Current Treatment Options in Cardiovascular Medicine

, Volume 10, Issue 4, pp 294–303

Therapeutic options for premature coronary artery disease


DOI: 10.1007/s11936-008-0050-9

Cite this article as:
Person, A.F. & Patterson, C. Curr Treat Options Cardiovasc Med (2008) 10: 294. doi:10.1007/s11936-008-0050-9

Opinion statement

Although cardiovascular disease is commonly recognized as a disease of the elderly, young patients are also at risk for coronary atherosclerosis, which has a devastating impact on their more active lifestyle. In identifying patients at risk for a cardiovascular event, global risk models often fail to assess family history, an important risk factor in patients with premature coronary artery disease (P-CAD). P-CAD refers to the accelerated development of coronary atherosclerosis before age 55 in men and 65 in women, which may be the result of acquired or primary causes. Acquired P-CAD is associated with an underlying medical condition or influencing factor, such as systemic lupus erythematosus or cocaine use, that directly contributes to the rapid progression of coronary atherosclerosis. It is important to evaluate young patients for acquired P-CAD because in many instances treatment may be tailored to the underlying medical condition. Most cases of P-CAD, however, are the result of primary causes involving more complex interactions among genetic, metabolic, and environmental risk factors. Patients with primary P-CAD usually have a family history of coronary disease, suggesting a strong genetic component. With the use of genome-wide association analysis, several chromosome loci have been identified as being linked to the development of coronary atherosclerosis and risk factors. The chromosome 9p21.3 locus, which is the most replicated to date, has provided some insight into the pathologic mechanism of coronary disease. The confirmation and replication of these associations through further study will lead to earlier detection of P-CAD in at-risk patients and a better understanding of the underlying pathologic mechanisms, thereby influencing the development of preventive therapies.

Copyright information

© Current Medicine Group LLC 2008

Authors and Affiliations

  1. 1.Division of Cardiology and Carolina Cardiovascular Biology CenterThe University of North Carolina at Chapel HillChapel HillUSA