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Published on: October 12, 2017
The association of homocysteine and coronary artery disease
Gregory M Gauthier1, Jon G Keevil, Patrick E McBride
1Department of Medicine, University of Wisconsin Hospital and Clinics, Madison, Wisconsin 53792, USA. gm.gauthier@hosp.wisc.edu
Insights
High homocysteine levels (hyperhomocysteinemia) are linked to heart disease risk. Folic acid effectively lowers homocysteine, but its impact on preventing heart events requires further study.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Nutritional Science
Background:
- Hyperhomocysteinemia is associated with increased risk of atherosclerosis and myocardial infarction.
- Elevated homocysteine levels can result from genetic factors, nutritional deficiencies, diseases, or medications.
Purpose of the Study:
- To review the biochemistry of homocysteine metabolism.
- To discuss the etiology and pathogenesis of hyperhomocysteinemia.
- To explore the association between hyperhomocysteinemia and coronary artery disease, including screening and treatment options.
Main Methods:
- Literature review of prospective case-control studies.
- Analysis of biochemical pathways and genetic factors.
- Examination of clinical trial data on homocysteine-lowering therapies.
Main Results:
- Hyperhomocysteinemia is a risk factor for cardiovascular events.
- Folic acid and B-complex vitamins effectively reduce homocysteine concentrations.
- The clinical benefit of homocysteine reduction on coronary event risk remains uncertain.
Conclusions:
- Hyperhomocysteinemia is a significant risk factor for cardiovascular disease.
- While effective in lowering homocysteine, the role of folic acid in preventing coronary events needs further investigation.
- Comprehensive understanding of homocysteine metabolism and its clinical implications is crucial for cardiovascular health.
Abstract:
Hyperhomocysteinemia has been associated with increased risk of atherosclerosis and myocardial infarction by a number of prospective case-control studies. A variety of genetic mutations, nutritional deficiencies, disease states, and drugs can elevate homocysteine concentrations. Treatment with folic acid with or without B-complex vitamins effectively lowers homocysteine levels. Whether therapy corresponds with decreased risk of coronary events is unknown, but may be promising. This article reviews the biochemistry of homocysteine metabolism, pathogeneisis, and etiology of hyperhomocysteinemia, along with its association with coronary artery disease, screening, and treatment.
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