Pharmacogenomics in acute coronary syndrome

Abstract

Inheritance of cardiovascular diseases has been the subject of a large number of retrospective candidate gene studies and is now a topic of genome-wide, single-nucleotide-polymorphism investigations using chip-array techniques. The question as to whether or not genetic variants could also influence drug response is much less well investigated, although many factors involved in the etiology of coronary artery disease or acute coronary syndromes may also contribute to the clinical response to drug treatment. Moreover, inter-individual differences in the pharmacokinetics and pharmacodynamics were partly shown to affect the clinical outcome of long-term coronary artery disease treatment. However, except for the prevention of thrombosis by vitamin K antagonists, there is only weak evidence that the short-term treatment of acute coronary syndromes is dependent on any genetic trait. This review focuses on the role of polymorphic platelet aggregation, clotting factors, vascular function, and lipid metabolism and transport. The present picture is complex and many findings could not be reproduced or are often contradictory. In conclusion, statistically well-powered, prospective studies are required considering multiple genetic traits in order to estimate the impact of pharmacogenomics in acute coronary syndrome risk and individualized drug treatment. At present, no data are available that should influence a physicians decision on drug treatment in acute situations. However, for long-term treatment distinct genetic markers may be applied in the future.

Keywords::

• coronary artery disease
• genetic polymorphism
• glycoprotein
• leukocyte adhesion
• myocardial infarction
• thrombocyte aggregation

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