Cardiovascular disease (CVD), including stroke, is the leading cause of illness and death worldwide, and is eminently preventable. Genetic studies have demonstrated that in most cardiovascular conditions, specific inherited polymorphisms can influence the therapeutic response. Moreover, it is apparent that there is considerable interindividual variation in the effectiveness of cardiovascular system drugs. These differences are due to both environmental factors (e.g., salt intake, smoking) and genetic variation. Ultimately, they result in abnormalities in gene expression (over-, under-, zero-, or defective production of an enzyme) that yield phenotypic changes that are of pathological significance in such disorders as hypertension, atherosclerosis, coronary heart disease, myocardial infarction, and arterial stiffness. Molecular genetic studies have also identified defects in ion channels, contractile or structural proteins, and signaling molecules that play a role in disease pathogenesis.

Inherited differences in drug metabolizing enzymes are usually monogenic codomi-nant traits. However, the overall clinical effect of most drugs is influenced by multiple genes involved in the mechanistic pathways of drug absorption, metabolism, disposition, and interaction with the target receptor (1). Therefore, for any given drug, one gene may determine the extent of drug activation, a second may affect drug excretion, and still a third may determine receptor sensitivity. The overall effect of a given drug may thus be influenced by polymorphism in a number of different genes and therefore potentially by individual-specific combinations and permutations of polymorphic alleles.

In the following sections, we review polymorphisms that are thought to play an important role in the treatment of CVD.

Your Heart and Nutrition

Your Heart and Nutrition

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