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The Role of Genetic Risk Factors in Coronary Artery Disease

  • Diabetes and Cardiovascular Disease (S Malik, Section Editor)
  • Published:
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Abstract

Genome-wide association studies for coronary artery disease utilizing the case control association study approach has identified 50 genetic risk variants associated with coronary artery disease or myocardial infarction. All of these genetic variants are of genome wide significance and replicated in an independent population. It is of note that 35 of these 50 genetic risk variants act through mechanisms as yet unknown. These findings have great implications for the pathogenesis of atherosclerosis, as well as new targets for the development of novel therapies for the prevention and treatment of CAD. The genetic variant PCSK9 has already led to the development of a monoclonal anti-body which is undergoing assessment in phases I, II, and III clinical trials. This therapy shows very promising results and since it increases removal of LDL-C, it is complementary to current statin therapy. Assessing the beneficial or deleterious effects of a lifelong exposure to a genetic risk variant (Mendelian randomization) will be an important adjunct to clinical trials.

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Acknowledgments

In the preparation of this document, the authors would like to acknowledge the efforts of Peggy Offley and Heather Stevenson.

Robert Roberts has received grant support from CIHR #MOP82810 Canada, CFI # 11966 Canada.

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Conflict of Interest

Sonny Dandona declares that he has no conflict of interest.

Robert Roberts is a consultant to Cumberland Pharmaceuticals.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

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Correspondence to Robert Roberts.

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This article is part of the Topical Collection on Diabetes and Cardiovascular Disease

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Dandona, S., Roberts, R. The Role of Genetic Risk Factors in Coronary Artery Disease. Curr Cardiol Rep 16, 479 (2014). https://doi.org/10.1007/s11886-014-0479-2

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  • DOI: https://doi.org/10.1007/s11886-014-0479-2

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