Coronary Artery Disease

Coronary artery disease (CAD) resulting in inadequate blood supply to the heart, or ischemia, is a major public health problem. CAD is the leading cause of death in the United States, accounting for 1 of every 4.8 deaths. According to current ACC/AHA estimates there may be as many as 16.5 million stable angina patients in the United States, with 500,000 new diagnoses annually.1,2

Assessment of obstructive CAD begins with an evaluation of a patient’s symptoms, medical history and cardiovascular risk factors. Further non-invasive evaluation may include studies such as Stress Echocardiography, Myocardial Perfusion Imaging (MPI), and/or Computed Tomography Angiography (CTA) to assess the anatomy and function of the heart and its vessels. Despite advances in imaging technology, non-invasive assessment of obstructive CAD continues to be challenging. The complexity of CAD assessment lies not only in the variation of presenting symptoms, but also in the patient’s unique characteristics. Moreover, implementation of standard of care involving non-invasive imaging assessment of CAD is highly variable regarding the type, number, and sequence of tests ordered by physicians.3-5

Developments in the area of genomic medicine have enabled CardioDx to provide cardiologists with a new tool to assess the likelihood of obstructive* CAD in patients with stable chest pain. Recently, scientific research has shown that circulating blood cells respond to the presence of coronary atherosclerotic plaque by altering their gene expression patterns. The development of atherosclerotic plaque is a multi-step process that starts with the deposition of cholesterol and oxidized lipids, leading to plaque formation. Plaque deposition creates an inflammatory stimulus that is recognized by circulating monocytes, which then adhere to the diseased areas in the arterial wall. These cells ingest the oxidized lipids and become foam cells, which are macrophages containing globules of lipid. These cells secrete chemical messengers, which may interact with other circulating cells, altering their gene expression pattern. Such mechanistic considerations of atherogenesis, atherosclerotic progression, and the response to the presence of atherosclerotic disease help to explain how a gene expression test can be developed to effectively assess CAD.

Introducing Corus™ CAD

Ground-breaking work from CardioDx in cardiovascular genomic diagnostics has culminated in the commercial release of Corus CAD, an entirely new way to assess obstructive CAD. Corus CAD is the first and only clinically validated gene expression test that objectively quantifies the likelihood of obstructive CAD in stable chest pain patients. Find more detailed information about Corus CAD here.

 

* Obstructive CAD is defined as at least one atherosclerotic plaque causing ≥50% luminal diameter stenosis in a major coronary artery (≥1.5 mm lumen diameter) as determined by invasive quantitative coronary angiography (QCA).
  1. Lloyd-Jones D, Adams R, Carnethon M, et al. for the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009;119(3):480-486.
  2. Gibbons RJ, Abrams J, Chatterjee K, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on the Management of Patients With Chronic Stable Angina). J Am Coll Cardiol. 2003;41(1):159-168.
  3. Anderson JL. Beyond Framingham: contemporary evolution of individualized coronary heart disease risk assessment. Available at: http://www.medscape.com/infosite/cardiodx/article-2. Accessed on May 19, 2009.
  4. Akosah KO, Schaper A, Cogbill C, Schoenfeld P. Preventing myocardial infarction in the young adult in the first place: how do the National Cholesterol Education Panel III guidelines perform? J Am Coll Cardiol. 2003;41(9):1475-1479.
  5. Lauer MS. Primary prevention of atherosclerotic cardiovascular disease: the high public burden of low individual risk. JAMA. 2007;297(12):1376-1378. Epub 2007 Mar 25.
  6. Libby P, Theroux P. Pathophysiology of coronary artery disease. Circulation. Jun 28 2005;111(25):3481-3488.
  7. Seo D, Wang T, Dressman H, et al. Gene expression phenotypes of atherosclerosis. Arterioscler Thromb Vasc Biol. Oct 2004;24(10):1922-1927.
  8. Tabibiazar R, Wagner RA, Ashley EA, et al. Signature patterns of gene expression in mouse atherosclerosis and their correlation to human coronary disease. Physiol Genomics. Jul 14 2005;22(2):213-226.
  9. Wingrove, J., Daniels, SE, Sehnert, AJ, Tingley, W, Elashoff, MR, Rosenberg, S, Buellesfeld L, Grube, E, Newby, K, Ginsburg, GS, Kraus, WE Correlation of Peripheral Blood Gene Expression with Extent of Coronary Artery Stenosis. Circulation: Cardiovascular Genetics. 1(1):31-38, October 2008.

Last Publication

Circulation: Cardiovascular Genetics Correlation of Peripheral Blood Gene Expression with the Extent of Coronary Artery Stenosis
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