basis for CIMT variation is almost unknown. Cardiovascular genetics has led to numerous clinical studies
generally focused on only one candidate gene and were frequently conducted in subjects with cardiovascular diseases
and/or taking drugs that could affect CIMT.
Pharmacogenetics is the study of the effect of a medication as it relates to single or defined sets of genes. An important
goal of pharmacogenetics in cardiovascular disorders is to integrate the two (drugs plus genes) so that true personalized
therapy can be delivered. In this paper, we will discuss the interaction between genes involved in lipid metabolism and
statin therapy that affects intermediate phenotype (plasma lipid levels) and CIMT in patients with type 2 diabetes.
Keywords: B-mode ultrasound, carotid atherosclerosis, carotid intima-media thickness, epigenetics, gene polymorphisms,
intervention trials, personalized medicine, statins, therapeutic efficacy assessment, type 2 diabetes
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