Abstract
Coronary artery disease (CAD) and its major complication, myocardial infarction (MI), remain the number one cause of death in industrialized society, causing approximately one in every six deaths in the United States in 2010. Today, it is well established that CAD/MI arises from the interaction of multiple genetic and environmental factors. On a cellular level, atherosclerosis is a complex process characterized by endothelial dysfunction, lipid and matrix accumulation, migration and local transformation of circulating cells, smooth muscle cell (SMC) proliferation, calcification, inflammation, and, finally, thrombus formation. In this scenario, the potential influence of genetically modulated mechanisms may occur at multiple points during the development of the disease. Here, we describe the current knowledge about the underlying genetics of CAD and MI generated over the past 10 years.
| Original language | English |
|---|---|
| Title of host publication | Clinical Cardiogenetics |
| Subtitle of host publication | Third Edition |
| Publisher | Springer International Publishing |
| Pages | 413-430 |
| Number of pages | 18 |
| ISBN (Electronic) | 9783030454579 |
| ISBN (Print) | 9783030454562 |
| DOIs | |
| State | Published - 1 Jan 2020 |
Keywords
- 9p21
- Coronary artery disease
- Genetics
- Genome-wide association study
- Myocardial infarction
- Precision medicine
- Risk prediction
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