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Experimental hyperhomocysteinemia impairs coronary flow velocity reserve
Kazuhito Yamashita1, Hiromi Tasaki, Yoshitaka Nagai
1The 2nd Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Yahatanishi-ku, Kitayushu 807-8555, Japan. wajinn@med.uoeh-u.ac.jp
International Journal of Cardiology
|September 20, 2005
Summary
High homocysteine levels impair coronary flow reserve, a key indicator of heart health. Vitamin C effectively reverses this impairment, suggesting its protective role against homocysteine-induced vascular damage.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Nutritional Science
Background:
- Hyperhomocysteinemia is an independent risk factor for coronary artery disease.
- Endothelial dysfunction is a proposed mechanism linking hyperhomocysteinemia to cardiovascular disease.
- Vitamin C is known to improve endothelial function, but its direct effect on coronary circulation requires investigation.
Purpose of the Study:
- To test the hypothesis that experimentally induced hyperhomocysteinemia impairs coronary flow velocity reserve (CFR).
- To investigate the role of oxidative stress in the deleterious effects of homocysteine on coronary circulation.
- To determine if vitamin C administration can prevent the impairment of CFR by hyperhomocysteinemia.
Main Methods:
- Eleven healthy male volunteers participated in a randomized, placebo-controlled study.
- Coronary flow velocity reserve (CFR) was measured using transthoracic-Doppler echocardiography after adenosine triphosphate infusion.
- Measurements were taken following administration of placebo, methionine, or methionine plus vitamin C.
Main Results:
- Methionine administration significantly increased plasma homocysteine levels and decreased CFR.
- A significant inverse correlation was observed between plasma homocysteine and CFR.
- Vitamin C administration prevented the decrease in CFR despite elevated homocysteine levels.
Conclusions:
- Experimentally induced hyperhomocysteinemia significantly reduces coronary flow velocity reserve.
- Vitamin C administration effectively reverses the detrimental effects of hyperhomocysteinemia on coronary microcirculation.
- Oxidative stress is implicated as a key mediator in homocysteine-induced coronary vascular dysfunction.